Germ cells are sensitive to genotoxins, and ovarian failure and infertility are major side effects of chemotherapy in young patients with cancer. Here we describe the c-Abl–TAp63 pathway activated by chemotherapeutic DNA-damaging drugs in model human cell lines and in mouse oocytes and its role in cell death. In cell lines, upon cisplatin treatment, c-Abl phosphorylates TAp63 on specific tyrosine residues. Such modifications affect p63 stability and induce a p63-dependent activation of proapoptotic promoters.
For many individuals with cancer, protecting fertility from the damaging effects of radiation and chemotherapy is complicated by factors such as age, marital status, the time they have to delay treatment, even the uncertainty of surviving their disease.
Recent research and access to information about the fertility threats of treatment and the options for fertility preservation have improved significantly.
This can only be a good thing.
While this research is preclinical, it does offer hope for cancer patients because the findings could lead to new ways to protect germ cells from the damaging effects of toxic cancer treatments such as cisplatin, which is commonly used for treating breast and gynaecologic cancers.