ORIGINAL_ARTICLE
Predictive Markers for Hepatocellular Carcinoma Development in Patients with Chronic Hepatitis C Virus Genotype4a
Background: Egypt has the highest prevalence of hepatitis C virus worldwide. Monitoring hepatitis C-infected patients for hepatocellular carcinoma development is an important clinical issue to diagnose these patients during the potentially curable early-stage of disease. This study aims to evaluate the role of N-terminal procollagen III, matrix metalloproteinase- 2, tissue inhibitor of matrix metalloproteinase-1, alpha-fetoprotein, and conventional liver function tests as predictors of hepatocellular carcinoma development upon long-term followup of non-responding hepatitis C virus patients.Methods: The study included 850 treatment-naïve hepatitis C virus genotype 4a adult patients; after treatment, 360 achieved sustained viral response while 490 did not. Nonresponding patients had a 5-year rate for hepatocarcinogenesis of 8.4% and a 10-year rate of 27.5%. N-terminal procollagen III, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase-1, alpha-fetoprotein, and conventional liver function tests were evaluated in all patients before and after treatment, and after hepatocellular carcinoma development. The study also included a group of 50 hepatocellular carcinoma patients who were negative for hepatitis C and hepatitis B viruses, and a group of 50 healthy subjects as controls.Results: The non-responders had significantly higher age, stage, grade, viral load, alanine aminotransferase, and aspartate aminotransferase than responders. Also N-terminal procollagen III, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase-1, and alphafetoprotein were significantly higher in non-responders; after treatment they decreased in responders. In non-responders they remained higher than the control. The most significant risk factors for hepatocellular carcinoma development in non-responding hepatitis C virus patients were male gender and increased age, stage, grade, aspartate aminotransferase, Nterminal procollagen III, and tissue inhibitor of matrix metalloproteinase-1. Patients with viral-hepatocellular carcinoma were of significantly lower age, higher grade, stage, γ-glutamyltransferase, N-terminal procollagen III, and matrix metalloproteinase-2 than non-viral hepatocellular carcinoma patients. Percent positive N-terminal procollagen III, tissue inhibitor of matrix metalloproteinase-1, and alpha-fetoprotein were significantly higher in viral hepatocellular carcinoma patients.Conclusion: Data suggest that high N-terminal procollagen III and tissue inhibitor of matrix metalloproteinase-1levels after treatment might be particularly important as markers of hepatitis C virus-non-responding patients who are at higher risk of developing hepatocellular carcinoma, especially in older males with high stage and grade liver disease. However, studies of larger scale are needed to verify this suggestion.
https://mejc.sums.ac.ir/article_42132_44475e6127acab44db94d125246636c9.pdf
2018-10-01
261
273
10.30476/mejc.2018.42132
Ebtsam
Zaher
ebtsam.zaher@alexu.edu.eg
1
Radiation Sciences Department, Medical Research Institute, Alexandria University, Alexandria, Egypt
LEAD_AUTHOR
Abeer
Ghazal
2
Microbiology Department, Medical Research Institute, Alexandria University, Alexandria, Egypt
AUTHOR
Wael
Ellabban
3
Queen’s Medical Center, Durham, UK
AUTHOR
Mona
El-Deeb
4
Clinical Pathology Department, Medical Research Institute, Alexandria University, Alexandria, Egypt
AUTHOR
Lamyaa
Al-Ghaleed
5
Internal Medicine Department, Medical Research Institute, Alexandria University, Alexandria, Egypt
AUTHOR
Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015;136(5):E359-86.
1
Bosetti C, Levi F, Boffetta P, Lucchini F, Negri E, La Vecchia C. Trends in mortality from hepatocellular carcinoma in Europe, 1980-2004. Hepatology. 2008;48(1):137-45.
2
Alter MJ. Epidemiology of hepatitis C virus infection. World J Gastroenterol. 2007;13(17):2436-41.
3
Ahmad W, Ijaz B, Gull S, Asad S, Khaliq S, Jahan S,et al. A brief review on molecular, genetic and imaging techniques for HCV fibrosis evaluation. Virol J. 2011;8:53.
4
Kamal SM, Nasser IA. Hepatitis C genotype 4: What we know and what we don't yet know. Hepatology. 2008;47(4):1371-83.
5
Madhoun MF, Fazili J, Bright BC, Bader T, Roberts DN, Bronze MS. Hepatitis C prevalence in patients with hepatocellular carcinoma without cirrhosis. Am J Med Sci. 2010;339(2):169-73.
6
El-Serag HB, Kramer JR, Chen GJ, Duan Z, Richardson PA, Davila JA. Effectiveness of AFP and ultrasound tests on hepatocellular carcinoma mortality in HCV-infected patients in the USA. Gut. 2011;60(7):992-7.
7
El-Zanaty F, Way A. Egypt Demographic and Health Survey 2008. Cairo, Egypt: Ministry of Health, El-Zanaty and Associates, and Macro International, 2009.
8
Deuffic-Burban S, Mohamed MK, Larouze B, Carrat F, Valleron AJ. Expected increase in hepatitis C-related mortality in Egypt due to pre-2000 infections. J Hepatol. 2006;44(3):455-61.
9
Zakaria S, Fouad R, Shaker O, Zaki S, Hashem A, El-Kamary SS, et al. Changing patterns of acute viral hepatitis at a major urban referral center in Egypt. Clin Infect Dis. 2007;44(4):e30-6.
10
Kamal SM, Nasser IA. Hepatitis C genotype 4: What we know and what we don't yet know. Hepatology. 2008;47(4):1371-83.
11
Roulot D, Bourcier V, Grando V, Deny P, Baazia Y, Fontaine H, et al. Epidemiological characteristics and response to peginterferon plus ribavirin treatment of hepatitis C virus genotype 4 infection. J Viral Hepat. 2007;14(7):460-7.
12
Ghany MG, Strader DB, Thomas DL, Seeff LB; American Association for the Study of Liver Diseases. Diagnosis, management, and treatment of hepatitis C: an update. Hepatology. 2009;49(4):1335-74.
13
Kamal SM, El Kamary SS, Shardell MD, Hashem M, Ahmed IN, Muhammadi M, et al. Pegylated interferon alpha-2b plus ribavirin in patients with genotype 4 chronic hepatitis C: The role of rapid and early virologic response. Hepatology. 2007;46(6):1732-40.
14
Alfaleh FZ, Hadad Q, Khuroo MS, Aljumah A, Algamedi A, Alashgar H, et al. Peginterferon alpha-2b plus ribavirin compared with interferon alpha-2b plus ribavirin for initial treatment of chronic hepatitis C in Saudi patients commonly infected with genotype 4. Liver Int. 2004;24(6):568-74.
15
Dimitroulopoulos D, Elefsiniotis I, Pavlidis C, Xinopoulos D, Tsamakidis K, Patsavela S, et al. European vs. Egyptian HCV-4 patients with elevated baseline HCV RNA, treated with PEG-IFN-α2a and ribavirin: the role of rapid and early virologic response. Hepat Mon. 2010;10(3):193-8.
16
Santantonio T, Medda E, Ferrari C, Fabris P, Cariti G, Massari M, et al. Risk factors and outcome among a large patient cohort with community-acquired acute hepatitis C in Italy. Clin Infect Dis. 2006;43(9):1154-9.
17
Ahmad W, Ijaz B, Javed FT, Kausar H, Sarwar MT, Gull S, et al. HCV genotype-specific correlation with serum markers: higher predictability for genotype 4a.Virol J.2011;8:293.
18
Kasahara A, Hayashi N, Mochizuki K, Oshita M, Katayama K, Kato M, et al. Circulating matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-1 as serum markers of fibrosis in patients with chronic hepatitis C. Relationship to interferon response. J Hepatol. 1997;26(3):574-83.
19
De Giorgi V, Monaco A, Worchech A, Tornesello M, Izzo F, Buonaguro L, et al. Gene profiling, biomarkers and pathways characterizing HCV-related hepatocellular carcinoma. J Transl Med. 2009;7:85.
20
Daniele B, Bencivenga A, Megna AS, Tinessa V. Alpha-fetoprotein and ultrasonography screening for hepatocellular carcinoma. Gastroenterology. 2004;127(5 Suppl 1):S108-12.
21
Bruno S, Di Marco V, Iavarone M, Roffi L, Crosignani A, Calvaruso V, et al. Survival of patients with HCV cirrhosis and sustained virologic response is similar to the general population. J Hepatol. 2016;64(6):1217-23.
22
Hirakawa M, Ikeda K, Arase Y, Kawamura Y, Yatsuji H, Hosaka T, et al. Hepatocarcinogenesis following HCV RNA eradication by interferon in chronic hepatitis patients. Intern Med. 2008;47(19):1637-43.
23
Ikeda K, Arase Y, Saitoh S, Kobayashi M, Someya T, Hosaka T, et al. Prediction model of hepatocarcinogenesis for patients with hepatitis C virus-related cirrhosis. Validation with internal and external cohorts. J Hepatol. 2006;44(6):1089-97.
24
Carloni V, Luong TV, Rombouts K. Hepatic stellate cells and extracellular matrix in hepatocellular carcinoma: more complicated than ever. Liver Int. 2014;34(6):834-43.
25
Banerjee A, Ray RB, Ray R. Oncogenic potential of hepatitis C virus proteins. Viruses. 2010;2(9):2108-33.
26
Hassan M, Selimovic D, Ghozlan H, Abdel-kader O. Hepatitis C virus core protein triggers hepatic angiogenesis by a mechanism including multiple pathways. Hepatology. 2009;49(5):1469-82.
27
Nakajima T, Nakashima T, Yamaoka J, Shibuya A, Konishi E, Okada Y, et al. Greater age and hepatocellular aging are independent risk factors for hepatocellular carcinoma arising from non-B non-C non-alcoholic chronic liver disease. Pathol Int. 2011;61(10):572-6.
28
Tanaka N, Moriya K, Kiyosawa K, Koike K, Gonzalez FJ, Aoyama T. PPARalpha activation is essential for HCV core protein-induced hepatic steatosis and hepatocellular carcinoma in mice. J Clin Invest. 2008;118(2):683-94.
29
Liang TJ, Heller T. Pathogenesis of hepatitis C-associated hepatocellular carcinoma. Gastroenterology. 2004;127(5 Suppl 1):S62-71.
30
Laurent-Puig P, Legoix P, Bluteau O, Belghiti J, Franco D, Binot F, et al. Genetic alterations associated with hepatocellular carcinomas define distinct pathways of hepatocarcinogenesis. Gastroenterology. 2001;120(7):1763-73.
31
Grando-Lemaire V, Guettier C, Chevret S, Beaugrand M, Trinchet JC. Hepatocellular carcinoma without cirrhosis in the West: epidemiological factors and histopathology of the non-tumorous liver. Groupe d'Etude et de Traitement du Carcinome Hépatocellulaire. J Hepatol. 1999;31(3):508-13.
32
Fattovich G, Stroffolini T, Zagni I, Donato F. Hepatocellular carcinoma in cirrhosis: incidence and risk factors. Gastroenterology. 2004;127(5 Suppl 1):S35-50.
33
Friedman SL. Mechanisms of hepatic fibrogenesis. Gastroenterology. 2008;134(6):1655-69.
34
Plebani M, Basso D. Non-invasive assessment of chronic liver and gastric diseases. Clin Chim Acta. 2007;381(1):39-49.
35
Valva P, Casciato P, Diaz Carrasco JM, Gadano A, Galdame O, Galoppo MC, et al. The role of serum biomarkers in predicting fibrosis progression in pediatric and adult hepatitis C virus chronic infection. PLoS One. 2011;6(8):e23218.
36
Osaki Y, Ueda Y, Marusawa H, Nakajima J, Kimura T, Kita R, et al. Decrease in alpha-fetoprotein levels predicts reduced incidence of hepatocellular carcinoma in patients with hepatitis C virus infection receiving interferon therapy: a single center study. J Gastroenterol. 2012;47(4):444-51.
37
ORIGINAL_ARTICLE
Identification of Three BRCA1/2 Mutations and a Study of the Likelihood of an Association with Certain Characteristics in Syrian Familial Breast Cancer Patients
Background: The main goal of the present study was to investigate BRCA1 and BRCA2 mutations in a number of Syrian familial breast cancer cases. We included 50 early onset invasive breast cancer patients from different Syrian families (48 females and 2 males) and 20 healthy women (control group) in the study. All participants were matched for age (28 to 49 years). There were 64% of breast cancer patients who had a significant family history of breast cancer.Methods: DNA was isolated from blood samples and we performed polymerase chain reaction on the isolated DNA to amplify specific target regions (hotspots): exon 2 of the BRCA1 gene and exon 11 of the BRCA2 gene. Polymerase chain reaction products were then sequenced to investigate possible genetic variations that could be present in the examined regions.Results: The sequenced polymerase chain reaction products revealed 3 point mutations that included two deletions and one substitution. An exon 2 mutation was found in 2% of the breast cancer patients. Mutations of exon 11 were each found in 4% of the patient group. We detected no founder mutations. The detected exon 2 mutation was previously mentioned by other researchers and classified as a harmful mutation.Conclusion: To the best of our knowledge, the detected mutations in exon 11 of the BRCA2 gene were not previously identified. A significant association existed between those mutations and the triple negative subtype of breast cancer in Syrian familial breast cancer patients.
https://mejc.sums.ac.ir/article_42135_8a067eb4789738327e89aae8f73fb5bb.pdf
2018-10-01
274
281
10.30476/mejc.2018.42135
Husam
Khalil
husam.khalil86@gmail.com
1
Department of Biochemistry and Microbiology, Faculty of Pharmacy, Damascus University, Damascus, Syria
LEAD_AUTHOR
Fawza
Monem
fawzamonem@hotmail.com
2
Department of Biochemistry and Microbiology, Faculty of Pharmacy, Damascus University, Damascus, Syria
AUTHOR
Faizeh
Al-Quobaili
faizehalquobaili@gmail.com
3
Department of Biochemistry and Microbiology, Faculty of Pharmacy, Damascus University, Damascus, Syria
AUTHOR
1.Bensam M, Hafez E, Awad D, El-Saadani M, Balbaa M. Detection of new point mutations of BRCA1 and BRCA2 in breast cancer patients. Biochem Genet. 2013;52(1-2):15-28.
