ROLE OF GENETIC ALTERATIONS IN BREAST CANCER PROGRESSION.

Breast cancer is a multifactorial disease and represents the tumor formation through non-controlled cellular proliferation in the breast tissue. To understand the concept of breast cancer, one has to study the types, risk factors, diagnosis, treatment and latest research about the disease[1].While breast cancer remains a premier health concern, the advances made in research methods and tools, early detection and treatments have dramatically improved survival rates and quality of life for many patients [2].The incidence rates for breast cancer have been on the increase due to increased awareness, better diagnostic facilities and changes in lifestyle[3].The Wnt signaling pathway normally plays a very fundamental role in cell growth, differentiation and embryonic development. Understanding this pathway is important for the development of targeted therapies and advanced understanding in the advancement of regenerative medicine[4].HCCRI is an abbreviation of Human Cervical cancer Related 1, a gene implicated in the development of cancer especially in cervical cancer. It encodes for a protein involved in regulating all proliferation and apoptosis. Overexpression of HCCRI has been implicated in tumor progressions and prognosis in various cancers. Research indicates that HCCRI could be utilized as a biomarker for diagnosis in cancer and prognosis while the targeting of HCCRI can offer new therapeutic strategies in managing cancer[5].The TIMP2 gene encodes a tissue inhibitor of metalloproteinases 2-a protein that plays a critical role in regulating extracellular matrix remodeling through the inhibition of matrix metalloproteinases. This inhibition controls the degradation and remodeling of tissue leading to various physiological processes such as wound healing and embryogenesis. TIMP2 is involved in maintaining tissue integrity and has been implicated in various pathological conditions including cancer metastasis and cardiovascular diseases. It operates by binding to MMPs, thus preventing their activity and subsequent breakdown of extracellular characterized by excessive tissue remodelling or insufficient tissue repair[6].