Supporting an Athlete With Breast Cancer: A Case Report.

For cancer survivors who also identify as athletes, a rigorous exercise that was once part of their daily routine and fundamental to their physical, psychological, and potentially financial well-being, may be temporarily or permanently altered in ways that exacerbate cancer-related changes in quality of life. This report presents an illustrative case of an endurance athlete who underwent breast cancer treatment and her subsequent return to high-performance, high elevation sport. We identify gaps in oncology research and patient educational tools to counsel athletes with cancer regarding the acute and long-term effects of cancer treatment and possibility of returning to a precancer level of fitness and performance. The report also highlights the need to tailor individualized cancer care treatment, rehabilitation, and the ability to preempt potential clinical and psychological side effects that may substantially impact training and competition.

Attenuated DNA damage repair delays therapy-related myeloid neoplasms in a mouse model.

Therapy-related cancers are potentially fatal late life complications for patients who received radio- or chemotherapy. So far, the mouse model showing reduction or delay of these diseases has not been described. We found that the disruption of Aplf in mice moderately attenuated DNA damage repair and, unexpectedly, impeded myeloid neoplasms after exposure to ionizing radiation (IR). Irradiated mutant mice showed higher rates of p53-dependent cell death, fewer chromosomal translocations, and a delay in malignancy-induced mortality. Simultaneous deficiency of p53 abrogated IR-induced apoptosis and the benefit of impaired DNA repair on mortality in irradiated Aplf­/­ mice. Depletion of APLF in non-tumorigenic human cells also markedly reduced the risk of radiation-induced chromosomal aberrations. We therefore conclude that proficient DNA damage repair may promote chromosomal aberrations in normal tissues after irradiation and induce malignant evolution, thus illustrating the potential benefit in sensitizing p53 function by manipulating DNA repair efficiency in cancer patients undergoing genotoxic therapies.