1
2. ParkinDM, BrayF, FerlayJ, PisaniP. Global cancer statistics, 2002. CA Cancer J Clin. 2005;55(2):74-108.
2
3. Rapid Assessment of Cancer Management Care in Syria. A report by WHO Syria Office in coordination with WHO Headquarters, WHO Regional Office and the National Committee for Cancer Care. Syria: Ministry of Health; 2016. Available from: http://www.moh.gov.sy/Default.aspx?tabid=565&language=ar-YE. [Accessed date: July 2017].
3
4. Barlow-Stewart, K; Emery, J; Metcalfe, S; Dunlop, K; Kirk, J; Tucker, K. Genetics in family medicine: The Australian Handbook for General Practitioners. In: Barlow-Stewart, K; Emery, J; Metcalfe, S, editors. Australia: The Australian Government Agency Biotechnology, Australia; 2007. Chapter 4, Cancer in the family.p. 1-23.
4
5. Branković-Magić M, Dobricić J, Krivokuća A. Genetics of breast cancer: contribution of BRCA1/2 genes alterations to hereditary predisposition. Vojnosanit Pregl. 2012;69(8):700-6.
5
6. Lin PH, Kuo WH, Huang AC, Lu YS, Lin CH, Kuo SH, et al. Multiple gene sequencing for risk assessment in patients with early-onset or familial breast cancer.Oncotarget. 2016;7(7):8310-20.
6
7. Walsh T, King MC. Ten genes for inherited breast cancer. Cancer Cell. 2007;11(2):103-5.
7
8. McClellan J, King MC. Genetic heterogeneity in human disease. Cell. 2010;141(2):210-7.
8
9. Metcalfe KA, Lubinski J, Gronwald J, Huzarski T, McCuaig J, Lynch HT, et al. The risk of breast cancer in BRCA1 and BRCA2 mutation carriers without a first-degree relative with breast cancer. Clin Genet. 2017; [Epub ahead of print].
9
10. Pinsky LE, Culver JB, Hull J, Levy-Lahad E, Daly M, Burke W. Why should primary care physicians know about breast cancer genetics? West J Med. 2001;175(3):168-73.
10
11. Karami F, Mehdipour P. A comprehensive focus on global spectrum of BRCA1 and BRCA2 mutations in breast cancer. Biomed Res Int. 2013;2013:928562.
11
12. Narod SA, Foulkes WD. BRCA1 and BRCA2: 1994 and beyond. Nat Rev Cancer. 2004;4(9):665-76.
12
13. Lindor NM, McMaster ML, Lindor CJ, Greene MH; National Cancer Institute, Division of Cancer Prevention, et al. Concise handbook of familial cancer susceptibility syndromes - second edition.J Natl Cancer Inst Monogr.2008;(38):1-93.
13
14. Ferla R, Calò V, Cascio S, Rinaldi G, Badalamenti G, Carreca I, et al. Founder mutations in BRCA1 and BRCA2 genes. Ann Oncol. 2007;18 Suppl 6:vi93-8.
14
15. Simard J, Tonin P, Durocher F, Morgan K, Rommens J, Gingras S, et al. Common origins of BRCA1 mutations in Canadian breast and ovarian cancer families. Nat Genet. 1994;8(4):392-8.
15
16. Oddoux C, Struewing JP, Clayton CM, Neuhausen S, Brody LC, Kaback M, et al. The carrier frequency of the BRCA2 6174delT mutation among Ashkenazi Jewish individuals is approximately 1%. Nat Genet. 1996;14(2):188-90.
16
17. Brankovic-Magic M, Dobricic J, Jankovic R, Konstantopoulou I, Yannoukakos D, Radulovic S. Identifying and testing for hereditary susceptibility to breast/ovarian cancer in Serbia: Where are we now? Arch Oncol. 2006;14(3-4):131-5.
17
18. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92(14):1126-35.
18
19. Onitilo AA, Engel JM, Greenlee RT, Mukesh BN. Breast cancer subtypes based on ER/PR and Her2 expression: comparison of clinicopathologic features and survival. Clin Med Res. 2009;7(1-2):4-13.
19
20. Anagha PP, Sen S. The efficacy of bisphosphonates in preventing aromatase inhibitor induced bone loss for postmenopausal women with early breast cancer: a systematic review and meta-analysis. J Oncol. 2014;2014:625060.
20
21. Foulkes WD, Smith IE, Reis-Filho JS. Triple-negative breast cancer. N Engl J Med. 2010;363(20):1938-48.
21
22. Liedtke C, Mazouni C, Hess KR, André F, Tordai A, Mejia JA, et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. J Clin Oncol. 2008;26(8):1275-81.
22
23. Couch FJ, Hart SN, Sharma P, Toland AE, Wang X, Miron P, et al. Inherited mutations in 17 breast cancer susceptibility genes among a large triple-negative breast cancer cohort unselected for family history of breast cancer. J Clin Oncol. 2015;33(4):304-11.
23
24. Lang GT, Shi JX, Hu X, Zhang CH, Shan L, Song CG, et al. The spectrum of BRCA mutations and characteristics of BRCA-associated breast cancers in China: Screening of 2,991 patients and 1,043 controls by next-generation sequencing. Int J Cancer. 2017;141(1):129-142.
24
25. Dobricić J, Branković-Magić M, Filipović S, Radulović S. Novel BRCA1/2 mutations in Serbian breast and breast-ovarian cancer patients with hereditary predisposition. Cancer Genet Cytogenet. 2010;202(1):27-32.
25
26. Sweet K, Senter L, Pilarski R, Wei L, Toland AE. Characterization of BRCA1 ring finger variants of uncertain significance. Breast Cancer Res Treat. 2010;119(3):737-43.
26
27. Tavtigian SV, Byrnes GB, Goldgar DE, Thomas A. Classification of rare missense substitutions, using risk surfaces, with genetic- and molecular-epidemiology applications. Hum Mutat. 2008;29(11):1342-54.
27
28. Yeh J, Chun J, Schwartz S, Wang A, Kern E, Guth AA, et al. Clinical characteristics in patients with triple negative breast cancer. Int J Breast Cancer. 2017;2017:1796145.
28
29. Luporsi E, Bronner M, Lesur A, Saint-Dizier D, Sokolowska J, Mansuy L, et al. Characteristics of the BRCA mutation profile of a population of patients with triple negative breast cancer. Cancer Res. 2013;73(24):2-12.
29
30. de Juan Jiménez I, García Casado Z, Palanca Suela S, Esteban Cardeñosa E, López Guerrero JA, Segura Huerta Á, et al. Novel and recurrent BRCA1/BRCA2 mutations in early onset and familial breast and ovarian cancer detected in the Program of Genetic Counseling in Cancer of Valencian Community (eastern Spain). Relationship of family phenotypes with mutation prevalence. Fam Cancer. 2013;12(4):767-77.
30
1.Bensam M, Hafez E, Awad D, El-Saadani M, Balbaa M. Detection of new point mutations of BRCA1 and BRCA2 in breast cancer patients. Biochem Genet. 2013;52(1-2):15-28.
31
2. ParkinDM, BrayF, FerlayJ, PisaniP. Global cancer statistics, 2002. CA Cancer J Clin. 2005;55(2):74-108.
32
3. Rapid Assessment of Cancer Management Care in Syria. A report by WHO Syria Office in coordination with WHO Headquarters, WHO Regional Office and the National Committee for Cancer Care. Syria: Ministry of Health; 2016. Available from: http://www.moh.gov.sy/Default.aspx?tabid=565&language=ar-YE. [Accessed date: July 2017].
33
4. Barlow-Stewart, K; Emery, J; Metcalfe, S; Dunlop, K; Kirk, J; Tucker, K. Genetics in family medicine: The Australian Handbook for General Practitioners. In: Barlow-Stewart, K; Emery, J; Metcalfe, S, editors. Australia: The Australian Government Agency Biotechnology, Australia; 2007. Chapter 4, Cancer in the family.p. 1-23.
34
5. Branković-Magić M, Dobricić J, Krivokuća A. Genetics of breast cancer: contribution of BRCA1/2 genes alterations to hereditary predisposition. Vojnosanit Pregl. 2012;69(8):700-6.
35
6. Lin PH, Kuo WH, Huang AC, Lu YS, Lin CH, Kuo SH, et al. Multiple gene sequencing for risk assessment in patients with early-onset or familial breast cancer.Oncotarget. 2016;7(7):8310-20.
36
7. Walsh T, King MC. Ten genes for inherited breast cancer. Cancer Cell. 2007;11(2):103-5.
37
8. McClellan J, King MC. Genetic heterogeneity in human disease. Cell. 2010;141(2):210-7.
38
9. Metcalfe KA, Lubinski J, Gronwald J, Huzarski T, McCuaig J, Lynch HT, et al. The risk of breast cancer in BRCA1 and BRCA2 mutation carriers without a first-degree relative with breast cancer. Clin Genet. 2017; [Epub ahead of print].
39
10. Pinsky LE, Culver JB, Hull J, Levy-Lahad E, Daly M, Burke W. Why should primary care physicians know about breast cancer genetics? West J Med. 2001;175(3):168-73.
40
11. Karami F, Mehdipour P. A comprehensive focus on global spectrum of BRCA1 and BRCA2 mutations in breast cancer. Biomed Res Int. 2013;2013:928562.
41
12. Narod SA, Foulkes WD. BRCA1 and BRCA2: 1994 and beyond. Nat Rev Cancer. 2004;4(9):665-76.
42
13. Lindor NM, McMaster ML, Lindor CJ, Greene MH; National Cancer Institute, Division of Cancer Prevention, et al. Concise handbook of familial cancer susceptibility syndromes - second edition.J Natl Cancer Inst Monogr.2008;(38):1-93.
43
14. Ferla R, Calò V, Cascio S, Rinaldi G, Badalamenti G, Carreca I, et al. Founder mutations in BRCA1 and BRCA2 genes. Ann Oncol. 2007;18 Suppl 6:vi93-8.
44
15. Simard J, Tonin P, Durocher F, Morgan K, Rommens J, Gingras S, et al. Common origins of BRCA1 mutations in Canadian breast and ovarian cancer families. Nat Genet. 1994;8(4):392-8.
45
16. Oddoux C, Struewing JP, Clayton CM, Neuhausen S, Brody LC, Kaback M, et al. The carrier frequency of the BRCA2 6174delT mutation among Ashkenazi Jewish individuals is approximately 1%. Nat Genet. 1996;14(2):188-90.
46
17. Brankovic-Magic M, Dobricic J, Jankovic R, Konstantopoulou I, Yannoukakos D, Radulovic S. Identifying and testing for hereditary susceptibility to breast/ovarian cancer in Serbia: Where are we now? Arch Oncol. 2006;14(3-4):131-5.
47
18. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92(14):1126-35.
48
19. Onitilo AA, Engel JM, Greenlee RT, Mukesh BN. Breast cancer subtypes based on ER/PR and Her2 expression: comparison of clinicopathologic features and survival. Clin Med Res. 2009;7(1-2):4-13.
49
20. Anagha PP, Sen S. The efficacy of bisphosphonates in preventing aromatase inhibitor induced bone loss for postmenopausal women with early breast cancer: a systematic review and meta-analysis. J Oncol. 2014;2014:625060.
50
21. Foulkes WD, Smith IE, Reis-Filho JS. Triple-negative breast cancer. N Engl J Med. 2010;363(20):1938-48.
51
22. Liedtke C, Mazouni C, Hess KR, André F, Tordai A, Mejia JA, et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. J Clin Oncol. 2008;26(8):1275-81.
52
23. Couch FJ, Hart SN, Sharma P, Toland AE, Wang X, Miron P, et al. Inherited mutations in 17 breast cancer susceptibility genes among a large triple-negative breast cancer cohort unselected for family history of breast cancer. J Clin Oncol. 2015;33(4):304-11.
53
24. Lang GT, Shi JX, Hu X, Zhang CH, Shan L, Song CG, et al. The spectrum of BRCA mutations and characteristics of BRCA-associated breast cancers in China: Screening of 2,991 patients and 1,043 controls by next-generation sequencing. Int J Cancer. 2017;141(1):129-142.
54
25. Dobricić J, Branković-Magić M, Filipović S, Radulović S. Novel BRCA1/2 mutations in Serbian breast and breast-ovarian cancer patients with hereditary predisposition. Cancer Genet Cytogenet. 2010;202(1):27-32.
55
26. Sweet K, Senter L, Pilarski R, Wei L, Toland AE. Characterization of BRCA1 ring finger variants of uncertain significance. Breast Cancer Res Treat. 2010;119(3):737-43.
