Chlamydia infection – a risk factor for ovarian and cervix carcinoma?
Chlamydia infection induces stress in the host cell that leads to DNA damage. In order to survive these bacteria must downregulate the TP53 tumor suppressor protein that mediates either cell-cycle arrest, suppression of nutrient availability or apoptosis in stressed cells. TP53-dependent pathways are also activated by oncogenes in early tumorigenesis. Evasion of p53-dependent apoptosis is thus a common response of the host to both Chlamydia infection and oncogenic transformation. Strong evidence has accumulated suggesting fallopian tubes, the sites for chronic infections with Chlamydia are the site of origin for ovarian cancer cells and pelvic inflammatory disease (a frequent disease connected to Chlamydia infection) which has been identified as a major risk factor for ovarian cancer. We investigate in this project how chlamydial infection may contribute to the development of ovarian and cervix cancer (read more).
We also follow the hypothesis, that Chlamydia – virus co-infections causes genomic instability and increased mutation rates supporting ovarian cancer (read more).