Relationship between MMP-11 Expression in Invasive Ductal Breast Carcinoma with its Clinicopathologic Parameters

Farshad Naghshvar, Zhila Torabizadeh, Jamshid Yazdani Charati, Mohammad Akbarnezhad


Background: Breast cancer is one of the most common cancers in the world, particularly in Iran. There are many genomic and molecular factors that cause the occurrence of breast cancer. Many markers are associated with tumor invasiveness. Matrix metalloproteinase includes a family of zinc-dependent endopeptidases that degrade various components of the extracellular matrix and basement membrane. Matrix metalloproteinase expressions increase in thyroid, colorectal, head and neck squamous cell carcinoma, lung, and ovarian cancers. It is correlated with tumor angiogenesis, invasion, and metastasis. Matrix metalloproteinase 11 is a member of the stromelysin subclass of the matrix metalloproteinase family. This enzyme is secreted to become a potentially active form against other matrix metalloproteinases. Contradictory results exist regarding the correlation between matrix metalloproteinase 11 expression and clinicopathologic parameters in breast cancer.

Methods: This case-control study examined 80 invasive ductal carcinoma of the breast and 80 adjacent nonneoplastic breast tissue paraffin blocks to identify the relationship between matrix metalloproteinase 11 expression and clinicopathologic parameters such as age, tumor size, microscopic grade, perineural and vascular invasion, lymph node involvement, and stage by immunohistochemistry analyses

Results: Among the 80 patients, 86.3% showed matrix metalloproteinase 11 expression in tumor cells and 17.5% had matrix metalloproteinase 11 expression in adjacent normal breast tissue. This expression correlated with stage, grade, lymph node metastasis, and perineural and vascular invasion (P0.05).

Conclusion: Matrix metalloproteinase 11 expression is increased in breast cancer and may be used as a predictive factor for tumor invasiveness.

Full Text:



  • There are currently no refbacks.

eISSN: 2008-6687           pISSN: 2008-6709