56
27. Tavtigian SV, Byrnes GB, Goldgar DE, Thomas A. Classification of rare missense substitutions, using risk surfaces, with genetic- and molecular-epidemiology applications. Hum Mutat. 2008;29(11):1342-54. 28. Yeh J, Chun J, Schwartz S, Wang A, Kern E, Guth AA, et al. Clinical characteristics in patients with triple negative breast cancer. Int J Breast Cancer. 2017;2017:1796145.
57
29. Luporsi E, Bronner M, Lesur A, Saint-Dizier D, Sokolowska J, Mansuy L, et al. Characteristics of the BRCA mutation profile of a population of patients with triple negative breast cancer. Cancer Res. 2013;73(24):2-12.
58
30. de Juan Jiménez I, García Casado Z, Palanca Suela S, Esteban Cardeñosa E, López Guerrero JA, Segura Huerta Á, et al. Novel and recurrent BRCA1/BRCA2 mutations in early onset and familial breast and ovarian cancer detected in the Program of Genetic Counseling in Cancer of Valencian Community (eastern Spain). Relationship of family phenotypes with mutation prevalence. Fam Cancer. 2013;12(4):767-77.
59
ORIGINAL_ARTICLE
Prognostic Factors of Anaplastic Thyroid Carcinoma: An Egyptian Single Institution Experience
Background: Anaplastic thyroid carcinoma is an extremely aggressive cancer that has a very poor outcome. We have analyzed predictive factors for overall survival and different therapeutic modalities that could help to determine the optimal therapy for this carcinoma.Methods: We performed a retrospective analysis of data from 54 cases of anaplastic thyroid carcinoma to evaluate demographic, pathological, and clinical characteristics, along with therapeutic modalities that affected survival. The Kaplan-Meier curve was used to visualize the cumulative probability of survival and comparison among/between groups was performed with the log-rank test. A multivariate Cox proportional hazards model was used to examine overall survival.Results: We observed overall survival percentages of 50% (one-year), 25% (2- year), and 5.6% (5-year). The 2-year overall survival was 41.7% for stage IVA, 31.5% for stage IVB, and 7.4% for stage IVC (P= 0.04). The 2-year overall survival rates were 59.3% for patients with negative margins, 30.1% for those with positive margins, and 0.0% in the group without thyroidectomy (P=0.005). Surgery plus postoperative radiotherapy indicated better 2-year overall survival (56%) compared to surgery alone (34.7%, Pone month, no reported metastasis at presentation, negative surgical margins, surgery, radiotherapy, and/or chemotherapy.Conclusion: Anaplastic thyroid carcinoma is an aggressive cancer with a very poor prognosis. Multimodality treatment may improve overall survival in these patients. Duration of symptoms, primary tumor size, distant metastases, surgical treatment, surgical margin status, radiotherapy, and chemotherapy are independent factors that affect prognosis.
https://mejc.sums.ac.ir/article_42137_ebae6d1066ef5240cadc3ee59a276be9.pdf
2018-10-01
282
287
10.30476/mejc.2018.42137
Rasha
Hamed
rashahamdy532@yahoo.com
1
Clinical Oncology and Nuclear Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
LEAD_AUTHOR
Hanem
Sakr
hanemsakr@mans.edu.eg
2
Clinical Oncology and Nuclear Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
AUTHOR
Ahmed
Lotfy
ahmedlotfy@mans.edu.eg
3
General Surgery Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
AUTHOR
1. Are C, Shaha AR. Anaplastic thyroid carcinoma: biology, pathogenesis, prognostic factors, and treatment approaches. Ann Surg Oncol. 2006;13(4):453-64
1
2. Smallridge RC, Copland JA. Anaplastic thyroid carcinoma: pathogenesis and emerging therapies. Clin Oncol (R Coll Radiol). 2010;22(6):486-97.
2
3. Ranganath R, Shah MA, Shah AR. Anaplastic thyroid cancer. Curr Opin Endocrinol Diabetes Obes. 2015;22(5):387-91.
3
4. Chen J, Tward JD, Shrieve DC, Hitchcock YJ. Surgery and radiotherapy improves survival in patients with anaplastic thyroid carcinoma: analysis of the surveillance, epidemiology, and end results 1983-2002. Am J Clin Oncol. 2008;31(5):460-4.
4
5. Kim TY, Kim KW, Jung TS, Kim JM, Kim SW, Chung KW, et al. Prognostic factors for Korean patients with anaplastic thyroid carcinoma. Head Neck. 2007;29(8):765-72.
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6. Sugitani I, Miyauchi A, Sugino K, Okamoto T, Yoshida A, Suzuki S. Prognostic factors and treatment outcomes for anaplastic thyroid carcinoma: ATC Research Consortium of Japan cohort study of 677 patients. World J Surg. 2012;36(6):1247-54.
6
7. Mohebati A, Dilorenzo M, Palmer F, Patel SG, Pfister D, Lee N, et al. Anaplastic thyroid carcinoma: a 25-year single-institution experience. Ann Surg Oncol. 2014;21(5):1665-70.
7
8. Tennvall J, Lundell G, Wahlberg P, Bergenfelz A, Grimelius L, Akerman M, et al. Anaplastic thyroid carcinoma: three protocols combining doxorubicin, hyperfractionated radiotherapy and surgery. Br J Cancer. 2002;86(12):1848-53.
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9. Haigh PI. Anaplastic thyroid carcinoma. Curr Treat Options Oncol. 2000;1(4):353-7.
9
10. Ain KB, Egorin MJ, DeSimone PA. Treatment of anaplastic thyroid carcinoma with paclitaxel: phase 2 trial using ninety-six-hour infusion. Collaborative Anaplastic Thyroid Cancer Health Intervention Trials (CATCHIT) Group. Thyroid. 2000;10(7):587-94.
10
11. Akaishi J, Sugino K, Kitagawa W, Nagahama M, Kameyama K, Shimizu K, et al. Prognostic factors and treatment outcomes of 100 cases of anaplastic thyroid carcinoma. Thyroid. 2011;21(11):1183-9.
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12. Ruhstaller T, Roe H, Thürlimann B, Nicoll JJ. The multidisciplinary meeting: An indispensable aid to communication between different specialities. Eur J Cancer. 2006;42(15):2459-62.
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13. Kebebew E, Greenspan FS, Clark OH, Woeber KA, McMillan A. Anaplastic thyroid carcinoma. Treatment outcome and prognostic factors. Cancer. 2005;103(7):1330-5.
13
14. Stavas MJ, Shinohara ET, Attia A, Ning MS, Friedman JM, Cmelak AJ. Short course high dose radiotherapy in the treatment of anaplastic thyroid carcinoma. J Thyroid Res. 2014;2014:764281.
14
15. Liu TR, Xiao ZW, Xu HN, Long Z, Wei FQ, Zhuang SM, et al. Treatment and prognosis of anaplastic thyroid carcinoma: A clinical study of 50 cases. PLoS One. 2016;11(10):e0164840.
15
16. Polistena A, Monacelli M, Lucchini R, Triola R, Conti C, Avenia S, et al. The role of surgery in the treatment of thyroid anaplastic carcinoma in the elderly. Int J Surg. 2014;12 Suppl 2:S170-S176.
16
17. Lee DY, Won JK, Lee SH, Park DJ, Jung KC, Sung MW, et al. Changes of clinicopathologic characteristics and survival outcomes of anaplastic and poorly differentiated thyroid carcinoma. Thyroid. 2016;26(3):404-13.
17
18.Sugitani I, Miyauchi A, Sugino K, Okamoto T, Yoshida A, Suzuki S. Prognostic factors and treatment outcomes for anaplastic thyroid carcinoma: ATC Research Consortium of Japan cohort study of 677 patients. World J Surg. 2012;36(6):1247-54.
18
19. Yau T, Lo CY, Epstein RJ, Lam AK, Wan KY, Lang BH. Treatment outcomes in anaplastic thyroid carcinoma: survival improvement in young patients with localized disease treated by combination of surgery and radiotherapy. Ann Surg Oncol. 2008;15(9):2500-5.
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20. Glaser SM, Mandish SF, Gill BS, Balasubramani GK, Clump DA, Beriwal S. Anaplastic thyroid cancer: Prognostic factors, patterns of care, and overall survival. Head Neck. 2016;38 Suppl 1:E2083-90.
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21. Smallridge RC. Approach to the patient with anaplastic thyroid carcinoma. J Clin Endocrinol Metab. 2012;97(8):2566-72.
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22. Pushkarev VM, Starenki DV, Saenko VA, Pushkarev VV, Kovzun OI, Tronko MD, et al. Differential effects of low and high doses of Taxol in anaplastic thyroid cancer cells: possible implication of the Pin1 prolyl isomerase. Exp Oncol. 2008;30(3):190-4.
22
23. Sun C, Li Q, Hu Z, He J, Li C, Li G, et al. Treatment and prognosis of anaplastic thyroid carcinoma: experience from a single institution in China. PLoS One. 2013;8(11):e80011.
23
ORIGINAL_ARTICLE
An Immunohistochemical Study of Vascular Endothelial Growth Factor Expression in Meningioma and Its Correlation with Tumor Grade
Background: Meningiomas are one of the most common primary brain tumors and the most common intradural spinal tumors. Vascular endothelial growth factor has been demonstrated to play an important role in the stimulation of angiogenesis in many types of cancers. Agents that block the vascular endothelial growth factor pathway, such as bevacizumab, have the capability to decrease vascular permeability. The aim of this study is to evaluate vascular endothelial growth factor expression in meningioma patients.Methods: This retrospective, cross-sectional study used an immunohistochemical method to assess vascular endothelial growth factor expression in meningioma. We randomly chose 83 paraffin-embedded tissue blocks of meningiomas diagnosed during 2015 from the files of the Pathology Laboratory of Al-Zahra Hospital, affiliated with Isfahan University of Medical Sciences, Iran.Results: All of the meningioma samples (100%) were vascular endothelial growth factor-immunoreactive. There was a vascular endothelial growth factor score of 1 in 6 (7.2%) cases, a score of 2 in 54 (65.1%) cases, and score of 3 in 23 (27.7%) cases. A correlation existed between vascular endothelial growth factor score and tumor grade. However, there was no correlation between vascular endothelial growth factor score and age and sex of patients.Conclusion: Our study demonstrated a significant role of vascular endothelial growth factor expression in the pathogenesis of peritumoral brain edema in low- and high-grade meningiomas as well as in recurrence or malignant transformation. Thus, anti-vascular endothelial growth factor agents such as bevacizumab might be useful as a treatment of this condition.
https://mejc.sums.ac.ir/article_42139_50bbe499a883cd78ab5e6142ddd78595.pdf
2018-10-01
288
294
10.30476/mejc.2018.42139
Parvin
Mahzouni
mahzouni@med.mui.ac.ir
1
Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Elham
Aghili
aghili_elham@yahoo.com
2
Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Behnaz
Sabaghi
sabaghi_beh@yahoo.com
3
Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
1. Saraf S, McCarthy BJ, Villano JL.Update on meningiomas.Oncologist. 2011;16(11):1604-13. doi: 10.1634/theoncologist.2011-0193.
1
2. Schellinger KA, Propp JM, Villano JL, McCarthy BJ.Descriptive epidemiology of primary spinal cord tumors.J Neurooncol. 2008;87(2):173-9.
2
3. Mahzouni P, Movahedipour M.An immunohistochemical study of HER2 expression in meningioma and its correlation with tumor grade.Pathol Res Pract. 2012;208(4):221-4. doi: 10.1016/j.prp.2012.01.009.
3
4. Rogers L, Gilbert M, Vogelbaum MA.Intracranial meningiomas of atypical (WHO grade II) histology.J Neurooncol. 2010;99(3):393-405. doi: 10.1007/s11060-010-0343-1.
4
5. Rooprai HK, Martin AJ, King A, Appadu UD, Jones H, Selway RP et al. Comparative gene expression profiling of ADAMs, MMPs, TIMPs, EMMPRIN, EGF-R and VEGFA in low grade meningioma.Int J Oncol. 2016;49(6):2309-2318. doi: 10.3892/ijo.2016.3739.
5
6. Nassehi D. Intracranial meningiomas, the VEGF-A pathway, and peritumoral brain oedema.Dan Med J. 2013;60(4):B4626.
6
7. Dietrich J, Rao K, Pastorino S, Kesari S.Corticosteroids in brain cancer patients: benefits and pitfalls.Expert Rev ClinPharmacol. 2011;4(2):233-42. doi: 10.1586/ecp.11.1.
7
8. Hawasli AH, Rubin JB, Tran DD, Adkins DR, Waheed S, Hullar TE, et al. Antiangiogenic agents for nonmalignant brain tumors.J NeurolSurg B Skull Base. 2013;74(3):136-41. doi: 10.1055/s-0033-1338262.
8
9. Gerstner ER, Duda DG, di Tomaso E, Ryg PA, Loeffler JS, Sorensen AG, et al. VEGF inhibitors in the treatment of cerebral edema in patients with brain cancer.Nat Rev ClinOncol. 2009;6(4):229-36. doi: 10.1038/nrclinonc.2009.14.
9
10. Pfister C, Pfrommer H, Tatagiba MS, Roser F.Vascular endothelial growth factor signals through platelet-derived growth factor receptor β in meningiomasin vitro.Br J Cancer. 2012;107(10):1702-13. doi: 10.1038/bjc.2012.459.
10
11. Reszec J, Hermanowicz A, Rutkowski R, Turek G, Mariak Z, Chyczewski L. Expression of MMP-9 and VEGF in meningiomas and their correlation with peritumoral brain edema.Biomed Res Int. 2015;2015:646853. doi: 10.1155/2015/646853.
