Home Index

AU-KBC RESEARCH CENTRE  Life Sciences Research Faculty

The Breast Cancer Research Group
                                                                                                                    - P.Gajalakshmi & S.Bagavathi

Overview :

 BRCA1 Mutation screening

Germline mutations in the BRCA1 gene have been identified in a large number of families with multiple cases of early-onset breast and/or ovarian cancer. The involvement of BRCA1 gene mutations in hereditary breast cancer patients for the local population is little explored, as opposed to the situation in western countries. BRCA1 is located on chromosome 17q12-21 and has 24 exons, coding for a tumor suppressor protein comprising of 1863 amino acids with a molecular mass of 220kD. This study will provide an insight into the prevalence of BRCA1 mutations and their role in the incidence of breast cancer in the TamilNadu population.

Since BRCA1 is very large, we adopted a bioinformatic strategy to identify mutational hotspots for preliminary experimental characterization.

We are also studying the following aspects of breast cancer:
The risk assessment of some epidemiological factors associated with breast cancer patients based on a dataset derived from hospital patients has been studied. An Oracle database has been created and maintained for patient data.
The major known risk factors for female breast cancer are associated with prolonged exposure to increased levels of estrogen. Low penetrant genes, such as estrogen receptor (ESR), cytochrome P4501A1 (CYP1A1) and N-acetyl transferase (NAT) for spradic breast cancer, code for enzymes which are involved in the metabolism of estrogen and carcinogen. Many researchers have already investigated these genes but their results are conflicting. We are interested in reinvestigating the association of these polymorphic genes in sporadic breast cancer patients by the case - control method in the South Indian population with particular reference to TamilNadu, India.


Suicide Gene Therapy

Antitumor suicide gene therapy is one of the emerging strategies against cancer. This strategy relies upon conversion of a nontoxic prodrug into a toxic drug by means of a therapeutic gene. Since the introduction of this therapaeutic gene into the whole cell tumor population is difficult, the successful eradication of tumors depends on a phenomenon called the "bystander effect", by which the introduced gene can affect even cells in which it is not itself present.

Gap junctions are perceived to be one of the primary pathways that mediate the "bystander effect" in the treatment of cancer. Low transduction efficiency is thus mitigated by a gap junction mediated intercellular pathway. Therefore, we are interested in studying human breast carcinoma cell lines primarily to understand the role of intrinsic and induced gap junctions in the bystander effect in these cell lines. The long term objective is to extensively study, quantify and model the extent of the bystander effect in breast cancer cells.