11
12. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK (eds) (2007) WHO Classification of tumours of the central nervous system. IARC, Lyon
12
13. Ding YS, Wang HD, Tang K, Hu ZG, Jin W, Yan W.Expression of vascular endothelial growth factor in human meningiomas and peritumoral brain areas.Ann Clin Lab Sci. 2008;38(4):344-51.
13
14. Kim BW, Kim MS, Kim SW, Chang CH, Kim OL.Peritumoral brain edema in meningiomas : correlation of radiologic and pathologic features.J Korean Neurosurg Soc. 2011;49(1):26-30. doi: 10.3340/jkns.2011.49.1.26.
14
15. Huang H, Held-Feindt J, Buhl R, Mehdorn HM, Mentlein R.Expression of VEGF and its receptors in different brain tumors.Neurol Res. 2005;27(4):371-7.
15
16. VokudaRS, Srinivas BH, Madhugiri VS, Verma SK. Vascular endothelial growth factor as an angiogenicmarker in malignant astrocytoma and oligodendroglioma: An Indian scenario. JJClinDiagn Res. 2017;11(2):EC05-EC07. doi: 10.7860/JCDR/2017/24353.9331.
16
17. Weindel K, Moringlane JR, Marmé D, Weich HA.Detection and quantification of vascular endothelial growth factor/vascular permeability factor in brain tumor tissue and cyst fluid: the key to angiogenesis?Neurosurgery. 1994;35(3):439-48; discussion 448-9.
17
18. Criscuolo GR. The genesis of peritumoralvasogenic brain edema and tumor cysts: a hypothetical role for tumor-derived vascular permeability factor.Yale J Biol Med. 1993;66(4):277-314.
18
19. Plate KH, Breier G, Weich HA, Risau W.Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.Nature. 1992;359(6398):845-8.
19
20. Maiuri F, De Caro MB, Esposito F, Cappabianca P, Strazzullo V, Pettinato G, et al. Recurrences of meningiomas: predictive value of pathological features and hormonal and growth factors.J Neurooncol. 2007;82(1):63-8.
20
21. Pistolesi S, Boldrini L, Gisfredi S, De Ieso K, Camacci T, Caniglia M, et al. Angiogenesis in intracranial meningiomas: immunohistochemical and molecular study.Neuropathol Appl Neurobiol. 2004;30(2):118-25.
21
22. Lou E, Sumrall AL, Turner S, Peters KB, Desjardins A, Vredenburgh JJ, et al. Bevacizumab therapy for adults with recurrent/progressive meningioma: a retrospective series. J Neurooncol. 2012;109(1):63-70. doi: 10.1007/s11060-012-0861-0.
22
23. Nayak L, Iwamoto FM, Rudnick JD, Norden AD, Lee EQ, Drappatz J, et al. Atypical and anaplastic meningiomas treated with bevacizumab. J Neurooncol. 2012;109(1):187-93. doi: 10.1007/s11060-012-0886-4.
23
24. Schmid S, Aboul-Enein F, Pfisterer W, Birkner T, Stadek C, Knosp E.Vascular endothelial growth factor: the major factor for tumor neovascularization and edema formation in meningioma patients.Neurosurgery. 2010;67(6):1703-8; discussion 1708. doi: 10.1227/NEU.0b013e3181fb801b.
24
25. Provias J, Claffey K, delAguila L, Lau N, Feldkamp M, Guha A.Meningiomas: role of vascular endothelial growth factor/vascular permeability factor in angiogenesis and peritumoral edema.Neurosurgery. 1997;40(5):1016-26.
25
26. Dharmalingam P, Roopesh Kumar VR, Verma SK. Vascular endothelial growth factor expression and angiogenesis in various grades and subtypes of meningioma.Indian J PatholMicrobiol. 2013;56(4):349-54. doi: 10.4103/0377-4929.125286.
26
27. Dvorak HF, Brown LF, Detmar M, Dvorak AM.Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis.Am J Pathol. 1995;146(5):1029-39.
27
28. Klein M, Picard E, Vignaud JM, Marie B, Bresler L, Toussaint B, et al. Vascular endothelial growth factor gene and protein: strong expression in thyroiditis and thyroid carcinoma.J Endocrinol. 1999;161(1):41-9.
28
29. Klein M, Vignaud JM, Hennequin V, Toussaint B, Bresler L, Plénat F, et al. Increased expression of the vascular endothelial growth factor is a pejorative prognosis marker in papillary thyroid carcinoma.J ClinEndocrinolMetab. 2001;86(2):656-8.
29
ORIGINAL_ARTICLE
IL-35 Serum Levels in Bladder Cancer Patients: An Analytical Cross-sectional Study
Background: Bladder cancer is a prevalent disease with significant health care costs and high rates of recurrence. Results from numerous studies to associate bladder cancer with serum biomarkers have been analyzed for prognostic indicators, or to develop agents for diagnostic and therapeutic applications. Interleukin-35 is a suppressive cytokine that has a role in tumor immunity as a regulatory cytokine by suppressing T cell anticancer responses. Methods: In the present study, we have investigated interleukin-35 serum levels in bladder cancer patients by ELISA, and compared these levels with a healthy comparison group, as well as among different clinicopathological subgroups.Results: We observed no difference in serum levels of interleukin-35 in bladder cancer patients and healthy controls; however, bladder cancer patients diagnosed at lower stages (0a, I, II) had significantly higher levels of interleukin-35 in their sera compared to high stage (III, IV) patients (P=0.018).Conclusion: Our results could indicate that interleukin-35 has no significant role in bladder cancer pathogenesis and progression. Interleukin-35 might not be a valuable biomarker for diagnosis or assessment of bladder cancer progression in clinical settings. However, further studies are needed in order to reach a definitive conclusion.
https://mejc.sums.ac.ir/article_42141_4b935a3bb82b6c6c77ec7ef323a9aec9.pdf
2018-10-01
295
299
10.30476/mejc.2018.42141
Ali
Ariafar
ali.ariafar@yahoo.com
1
Urology-Oncology Research Center, Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Sabereh
Davari
2
Shiraz Institute for Cancer Research, School of Medicine Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Shabnam
Abtahi
3
Shiraz Institute for Cancer Research, School of Medicine Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Abbas
Ghaderi
ghaderia@sums.ac.ir
4
Shiraz Institute for Cancer Research, School of Medicine Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1. Morales A, Eidinger D. Bacillus Calmette-Guerin in the treatment of adenocarcinoma of the kidney. J Urol. 1976;115(4):377-80.
1
2. Ploeg M, Aben KK, Kiemeney LA. The present and future burden of urinary bladder cancer in the world. World J Urol. 2009;27(3):289-93.
2
3. Letašiová S, Medve'ová A, Šovčíková A, Dušinská M, Volkovová K, Mosoiu C, et al. Bladder cancer, a review of the environmental risk factors. Environ Health. 2012;11 Suppl 1:S11.
3
4. Lee SJ, Lee EJ, Kim SK, Jeong P, Cho YH, Yun SJ, et al. Identification of pro-inflammatory cytokines associated with muscle invasive bladder cancer; the roles of IL-5, IL-20, and IL-28A. PLoS One. 2012;7(9):e40267.
4
5. Collison LW, Workman CJ, Kuo TT, Boyd K, Wang Y, Vignali KM, et al. The inhibitory cytokine IL-35 contributes to regulatory T-cell function. Nature. 2007;450(7169):566-9.
5
6. Collison LW, Chaturvedi V, Henderson AL, Giacomin PR, Guy C, Bankoti J, et al. IL-35-mediated induction of a potent regulatory T cell population. Nat Immunol. 2010;11(12):1093-101.
6
7. Wang RX, Yu CR, Dambuza IM, Mahdi RM, Dolinska MB, Sergeev YV, et al. Interleukin-35 induces regulatory B cells that suppress autoimmune disease. Nat Med. 2014;20(6):633-41.
7
8. Wang Z, Liu JQ, Liu Z, Shen R, Zhang G, Xu J, et al. Tumor-derived IL-35 promotes tumor growth by enhancing myeloid cell accumulation and angiogenesis. J Immunol. 2013;190(5):2415-23.
8
9. Jin P, Ren H, Sun W, Xin W, Zhang H, Hao J. Circulating IL-35 in pancreatic ductal adenocarcinoma patients. Hum Immunol. 2014;75(1):29-33.
9
10. Nicholl MB, Ledgewood CL, Chen XH, Bai Q, Qin CL, Cook KM, et al. IL-35 promotes pancreas cancer growth through enhancement of proliferation and inhibition of apoptosis: Evidence for a role as an autocrine growth factor. Cytokine. 2014;70(2):126-33.
10
11. Huang C, Li N, Li Z, Chang A, Chen Y, Zhao T, et al. Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression. Nat Commun. 2017;8:14035.
11
12. Fan YG, Zhai JM, Wang W, Feng B, Yao GL, An YH, et al. IL-35 over-expression is associated with genesis of gastric cancer. Asian Pac J Cancer Prev. 2015;16(7):2845-9.
12
13. Z Zeng JC, Zhang Z, Li TY, Liang YF, Wang HM, Bao JJ, et al. Assessing the role of IL-35 in colorectal cancer progression and prognosis. Int J Clin Exp Pathol. 2013;6(9):1806-16.
13
14. Zhou C, Zhang J, Chen Y, Wang H, Hou J. Interleukin-35 as a predictor of prostate cancer in patients undergoing initial prostate biopsy. Onco Targets Ther. 2017;10:3485-3491.
14
15. Chen G, Liang Y, Guan X, Chen H, Liu Q, Lin B, et al. Circulating low IL-23: IL-35 cytokine ratio promotes progression associated with poor prognosisin breast cancer. Am J Transl Res. 2016;8(5):2255-64.
15
16. Wu W, Jiang H, Li Y, Yan MX. IL-35 expression is increased in laryngeal squamous cell carcinoma and in the peripheral blood of patients. Oncol Lett. 2017;13(5):3303-8.
16
17. Wu H, Li P, Shao N, Ma J, Ji M, Sun X, et al. Aberrant expression of Treg-associated cytokine IL-35 along with IL-10 and TGF-beta in acute myeloid leukemia. Oncol Lett. 2012;3(5):1119-23.
17
18. Fu YP, Yi Y, Cai XY, Sun J, Ni XC, He HW, et al. Overexpression of interleukin-35 associates with hepatocellular carcinoma aggressiveness and recurrence after curative resection. Br J Cancer. 2016;114(7):767-76.
18
19. Gu X, Tian T, Zhang B, Liu Y, Yuan C, Shao L, et al. Elevated plasma interleukin-35 levels predict poor prognosis in patients with non-small cell lung cancer. Tumour Biol. 2015;36(4):2651-6.
19
20. Turnis ME, Sawant DV, Szymczak-Workman AL, Andrews LP, Delgoffe GM, Yano H, et al. Interleukin-35 limits anti-tumor immunity. Immunity. 2016;44(2):316-29.
20
21. Cheng L, Montironi R, Davidson DD, Lopez-Beltran A. Staging and reporting of urothelial carcinoma of the urinary bladder. Mod Pathol. 2009;22 Suppl 2:S70-95.
21
22. Comperat E, Varinot J. Immunochemical and molecular assessment of urothelial neoplasms and aspects of the 2016 World Health Organization classification. Histopathology. 2016;69(5):717-26.
22
23. Huang A, Cheng L, He M, Nie J, Wang J, Jiang K. Interleukin-35 on B cell and T cell induction and regulation. J Inflamm (Lond). 2017;14:16.
23
24. Jin L, Xu X, Ye B, Pan M, Shi Z, Hu Y. Elevated serum interleukin-35 levels correlate with poor prognosis in patients with clear cell renal cell carcinoma. Int J Clin Exp Med. 2015;8(10):18861-6.
24
25. Huang C, Li N, Li Z, Chang A, Chen Y, Zhao T, et al. Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression. Nat Commun. 2017;8:14035.
25
26. Wang K, Gong H, Chai R, Yuan H, Chen Y, Liu J. Aberrant frequency of IL-35 producing B cells in colorectal cancer patients. Cytokine. 2017. pii: S1043-4666(17): 30316-2.
26
27. Lu Y, Yuan Y. Serum level of interleukin-17 and interleukin-35 as a biomarker for diagnosis of thyroid cancer. J Cancer Res Ther. 2015;11(6):C209-C11.
27
28. Long J, Zhang X, Wen M, Kong Q, Lv Z, An Y, et al. IL-35 over-expression increases apoptosis sensitivity and suppresses cell growth in human cancer cells. Biochem Biophys Res Commun. 2013;430(1):364-9.
28
ORIGINAL_ARTICLE
HER2 Overexpression in Borderline and Malignant Ovarian Tumors: A Cross-sectional Study in an Iranian Population and Literature Review
Background: Different studies have investigated the overexpression of human epidermal growth factor receptor 2 in ovarian cancers, in addition to the association between the level of its overexpression and tumor characteristics (tumor grade, subtype, stage, and prognosis). However, the prognostic significance of human epidermal growth factor receptor 2/neu dysregulation in epithelial ovarian tumors is controversial. The current study aims to assess human epidermal growth factor receptor 2 overexpression in different types and stages of epithelial borderline and malignant ovarian tumors in a population of Iranian patients.Methods: We conducted this cross-sectional study on 100 patients diagnosed with epithelial borderline and malignant ovarian tumors who referred to the Cancer Institute of Imam Khomeini Hospital at Tehran between 2012 and 2014. After selection of the appropriate tissue block, we prepared slides for immunohistochemical staining with the human epidermal growth factor receptor 2 marker. Human epidermal growth factor receptor 2 positivity was evaluated and scored according to Ellis and Wolff recommendations. Cases with equivocal immunohistochemical results (score 2) also underwent chromogenic in situ hybridization.Results: The most prevalent tumor in our study was serous carcinoma (54%). Human epidermal growth factor receptor 2 scores were: 0 in 69%, 1+ in 26%, 2+ in 4%, and 3+ in 1% of tumors. Chromogenic in situ hybridization examination of cases with human epidermal growth factor receptor 2 score of 2 showed negative results for human epidermal growth factor receptor 2 gene amplification. We observed no association between human epidermal growth factor receptor 2 and the level of tumor differentiation, histologic subtype, clinical stage, tumor size, and patient’s age.Conclusion: Controversial results and wide range of prevalence in human epidermal growth factor receptor 2 overexpression in different studies could be due to several causes. Technical considerations, tumor heterogeneity, and lack of standard guidelines for interpretation could influence the results. We did not find any relationship between human epidermal growth factor receptor 2 overexpression and prognostic indices of grade, clinical stage or histologic subtype as many other reports. Future studies should be conducted on larger numbers of patients with different disease stages and adequate numbers of different histologic subtypes.
https://mejc.sums.ac.ir/article_42142_a32f5b50a94152378d5324ac52187a18.pdf
2018-10-01
300
309
10.30476/mejc.2018.42142
Elham
Asadinejad
1
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Afshin
Abdirad
2
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Fatemeh
Nili
f_nili@yahoo.com
3
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Vahid
Soleimani
4
Department of Pathology, Cancer Institute, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
1. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015;136(5):E359-86. doi: 10.1002/ijc.29210.
1
2. Allemani C, Weir HK, Carreira H, Harewood R, Spika D, Wang XS, et al. Global surveillance of cancer survival 1995-2009: analysis of individual data for 25,676,887 patients from 279 population-based registries in 67 countries (CONCORD-2). Lancet. 2015;385(9972):977-1010.
2
3. Sankaranarayanan R, Ferlay J. Worldwide burden of gynaecological cancer: the size of the problem. Best Pract Res Clin Obstet Gynaecol. 2006;20(2):207-25.
3
4. Ebell MH, Culp MB, Radke TJ. A Systematic Review of Symptoms for the Diagnosis of Ovarian Cancer. Am J Prev Med. 2016 Mar;50(3):384-394.
4
5. Kurman RJ, Shih IeM. The origin and pathogenesis of epithelial ovarian cancer: a proposed unifying theory. Am J Surg Pathol. 2010;34(3):433-43.
5
6. Kindelberger DW, Lee Y, Miron A, Hirsch MS, Feltmate C, Medeiros F, et al. Intraepithelial carcinoma of the fimbria and pelvic serous carcinoma: Evidence for a causal relationship. Am J Surg Pathol. 2007;31(2):161-9.
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7. Eltabbakh GH, Belinson JL, Kennedy AW, Biscotti CV, Casey G, Tubbs RR. p53 and HER-2/neu overexpression in ovarian borderline tumors. Gynecol Oncol. 1997;65(2):218-24.
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8. Bjørge T, Lie AK, Hovig E, Gislefoss RE, Hansen S, Jellum E, et al. BRCA1 mutations in ovarian cancer and borderline tumours in Norway: a nested case-control study. Br J Cancer. 2004;91(10):1829-34.
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8. Cho KR, Shih IeM. Ovarian cancer. Annu Rev Pathol. 2009;4:287-313. doi: 10.1146/annurev.pathol.4.110807.092246.
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9. Pritchard KI, Shepherd LE, O'Malley FP, Andrulis IL, Tu D, Bramwell VH, et al. HER2 and responsiveness of breast cancer to adjuvant chemotherapy. N Engl J Med. 2006;354(20):2103-11.
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10. Ellis IO, Bartlett J, Dowsett M, Humphreys S, Jasani B, Miller K, et al. Best Practice No 176: Updated recommendations for HER2 testing in the UK. J Clin Pathol. 2004;57(3):233-7.
11
11. Lanitis E, Dangaj D, Hagemann IS, Song DG, Best A, Sandaltzopoulos R, et al. Primary human ovarian epithelial cancer cells broadly express HER2 at immunologically-detectable levels. PLoS One. 2012;7(11):e49829. doi: 10.1371/journal.pone.0049829.
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12. Wang D, Zhu H, Ye Q, Wang C, Xu Y. Prognostic value of KIF2A and HER2-Neu overexpression in patients with epithelial ovarian cancer. Medicine (Baltimore). 2016;95(8):e2803.
13
13. de Toledo MC, Sarian LO, Sallum LF, Andrade LL, Vassallo J, de Paiva Silva GR, et al. Analysis of the contribution of immunologically-detectable HER2, steroid receptors and of the "triple-negative" tumor status to disease-free and overall survival of women with epithelial ovarian cancer. Acta Histochem. 2014;116(3):440-7.
14
14. Hsieh CY, Chen CA, Chou CH, Lai KP, Jeng YM, Kuo ML, et al. Overexpression of Her-2/NEU in epithelial ovarian carcinoma induces vascular endothelial growth factor C by activating NF-kappa B: implications for malignant ascites formation and tumor lymphangiogenesis. J Biomed Sci. 2004;11(2):249-59.
15
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17. Rubin SC, Finstad CL, Federici MG, Scheiner L, Lloyd KO, Hoskins WJ. Prevalence and significance of HER-2/neu expression in early epithelial ovarian cancer. Cancer. 1994;73(5):1456-9.
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18. Singleton TP, Perrone T, Oakley G, Niehans GA, Carson L, Cha SS, et al. Activation of c-erbB-2 and prognosis in ovarian carcinoma. Comparison with histologic type, grade, and stage. Cancer. 1994;73(5):1460-6.
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19. Meden H, Marx D, Rath W, Kron M, Fattahi-Meibodi A, Hinney B, et al. Overexpression of the oncogene c-erb B2 in primary ovarian cancer: evaluation of the prognostic value in a Cox proportional hazards multiple regression. Int J Gynecol Pathol. 1994;13(1):45-53.
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20. Felip E, Del Campo JM, Rubio D, Vidal MT, Colomer R, Bermejo B. Overexpression of c-erbB-2 in epithelial ovarian cancer. Prognostic value and relationship with response to chemotherapy. Cancer. 1995;75(8):2147-52.
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21. Fajac A, Benard J, Lhomme C, Rey A, Duvillard P, Rochard F, et al. c-erbB2 gene amplification and protein expression in ovarian epithelial tumors: evaluation of their respective prognostic significance by multivariate analysis. Int J Cancer. 1995;64(2):146-51.
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22. Simpson BJ, Phillips HA, Lessells AM, Langdon SP, Miller WR. c-erbB growth-factor-receptor proteins in ovarian tumours. Int J Cancer. 1995;64(3):202-6.
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23. van Haaften-Day C, Russell P, Boyer CM, Kerns BJ, Wiener JR, Jensen DN, et al. Expression of cell regulatory proteins in ovarian borderline tumors. Cancer. 1996;77(10):2092-8.
24
24. Goff BA, Shy K, Greer BE, Muntz HG, Skelly M, Gown AM. Overexpression and relationships of HER-2/neu, epidermal growth factor receptor, p53, Ki-67, and tumor necrosis factor alpha in epithelial ovarian cancer. Eur J Gynaecol Oncol. 1996;17(6):487-92.
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25. Auranen A, Grénman S, Kleml PJ. Immunohistochemically detected p53 and HER-2/neu expression and nuclear DNA content in familial epithelial ovarian carcinomas. Cancer. 1997;79(11):2147-53.
26
26. Høgdall EV1, Christensen L, Kjaer SK, Blaakaer J, Bock JE, Glud E, et al. Distribution of HER-2 overexpression in ovarian carcinoma tissue and its prognostic value in patients with ovarian carcinoma: from the Danish MALOVA Ovarian Cancer Study. Cancer. 2003;98(1):66-73.
27
27. Bookman MA, Darcy KM, Clarke-Pearson D, Boothby RA, Horowitz IR. Evaluation of monoclonal humanized anti-HER2 antibody, trastuzumab, in patients with recurrent or refractory ovarian or primary peritoneal carcinoma with overexpression of HER2: a phase II trial of the Gynecologic Oncology Group. J Clin Oncol. 2003;21(2):283-90.
28
28. Mano MS, Awada A, Di Leo A, Durbecq V, Paesmans M, Cardoso F, et al. Rates of topoisomerase II-alpha and HER-2 gene amplification and expression in epithelial ovarian carcinoma. Gynecol Oncol. 2004;92(3):887-95.
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29. Camilleri-Broët S1, Hardy-Bessard AC, Le Tourneau A, Paraiso D, Levrel O, Leduc B, et al. HER-2 overexpression is an independent marker of poor prognosis of advanced primary ovarian carcinoma: a multicenter study of the GINECO group. Ann Oncol. 2004;15(1):104-12.
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30. Nielsen JS, Jakobsen E, Hølund B, Bertelsen K, Jakobsen A. Prognostic significance of p53, Her-2, and EGFR overexpression in borderline and epithelial ovarian cancer. Int J Gynecol Cancer. 2004;14(6):1086-96.
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31. Lassus H, Leminen A, Vayrynen A, Cheng G, Gustafsson JA, Isola J, et al. ERBB2 amplification is superior to protein expression status in predicting patient outcome in serous ovarian carcinoma. Gynecol Oncol. 2004;92(1):31-9.
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32. Lee CH, Huntsman DG, Cheang MC, Parker RL, Brown L, Hoskins P, et al. Assessment of Her-1, Her-2, And Her-3 expression and Her-2 amplification in advanced stage ovarian carcinoma. Int J Gynecol Pathol. 2005;24(2):147-52.
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33. O'Neill CJ, Deavers MT, Malpica A, Foster H, McCluggage WG. An immunohistochemical comparison between low-grade and high-grade ovarian serous carcinomas: significantly higher expression of p53, MIB1, BCL2, HER-2/neu, and C-KIT in high-grade neoplasms. Am J Surg Pathol. 2005;29(8):1034-41.
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34. Verri E, Guglielmini P, Puntoni M, Perdelli L, Papadia A, Lorenzi P, et al. HER2/neu oncoprotein overexpression in epithelial ovarian cancer: evaluation of its prevalence and prognostic significance. Clinical study. Oncology. 2005;68(2-3):154-61.
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35. Mayr D1, Kanitz V, Amann G, Engel J, Burges A, Löhrs U, et al. HER-2/neu gene amplification in ovarian tumours: a comprehensive immunohistochemical and FISH analysis on tissue microarrays. Histopathology. 2006;48(2):149-56.
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36. Tuefferd M, Couturier J, Penault-Llorca F, Vincent-Salomon A, Broët P, Guastalla JP, et al. HER2 status in ovarian carcinomas: a multicenter GINECO study of 320 patients. PLoS One. 2007;2(11):e1138.
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37. Steffensen KD, Waldstrøm M, Brandslund I, Jakobsen A. Prognostic impact of prechemotherapy serum levels of HER2, CA125, and HE4 in ovarian cancer patients. Int J Gynecol Cancer. 2011;21(6):1040-7. doi: 10.1097/IGC.0b013e31821e052e.
38
38. Vermeij J, Teugels E, Bourgain C, Xiangming J, in 't Veld P, Ghislain V, et al. Genomic activation of the EGFR and HER2-neu genes in a significant proportion of invasive epithelial ovarian cancers. BMC Cancer. 2008;8:3. doi: 10.1186/1471-2407-8-3.
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39. Hoopmann M, Sachse K, Valter MM, Becker M, Neumann R, Ortmann M, et al. Serological and immunohistochemical HER-2/neu statuses do not correlate and lack prognostic value for ovarian cancer patients. Eur J Cancer Care (Engl). 2010;19(6):809-15. doi: 10.1111/j.1365-2354.2009.01112.x.
40
40. Kadkhodayan S, Ghaffarzadegan K, Homaee F, Esmaeily H, Torabi SH. Expression of HER-2/neu and P16 in epithelial ovarian tumors and its correlation with clinicopathologic variables. [Article in Persian] Iran J Obstetrics Gynecol Infertil. 2015;17(133):1-7. 41. Omar N, Yan B, Salto-Tellez M. HER2: An emerging biomarker in non-breast and non-gastric cancers. Pathogenesis. 2015; 2(3):1-9
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42. McCaughan H, Um I, Langdon SP, Harrison DJ, Faratian D. HER2 expression in ovarian carcinoma: caution and complexity in biomarker analysis. J Clin Pathol. 2012;65(7):670-1; author reply 671-2. doi: 10.1136/jclinpath-2011-200616.
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43
ORIGINAL_ARTICLE
Breast Cancer Trend: A Case Study of a Tertiary Health Institution in Nigeria
Background: Breast cancer is a major global health problem in women from both developing and developed countries. As the leading cause of death among women, breast cancer has contributed 19.5% to the mortality rate among women in Nigeria. This study investigated the trend of breast cancer among women who attended Federal Teaching Hospital, Ido-Ekiti, Nigeria.
Methods: This retrospective study examined the trend of breast cancer over a period of eight years and determined the most affected age group. Participants consisted of patients registered in the cancer registry who had histologically confirmed breast cancer. Data of 362 patients were examined between March and April 2016. Data were analyzed and presented using descriptive (frequency, charts, and percentages) and inferential statistics (Fisher’s exact) for hypothesis testing.
Results: Findings of this study revealed that the mean age of the participants was 45.04±16.94 years and all patients involved were females. The age group 20-39 years was most affected by breast cancer with a proportion of 41.7%. This study revealed a relationship between breast cancer classification and age of patients (P=0.011). Almost all (94.3%) cases seen within this time period were malignant.
Conclusion: Healthcare professionals should place more emphasis on prevention of breast cancer across all age groups, especially young adults. These young adults constitute the larger percentage of the adult population. An increase in mortality rate in this age group will reduce the labor force and affect the nation’s economy.
https://mejc.sums.ac.ir/article_42143_b426435919db3b80dcd77ce6c0369d0c.pdf
2018-10-01
311
317
10.30476/mejc.2018.42143
Deborah
Esan
esandt@abuad.edu.ng
1
Department of Nursing, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
LEAD_AUTHOR
Ayodeji
Fasoro
akinfasoro@abuad.edu.ng
2
Department of Community Medicine, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
AUTHOR
Oluwaseun
Olatoye
seun.jola@yahoo.com
3
Department of Nursing, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
AUTHOR
Elizabeth
Ojo
4
Department of Nursing, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
AUTHOR
Theophilus
Esan
esantolaide@yahoo.com
5
Department of E.N.T., Federal Teaching Hospital, Ido-Ekiti, Nigeria
AUTHOR
1. WHO. Global cancer rates could increase by 50% to 15 million by 2020 [Internet]. [cited 2016 May 13] Available from: http://www.who.int/mediacentre/news/releases/2003/pr27/en/
1
2. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al . Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015;136(5):E359-86.
2
3. Jedy-Agba E, Curado MP, Ogunbiyi O, Oga E, Fabowale T, Igbinoba F, et al. Cancer incidence in Nigeria: a report from population-based cancer registries. Cancer Epidemiol. 2012;36(5):e271-8.
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4. Mukherjee, M. Development and characterization of mouse models of human breast cancer. [Doctoral Dissertation]. The University of North Carolina at Chapel Hill; 2008. Available from: Carolina Digital Repository, Malini Mukherjee - Thesis 7-18-2008.
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5. Ferlay, J; Bray, F; Parkin, DM; Pisani, P. GLOBOCAN 2000: Cancer Incidence and Mortality Worldwide (IARC Cancer Bases No. 5). Lyon: IARC Press; 2001.
5
6. Bray F, McCarron P, Parkin DM. The changing global patterns of female breast cancer incidence and mortality. Breast Cancer Res. 2004;6(6):229-39.
6
7. Chintamani. The paradigm shifts in the management of breast cancer-have we finally arrived? Indian J Surg. 2013;75(6):419-23.
7
8. Smeltzer, SC; Bare, BG; Hinkle, JL. Brunner & Suddarth’s textbook of medical-surgical nursing. Philadelphia: Lippincott Williams &Wilkins; 2010.
8
9. Komen SG. Breast cancer statistic [Internet]. Available from: https://ww5.komen.org/BreastCancer/Statistics.html (Accessed date: May13, 2016).
9
10. Vanguard News. One in every 25 Nigerian women dies of cancer – Expert [Internet]. 2013 [cited 2016 April 22]. Available from: www.vanguardngr.com/2013/11/one-every-25-nigerian-women-dies-cancer-expert/
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11. Shulman LN, Willett W, Sievers A, Knaul FM. Breast cancer in developing countries: opportunities for improved survival. J Oncol. 2010;2010:595167.
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12. National Cancer Registry. Breast cancer incidence, mortality, treatment and survival in Ireland: 1994‐2009. Cork: National Cancer Registry; 2012, p. 5.
12
13. Singapore Cancer Registry. Interim Annual Report Trends in Cancer Incidence in Singapore 2010-2014. Singapore: Singapore National Registry of Disease Office (NRDO); 2015, p. 56.
13
14. Cancer Registry of Norway. Cancer in Norway 2012 - Cancer incidence, mortality, survival and prevalence in Norway. Oslo: Cancer Registry of Norway; 2014.
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15. Pukkala E, Weiderpass E. Time trends in socio-economic differences in incidence rates of cancers of the breast and female genital organs (Finland, 1971-1995). Int J Cancer. 1999;81(1):56-61.
15
16. Morris, CR; Epstein, J; Nasserem K; Hofer, BM; Rico, J; Bates, JH, et al. Trends in Cancer Incidence, Mortality, Risk Factors, and Health Behaviours in California. Sacramento: California Department of Public Health, Cancer Surveillance Section; 2010, p.17.
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17. Goodman MT, Cologne JB, Moriwaki H, Vaeth M, Mabuchi K. Risk factors for primary breast cancer in Japan: 8-year follow-up of atomic bomb survivors. Prev Med. 1997;26(1):144-53.
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18. Sanderson M, Williams MA, Daling JR, Holt VL, Malone KE, Self SG, et al. Maternal factors and breast cancer risk among young women. Paediatr Perinat Epidemiol. 1998;12(4):397-407.
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19. Kelsey JL, Gammon MD, John EM. Reproductive factors and breast cancer. Epidemiol Rev. 1993;15(1):36-47.
19
20. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet. 2008;371(9612):569-78.
20
21. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Collaborative Group on Hormonal Factors in Breast Cancer. Lancet. 1997;350(9084):1047-59, Erratum in: Lancet. 1997, 350:1484.
21
22. Moradi T, Adami HO, Ekbom A, Wedrén S, Terry P, Floderus B, et al. Physical activity and risk for breast cancer a prospective cohort study among Swedish twins. Int J Cancer. 2002;100(1):76-81.
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23. Moradi T, Nyrén O, Zack M, Magnusson C, Persson I, Adami HO. Breast cancer risk and lifetime leisure-time and occupational physical activity (Sweden). Cancer Causes Control. 2000;11(6):523-31.
23
24. Ferlay J, Shin HR, Bray F, Forman D, Mathers CD, Parkin D. GLOBOCAN 2008, Cancer Incidence and Mortality Worldwide: IARC Cancer Base No.10 [Internet]. Lyon, France: International Agency for Research on Cancer. 2010; Accessed from: http://globocan.iarc.fr (Accessed date: Apr 25, 2016).
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[25]. Gaudette LA, Silberberger C, Altmayer CA, Gao RN. Trends in breast cancer incidence and mortality. [Article in English, French] Health Rep. 1996;8(2):29-37(Eng); 31-40(Fre).
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[26]. Saika K, Sobue T. Epidemiology of breast cancer in Japan and the US. JMAJ. 2009; 52(1): 39-44.
26
27. Hirko KA, Soliman AS, Hablas A, Seifeldin IA, Ramadan M, Banerjee M, et al. Trends in Breast Cancer Incidence Rates by Age and Stage at Diagnosis in Gharbiah, Egypt, over 10 Years (1999-2008). J Cancer Epidemiol. 2013;2013:916394.
27
28. WHO. World Health Statistics 2009 [Internet]. [cited 2016 April 22] Available from: http://www.who.int/entity/whosis/whostat/EN_WHS09_Full.pdf?ua=1
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29. Beiki O, Hall P, Ekbom A, Moradi T. Breast cancer incidence and case fatality among 4.7 million women in relation to social and ethnic background: a population-based cohort study. Breast Cancer Res. 2012;14(1):R5.
29
30. American Cancer Society. Global Cancer Facts & Figures. Atlanta: American Cancer Society; 2011.p.1-52.
30
ORIGINAL_ARTICLE
Environmental Risk Factors Associated with Sporadic Colorectal Cancer in Isfahan, Iran
Background: Records from the cancer registry system of Iran indicate that colorectal cancer is the third most common cancer in Iranian men and fourth most common among Iranian women. In this study we have investigated the environmental factors associated with colorectal cancer in Isfahan, Iran.Methods: In this case-control study, we randomly selected 187 patients with colorectal cancer who had positive results by colonoscopy and pathology (case group) and 250 persons who had negative colonoscopy results (control group) from the Colonoscopy Unit of Al Zahra Hospital and Colorectal Cancer Center of Seyed Al Shohada Hospital from 2014 to mid-2015. This study aimed to find the risk factors for sporadic colorectal cancer; therefore, we excluded patients with positive family history. Participants completed a self-administered questionnaire that asked about sex, age, body mass index, smoking status, job-related physical activity, and nonsteroidal antiinflammatory drug consumption.Results: This study enrolled 187 colorectal cancer patients (98 males and 89 females) and 250 individuals without colorectal cancer (107 males and 143 females). Multiple analysis demonstrated a significant association of age (odds ratio: 1.04; 95% confidence interval: 1.02, 1.06) and body mass index (odds ratio: 1.09; 95% confidence interval: 1.03, 1.15) with colorectal cancer risk. Men had an almost two-fold risk compared with women (odds ratio: 1.85; 95% confidence interval: 1.14, 2.99). Subjects who did not use nonsteroidal anti-inflammatory drugs had an almost three-fold risk compared with nonsteroidal anti-inflammatory drug consumers (odds ratio: 0.34; 95% confidence interval: 0.19, 0.62). Analysis for job-related physical activity, also indicated an association between the no/low active group with colorectal cancer (odds ratio no activity: 36.09; 95% confidence interval: 10.94, 119 and odds ratio low activity: 2.96; 95% confidence interval: 1.43, 6.13).Conclusion: Knowledge of the risk factors involved in colorectal cancer incidence makes it possible to identify people at risk and begin risk reduction strategies as well as screening programs.
https://mejc.sums.ac.ir/article_42144_fb06b7121bb255c805d2ae2cfb9f5552.pdf
2018-10-01
318
322
10.30476/mejc.2018.42144
Miganoosh
Simonian
migasi88@yahoo.com
1
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Sharifeh
Khosravi
sharifeh.khosravi@yahoo.com
2
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Deniz
Mortazavi
hadi.bagheri.bio@gmail.com
3
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Hadi
Bagheri
4
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Rasoul
Salehi
5
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Akbar
Hassanzadeh
6
Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Meysam
Mosallaei
me.mosallayi@uswr.ac.ir
7
Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
1. Ferlay J, Shin H-R, Bray F, Forman D, Mathers C, Parkin DM. GLOBOCAN 2008, Cancer incidence and mortality worldwide: IARC CancerBase No. 10. Lyon, France: International Agency for Research on Cancer. 2010;2010:29.
1
2. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer. 2010;127(12):2893-917. doi: 10.1002/ijc.25516.
2
3. Hosseini SV, Izadpanah A, Yarmohammadi H. Epidemiological changes in colorectal cancer in Shiraz, Iran: 1980-2000. ANZ J Surg. 2004;74(7):547-9.
3
4. Malekzadeh R, Bishehsari F, Mahdavinia M, Ansari R. Epidemiology and molecular genetics of colorectal cancer in iran: a review. Arch Iran Med. 2009;12(2):161-9.
4
5. Poomphakwaen K, Promthet S, Suwanrungruang K, Kamsa-ard S, Wiangnon S. Risk Factors for Colorectal Cancer in Thailand. Asian Pac J Cancer Prev. 2015;16(14):6105-9.
5
6. Yee YK, Tan VP, Chan P, Hung IF, Pang R, Wong BC. Epidemiology of colorectal cancer in Asia. J Gastroenterol Hepatol. 2009;24(12):1810-6. doi: 10.1111/j.1440-1746.2009.06138.x.
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7. Mehrabani D, Tabei S, Heydari S, Shamsina S, Shokrpour N, Amini M, et al. Cancer occurrence in Fars Province, Southern Iran. Iran Red Crescent Med J. 2008;2008(4):314-22.
7
8. Sadjadi A, Malekzadeh R, Derakhshan MH, Sepehr A, Nouraie M, Sotoudeh M, et al. Cancer occurrence in Ardabil: results of a population-based cancer registry from Iran. Int J Cancer. 2003;107(1):113-8.
8
9. Aleksandrova K, Pischon T, Jenab M, Bueno-de-Mesquita HB, Fedirko V, Norat T, et al. Combined impact of healthy lifestyle factors on colorectal cancer: a large European cohort study. BMC Med. 2014;12:168. doi: 10.1186/s12916-014-0168-4.
9
10. Sanchez NF, Stierman B, Saab S, Mahajan D, Yeung H, Francois F. Physical activity reduces risk for colon polyps in a multiethnic colorectal cancer screening population. BMC Res Notes. 2012;5:312. doi: 10.1186/1756-0500-5-312.
10
11. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61(5):759-67.
11
12. Becker N. Epidemiology of colorectal cancer. [Article in German] Radiologe. 2003;43(2):98-104.
12
13. Durko L, Malecka-Panas E. Lifestyle modifications and colorectal cancer. Curr Colorectal Cancer Rep. 2014;10:45-54.
13
14. Pohl C, Hombach A, Kruis W. Chronic inflammatory bowel disease and cancer. Hepatogastroenterology. 2000;47(31):57-70.
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15. Lieberman DA, Prindiville S, Weiss DG, Willett W; VA Cooperative Study Group 380. Risk factors for advanced colonic neoplasia and hyperplastic polyps in asymptomatic individuals. JAMA. 2003;290(22):2959-67.
15
16. Hong SN, Kim JH, Choe WH, Han HS, Sung IK, Park HS, et al. Prevalence and risk of colorectal neoplasms in asymptomatic, average-risk screenees 40 to 49 years of age. Gastrointest Endosc. 2010;72(3):480-9. doi: 10.1016/j.gie.2010.06.022.
16
17. Chung SJ, Kim YS, Yang SY, Song JH, Park MJ, Kim JS, et al. Prevalence and risk of colorectal adenoma in asymptomatic Koreans aged 40-49 years undergoing screening colonoscopy. J Gastroenterol Hepatol. 2010;25(3):519-25. doi: 10.1111/j.1440-1746.2009.06147.x.
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18. W Winawer S, Fletcher R, Rex D, Bond J, Burt R, Ferrucci J, et al. Colorectal cancer screening and surveillance: clinical guidelines and rationale-Update based on new evidence. Gastroenterology. 2003;124(2):544-60.
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19. Haggar FA, Boushey RP. Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors. Clin Colon Rectal Surg. 2009;22(4):191-7. doi: 10.1055/s-0029-1242458.
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20. Aykan NF, Yalçın S, Turhal NS, Özdoğan M, Demir G, Özkan M, et al. Epidemiology of colorectal cancer in Turkey: A cross-sectional disease registry study (A Turkish Oncology Group trial). Turk J Gastroenterol. 2015;26(2):145-53. doi: 10.5152/tjg.2015.5685.
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21. O'Connell JB, Maggard MA, Liu JH, Etzioni DA, Livingston EH, Ko CY. Rates of colon and rectal cancers are increasing in young adults. Am Surg. 2003;69(10):866-72.
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22. Murphy G, Devesa SS, Cross AJ, Inskip PD, McGlynn KA, Cook MB. Sex disparities in colorectal cancer incidence by anatomic subsite, race and age. Int J Cancer. 2011;128(7):1668-75. doi: 10.1002/ijc.25481.
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23. Booth A, Magnuson A, Fouts J, Foster M. Adipose tissue, obesity and adipokines: role in cancer promotion. Horm Mol Biol Clin Investig. 2015;21(1):57-74. doi: 10.1515/hmbci-2014-0037.
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24. Donohoe CL, Doyle SL, Reynolds JV. Visceral adiposity, insulin resistance and cancer risk. Diabetol Metab Syndr. 2011;3:12. doi: 10.1186/1758-5996-3-12.
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25. Ashktorab H, Paydar M, Yazdi S, Namin HH, Sanderson A, Begum R, et al. BMI and the risk of colorectal adenoma in African-Americans. Obesity (Silver Spring). 2014;22(5):1387-91. doi: 10.1002/oby.20702.
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26. Zapatier J, Avalos D, Tandon K, Souqiyyeh A, Hernandez M, Rai S, et al. Can adjusting BMI for age and sex provide for a better predictor of colonic neoplasia?
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36
ORIGINAL_ARTICLE
The Life and Works of Sadid al-Din Kazeroni: An Iranian Physician and Anatomist
Background: One of the great physicians in Iran who had expertise in medicine, surgery, and pharmacy was Sadid al-Din Kazeroni. He was a 14th century physician. No information is available on his birth and death – only “Al-Mughni”, a book, has been left to make him famous in surgical and medical knowledge.Methods: We used desk and historical research methods in this research, with a historical approach. This commonly used research method in human sciences was used to criticize and study the birthplace and works of Sadid al-Din Kazeroni.Results and Conclusion: Sadid al-Din Kazeroni discussed the exact issues in the field of anatomy, surgery, and gynecology. He was fluent in pharmacology. In his pharmacology book, for the first time, he named drugs considered necessary before and after surgery. In this study, we reviewed the biography and introduction of the works and reviewed “Al-Mughni”, a book on breast cancer.
https://mejc.sums.ac.ir/article_42131_6bc105f7439b79347690acd977052a16.pdf
2018-10-01
323
327
10.30476/mejc.2018.42131
Seyyed Alireza
Golshani
golshani_22@yahoo.com
1
Department of History, Ferdowsi University of Mashhad, Mashhad, Iran
LEAD_AUTHOR
Seyyed Ehsan
Golshan
ehsangolshan551@gmail.com
2
Department of Foreign Languages, Marvdasht Azad University, Marvdasht, Iran
AUTHOR
Mohammad Ebrahim
Zohalinezhad
zohalinm@yahoo.com
3
Assistant Professor, Persian Medicine, Shiraz University of Medical Sciences, Shiraz, Iran; Eessence of Parsiyan Wisdom Institute, Traditional Medicine and Medicinal Plant Incubator, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
1. Siobhan R. Maryam Mirzakhani, pioneering mathematical legacy[Internet]. The New Yorker. Retrieved at: 2017-07-18. Available from: https://www.newyorker.com/tech/elements/maryam-mirzakhanis-pioneering-mathematical-legacy.
1
2. Ekmektzoglou KA, Xanthos T, German V, Zografos GC. Breast cancer: from the earliest times through to the end of the 20th century. Eur J Obstet Gynecol Reprod Biol. 2009;145(1):3-8. doi: 10.1016/j.ejogrb.2009.03.017.
2
3. Hilal Z, Bashar S. Cancer treatment in the Arab-Islamic medicine: Integration of tradition with modern experimental trails. Journal of Jami'a. 2010;14(1):13-40.
3
4. Mozaffarian M. Kazeroon in the Mirror of Iranian Culture. Shiraz: Navid;1994.p.405-6.
4
5. Zvi Ben-Dor, Benite, The Dao of Muhammad: A cultural history of Muslims in late imperial China. Cambridge: Harvard University Press;2005.p.151-152.
5
6. Fazel, M. Catalogue of manuscripts in the library of the Mosque of Jama Ghoharshad Mashhad. Volume 2, Mashhad: the library of the Mosque of Jama Ghoharshad Mashhad; 1984.p.550.
6
7. Safa, Z. A history of Iranian literature. Volume 3. Tehran: Ferdowsi;1984.p.275-7.
7
8. Irfanian, Gh. A descriptive catalogue of the Persian, Arabic. Volume 19. Mashhad: Central Library of Astan Quds Razavi; 2001.p.131-3.
8
9. Sadid al-Din al-Kazaruni. Al-Mughni fi sharh al-Mujiz. Tehran: Iran University of Medical Sciences; 2008.p.686.
9
10. Zarshenas MM, Zargaran A, Mehdizadeh A, Mohagheghzadeh A. Mansur ibn Ilyas (1380-1422 AD): A Persian anatomist and his book of anatomy, Tashrih-i Mansuri. J Med Biogr. 2016;24(1):67-71. doi: 10.1177/0967772013479474.
10
11. ZillurRahman, M. The Kanon of Ibn Sina, its commentators and translators. Tehran: Society for the National Heritage of Iran;2004.p.66-7.
11
12. Al-Biruni. Kitab al saydana fi'l-tibb. [Translator Bagher Mazafarzadeh]. Tehran: Academy of Persian Language and Literature;2004.p.36-7.
12
13. Akmal al-din Ughli AD, Ramazan Şeşen AD, Aghpkar J, Eizegi J. Catalog of Islamic medicine manuscripts in Turkish libraries. Istanbul: Research Center for History, History, Arts and Islamic Culture in Istanbul press; 1984.p.274.
13
ORIGINAL_ARTICLE
Unusual Site of Metastasis of Placental Site Trophoblastic Tumor: Case Report and Literature Review
Placental site trophoblastic tumor is a subtype of gestational trophoblastic neoplasm with unpredictable clinical behavior. Cytoreductive surgery is the cornerstone of treatment. The aim of this article is to present a case with an unusual site of metastases of placental site trophoblastic tumor. A 35-year-old woman was referred to the academic center of GTN as a persistent case gestational trophoblastic neoplasm for standard treatment. Based on pancreatic metastases in the patient’s work-up, she underwent cytoreductive surgery that resulted in significant improvement in her condition. Proper surgical approach of placental site trophoblastic tumor has a major role in the remission of this disease.
https://mejc.sums.ac.ir/article_42133_3a227197308c65074edc503005c1458f.pdf
2018-10-01
328
333
10.30476/mejc.2018.42133
Leila
Mousavi Seresht
lmousavilm@gmail.com
1
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hamed
Golmohamadzadeh
2
Department of Surgery, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zohreh
Yousefi
yousefiz@mums.ac.ir
3
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Amir Hosein
Jafarian
4
Department of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ali
Moghimi
5
Department of Surgery, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mojgan
Soltani
6
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1. Bouquet de la Jolinière J, Khomsi F, Fadhlaoui A, Ben Ali N, Dubuisson JB, Feki A. Placental site trophoblastic tumor: a case report and review of the literature. Front Surg. 2014;1:31.
1
2. Chiofalo B, Palmara V, Laganà AS, Triolo O, Vitale SG, Conway F, et al. Fertility sparing strategies in patients affected by placental site trophoblastic tumor. Curr Treat Options Oncol. 2017;18(10):58.
2
3. Santoro G, Laganà AS, Micali A, Barresi V, Giacobbe V, Palmara V. Historical, morphological and clinical overview of placental site trophoblastic tumors: from bench to bedside. Arch Gynecol Obstet. 2017;295(1):173-87.
3
4. Wang D, He Y, Hu Y, Xie C, Yin R. Placental site trophoblastic tumor with unusual presentation in the uterine cervix. Eur J Obstet Gynecol Reprod Biol. 2010;148(1):100-1.
4
5. Zwischenberger BA, Boren T. Placental site trophoblastic tumor presenting as a friable cervical mass. Eur J Gynaecol Oncol. 2010;31(5):570-2.
5
6. Pawar AA, Patil DB, Patel S, Mankad M, Dave P. Role of PET–CT Scan in Gynaeconcology. J Obstet Gynaecol India. 2016;66(5):339-44.
6
7. Niknejadi M, Ahmadi F, Akhbari F. Imaging and clinical data of placental site trophoblastic tumor: A case report. Iran J Radiol. 2016;13(2):e18480.
7
8. Baergen RN, Rutgers JL, Young RH, Osann K, Scully RE. Placental site trophoblastic tumor: a study of 55 cases and review of the literature emphasizing factors of prognostic significance. Gynecol Oncol. 2006;100(3):511-20.
8
9. Zeng X, Liu X, Tian Q, Xue Y, An R. Placental site trophoblastic tumor: A case report and literature review. Intractable Rare Dis Res. 2015;4(3):147-51.
9
10. Monclair T, Abeler VM, Kærn J, Walaas L, Zeller B, Hilstrøm C. Placental site trophoblastic tumor (PSTT) in mother and child: first report of PSTT in infancy. Med Pediatr Oncol. 2002;38(3):187-91; discussion 192.
10
11. Zhang X. Coexisting epithelioid trophoblastic tumor and placental site trophoblastic tumor of the uterus following a term pregnancy: report of a case and review of literature. Int J Clin Exp Pathol. 2015;8(6):7254-9.
11
12. Denny LA, Dehaeck K, Nevin J, Soeters R, VAN AL WI, Megevand E, et al. Placental site trophoblastic tumor: three case reports and literature review. Gynecol Oncol. 1995;59(2):300-3.
12
13. Batra V, Kalra OP, Mathur P, Dev G. Membranous glomerulopathy associated with placental site trophoblastic tumour: a case report. Nephrol Dial Transplant. 2007;22(6):1766-8.
13
14. Chang YL, Chang TC, Hsueh S, Huang KG, Wang PN, Liu HP, et al. Prognostic factors and treatment for placental site trophoblastic tumor—report of 3 cases and analysis of 88 cases. Gynecol Oncol. 1999;73(2):216-22.
14
15. Papadopoulos AJ, Foskett M, Seckl MJ, McNeish I, Paradinas FJ, Rees H, et al. Twenty-five years' clinical experience with placental site trophoblastic tumors. J Reprod Med. 2002;47(6):460-4.
15
16. Lucas R, Cunha TM, Santos FB. Placental site trophoblastic tumor: a case report and review of the literature. J Radiol Case Rep. 2015;9(4):14-22.
16
17. Lima LLA, Padron L, Câmara R, Sun SY, Rezende J Filho, Braga A. The role of surgery in the management of women with gestational trophoblastic disease. Rev Col Bras Cir. 2017;44(1):94-101.
17
18. Lan C, Li Y, He J, Liu J. Placental site trophoblastic tumor: lymphatic spread and possible target markers. Gynecol Oncol. 2010;116(3):430-7.
18
19. Papadopoulos AJ, Foskett M, Seckl MJ, McNeish I, Paradinas FJ, Rees H, et al. Twenty-five years' clinical experience with placental site trophoblastic tumors. J Reprod Med. 2002;47(6):460-4.
19
20. Schmid P, Nagai Y, Agarwal R, Hancock B, Savage PM, Sebire NJ, Lindsay I, et al. Prognostic markers and long-term outcome of placental-site trophoblastic tumours: a retrospective observational study. Lancet. 2009;374(9683):48-55.
20
21. Huang F, Zheng W, Liang Q, Yin T. Diagnosis and treatment of placental site trophoblastic tumor. Int J Clin Exp Pathol. 2013;6(7):1448-51.
21
22. How J, Scurry J, Grant P, Sapountzis K, Ostor A, Fortune D, et al. Placental site trophoblastic tumor. Report of three cases and review of the literature. Int J Gynecol Cancer. 1995;5(4):241-249.
22
ORIGINAL_ARTICLE
Neoadjuvant Chemotherapy of Cervical Squamous Cell Carcinoma during Pregnancy: A Case Report
Squamous cell carcinoma is one of the common malignancies among women, especially in the third and fourth decades of life. Human papillomavirus is the most important cause of squamous cell carcinoma among women worldwide. Early diagnosis and treatment of this carcinoma can prevent disease progression. Herein, we present the case of a pregnant woman with squamous cell carcinoma. A 35-year-old pregnant woman referred to our clinic for cervical cerclage. During the procedure, the gynecological surgeon observed a suspicious lesion. Accordingly, cervical conization was performed and a squamous cell carcinoma lesion was confirmed by the pathology reports. Neoadjuvant chemotherapy was initiated for the patient during pregnancy. Radical hysterectomy and bilateral lymphadenectomy were conducted toward caesarean section. As the patient was a young fertile woman, the ovaries were saved. Although chemotherapy is not a standard treatment for cervical cancer in pregnancy, but neoadjuvant chemotherapy followed by radical hysterectomy and bilateral pelvic lymphadenectomy during cesarean section was a successful treatment in our patient.
https://mejc.sums.ac.ir/article_42136_1ff0bd075c231bcc0ac1f18f74776233.pdf
2018-10-01
334
338
10.30476/mejc.2018.42136
Malihe
Hasanzadeh
1
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zohreh
Yousefi
yousefiz@mums.ac.ir
2
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Amir Hosein
Jafarian
3
Department of Pathology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Shohreh
Saeed
4
Gynecologist Oncologist, Fellowship of Gynecology Oncology, Mashhad, Iran
AUTHOR
Laya
Shirinzadeh
lashirinzadeh@gmail.com
5
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Behrouz
Davachi
6
Department of Radiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Marjaneh
Farazestanian
farazestanianm@mums.ac.ir
7
Department of Obstetrics and Gynecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Hecking T, Abramian A, Domröse C, Engeln T, Thiesler T, Leutner C, et al. Individual management of cervical cancer in pregnancy. Arch Gynecol Obstet. 2016;293(5):931-9.
1
2. Mocarska A, Starosławska E, Zelazowska-Cieślińska I, Łosicki M, Stasiewicz D, Kieszko D, et al. Epidemiology and risk factors of the cervical squamous cell carcinoma. [Article in Polish] Pol Merkur Lekarski. 2012;33(194):101-6.
2
3. Hiniker SM, Roux A, Murphy JD, Harris JP, Tran PT, Kapp DS, et al. Primary squamous cell carcinoma of the vagina: prognostic factors, treatment patterns, and outcomes. Gynecol Oncol. 2013;131(2):380-5.
3
4. Gadducci A, Fabrini MG, Lanfredini N, Sergiampietri C. Squamous cell carcinoma of the vagina: natural history, treatment modalities and prognostic factors. Crit Rev Oncol Hematol. 2015;93(3):211-24.
4
5. Madsen BS, Jensen HL, van den Brule AJ, Wohlfahrt J, Frisch M. Risk factors for invasive squamous cell carcinoma of the vulva and vagina--population-based case-control study in Denmark. Int J Cancer. 2008;122(12):2827-34.
5
6. Sadler L, Sykes P. How little is known about cervical cancer in pregnancy? Ann Oncol. 2005;16(3):341-3.
6
7. Morice P, Uzan C, Gouy S, Verschraegen C, Haie-Meder C. Gynaecological cancers in pregnancy. Lancet. 2012;379(9815):558-69.
7
8. Han SN, Gziri MM, Van Calsteren K, Amant F. Cervical cancer in pregnant women: treat, wait or interrupt? Assessment of current clinical guidelines, innovations and controversies. Ther Adv Med Oncol. 2013;5(4):211-9.
8
9. Eitan R, Abu-Rustum NR. Management of cervical carcinoma diagnosed during pregnancy. Primary Care Update for OB/GYNS. 2003;10(4):196-200.
9
10. Ribeiro F, Correia L, Paula T, Santana I, Pinto LV, Borrego J, et al. Cervical cancer in pregnancy: 3 cases, 3 different approaches. J Low Genit Tract Dis. 2013;17(1):66-70.
10
11. Ungár L, Smith JR, Pálfalvi L, Del Priore G. Abdominal radical trachelectomy during pregnancy to preserve pregnancy and fertility. Obstet Gynecol. 2006;108(3 Pt 2):811-4.
11
12. Van DeNIEUWENHOF H, VanHAM M, Lotgering F, Massuger L. First case of vaginal radical trachelectomy in a pregnant patient. Int J Gynecol Cancer. 200c;18(6):1381-5.
12
13. de Haan J, Vandecaveye V, Han S, Van de Vijver K, Amant F. Difficulties with diagnosis of malignancies in pregnancy. Best Pract Res Clin Obstet Gynaecol. 2016;33:19-32.
13
14. Robova H, Rob L, Pluta M, Kacirek J, Halaska Jr M, Strnad P, et al. Squamous intraepithelial lesion-microinvasive carcinoma of the cervix during pregnancy. Eur J Gynaecol Oncol. 2005;26(6):611-4.
14
15. Fruscio R, Villa A, Chiari S, Vergani P, Ceppi L, Dell'Orto F, et al. Delivery delay with neoadjuvant chemotherapy for cervical cancer patients during pregnancy: a series of nine cases and literature review. Gynecol Oncol. 2012;126(2):192-7.
15
16. Rabaiotti E, Sigismondi C, Montoli S, Mangili G, Candiani M, Viganò R. Management of locally advanced cervical cancer in pregnancy: a case report. Tumori. 2010;96(4):623-6.
16
ORIGINAL_ARTICLE
Intratumoral Heterogeneity in Breast Cancer: A Case Report and Molecular Discussion
The emerging era of personalized medicine makes it increasingly important to consider intratumoral heterogeneity, which has been found in some breast cancer cases. However, its identification criteria, form of reporting, and subsequent effects on the clinical course of this disease remain controversial and not fully defined. Here, we report and discuss a case of breast invasive ductal adenocarcinoma with substantial intratumoral heterogeneity, discrepancy between Her2/neu immunostaining and in situ hybridization, and disparity between estrogen receptor status before and after neoadjuvant therapy.
https://mejc.sums.ac.ir/article_42138_45a8895ef94736efe8147ee50365c0a2.pdf
2018-10-01
339
343
10.30476/mejc.2018.42138
Breast
Estrogen receptor
ErbB-2
Genetic heterogeneity
Personalized Medicine
Akbar
Safaei
safaei32akbar@yahoo.com
1
Department of Hematopathology, Molecular Pathology and Cytogenetics, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Ahmad
Monabati
ahmad_monabati@yahoo.com
2
Department of Hematopathology, Molecular Pathology and Cytogenetics, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Maral
Mokhtari
maral_mokhtari@yahoo.com
3
Department of Hematopathology, Molecular Pathology and Cytogenetics, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mehdi
Montazer
mehdi.montazer@gmail.com
4
Department of Hematopathology, Molecular Pathology and Cytogenetics, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1- Cho SH, Jeon J, Kim SI. Personalized medicine in breast cancer: a systematic review. J Breast Cancer. 2012;15(3):265-72.
1
2- Verma M. Personalized medicine and cancer. J Pers Med. 2012;2(1):1-14.
2
3- Tang P, Tse GM. Immunohistochemical surrogates for molecular classification of breast carcinoma: A 2015 update. Arch Pathol Lab Med. 2016;140(8):806-14.
3
4- Wolff AC, Hammond ME, Hicks DG, Dowsett M, McShane LM, Allison KH, et al. Recommendations for human epidermal growth factor receptor 2 testing in breast cancer: American Society of Clinical Oncology/College of American Pathologists clinical practice guideline update. Arch Pathol Lab Med. 2014;138(2):241-56.
4
5- Fitzgibbons PL, Dillon DA, Alsabeh R, Berman MA, Hayes DF, Hicks DG, et al. Template for reporting results of biomarker testing of specimens from patients with carcinoma of the breast. Arch Pathol Lab Med. 2014;138(5):595-601.
5
6- Varga Z, Tubbs RR, Moch H. Concomitant detection of HER2 protein and gene alterations by immunohistochemistry (IHC) and silver enhanced in situ hybridization (SISH) identifies HER2 positive breast cancer with and without gene amplification. PLoS One. 2014;9(8):e105961.
6
7- Seol H, Lee HJ, Choi Y, Lee HE, Kim YJ, Kim JH, et al. Intratumoral heterogeneity of HER2 gene amplification in breast cancer: its clinicopathological significance. Mod Pathol. 2012;25(7):938-48.
7
8- Makroo RN, Chowdhry M, Kumar M, Srivastava P, Tyagi R, Bhadauria P, et al. Correlation between HER2 gene amplification and protein overexpression through fluorescence in situ hybridization and immunohistochemistry in breast carcinoma patients. Indian J Pathol Microbiol. 2012;55(4):481-4.
8
9- Tamaki K, Sasano H, Ishida T, Miyashita M, Takeda M, Amari M, et al. Comparison of core needle biopsy (CNB) and surgical specimens for accurate preoperative evaluation of ER, PgR and HER2 status of breast cancer patients. Cancer Sci. 2010;101(9):2074-9.
9
10- Niikura N, Tomotaki A, Miyata H, Iwamoto T, Kawai M, Anan K, et al. Changes in tumor expression of HER2 and hormone receptors status after neoadjuvant chemotherapy in 21,755 patients from the Japanese breast cancer registry. Ann Oncol. 2016;27(3):480-7.
10
ORIGINAL_ARTICLE
Recurrent Neuroglycopenia: Do Not Forget Non-islet Cell Induced Tumor Hypoglycemia
Non-islet cell tumor hypoglycemia (NICTH) is an exceedingly rare paraneoplastic condition and often its commonest presenting symptom is hypoglycaemia. Most cases of NICTH are associated with underlying mesenchymal or epithelial neoplasm. However our case is unique as NICTH was associated with well differentiated liposarcoma, which has never been described before. Most of the reported cases of NICTH were diagnosed on the basis of biochemical tests. However NICTH can also be a diagnosis of exclusion as highlighted by our case report. This case also highlights both the diagnostic dilemma and the surgical challenges in the management of such cases. The elderly lady presented with repeated episodes of loss of unconsciousness for which she was hospitalised twice. Her symptoms closely resembled that of a cerebrovascular accident patient. However CT brain did not reveal any brain lesion. However she also had spontaneous episodes of hypoglycaemia which led to further investigations. Ultrasonography abdomen revealed presence of huge retroperitoneal mass on FNAB which was malignant. Subsequently, she was put on dextrose drip and thorough investigations ruled out metastatic disease. She underwent laparotomy and the mass was excised enbloc. Postoperative recovery was smooth and the hypoglycaemia resoled spontaneously. Final histopathologic examination was suggestive of well differentiated liposarcoma. At the 6-month follow-up, she was free from hypoglycemic episodes. This case highlights that NICTH can be a difficult diagnosis given its propensity to mimic several other benign conditions. NICTH can also be caused by liposarcomas. Diagnosis by excluding all other causes of hypoglycaemia is also an option where costly biochemical tests are unavailable. Surgical excision is the main stay of treatment.
https://mejc.sums.ac.ir/article_42140_b3664e8190d32682fdd4286f05606f6b.pdf
2018-10-01
344
347
10.30476/mejc.2018.42140
NICTH
Liposarcoma
Atypical lipomatous tumour
Paraneoplastic syndrome
hypoglycemia
Suvendu
Maji
drsuvendumaji@rediffmail.com
1
Department of Surgical Oncology, Chittaranjan National Cancer Institute, West Bengal, India
LEAD_AUTHOR
Indranil
Ghosh
2
Department of Surgical Oncology, Chittaranjan National Cancer Institute, West Bengal, India
AUTHOR
Escobar GA, Robinson WA, Nydam TL, Heiple DC, Weiss GJ, Buckley L, et al. Severe paraneoplastic hypoglycemia in a patient with a gastrointestinal stromal tumor with an exon 9 mutation: a case report. BMC Cancer. 2007;7:13.
1
Service FJ, McMahon MM, O'Brien PC, Ballard DJ. Functioning insulinoma--incidence, recurrence, and long-term survival of patients: a 60-year study. Mayo Clin Proc. 1991;66(7):711-9.
2
Blackman MR, Rosen SW, Weintraub BD. Ectopic hormones. Adv Intern Med. 1978;23:85-113.
3
Odell WD, Wolfsen AR. Humoral syndromes associated with cancer. Annu Rev Med. 1978;29:379-406.
4
Sluiter WJ, Marrink J, Houwen B. Monoclonal gammopathy with an insulin binding IgG(K) M-component, associated with severe hypoglycaemia. Br J Haematol. 1986;62(4):679-87.
5
Stuart CA, Prince MJ, Peters EJ, Smith FE, Townsend CM 3rd, Poffenbarger PL. Insulin receptor proliferation: a mechanism for tumor-associated hypoglycemia. J Clin Endocrinol Metab. 1986;63(4):879-85.
6
Kiang DT, Bauer GE, Kennedy BJ. Immunoassayable insulin in carcinoma of the cervix associated with hypoglycemia. Cancer. 1973;31(4):801-5.
7
Silbert CK, Rossini AA, Ghazvinian S, Widrich WC, Marks LJ, Sawin CT. Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion. Diabetes. 1976;25(3):202-6.
8
Dutta P, Aggarwal A, Gogate Y, Nahar U, Shah VN, Singla M, et al. Non-islet cell tumor-induced hypoglycemia: a report of five cases and brief review of the literature. Endocrinol Diabetes Metab Case Rep. 2013;2013:130046.
9
Dimitriadis GK, Gopalakrishnan K, Rao R, Grammatopoulos DK, Randeva HS, Weickert MO, et al. Severe paraneoplastic hypoglycemia secondary to a gastrointestinal stromal tumour masquerading as a stroke. Endocrinol Diabetes Metab Case Rep. 2015;2015:150062.
10
ORIGINAL_ARTICLE
Calendar of Events
https://mejc.sums.ac.ir/article_42134_c041fdee684ef499061751fb5fe45c3c.pdf
2018-10-01
348