Scientists have shown why a drug widely used to treat chemotherapy-induced anemia in ovarian and breast cancer patients also may shorten survival times in some patients by inadvertently stimulating tumor growth.
Anil Sood, M.D., professor of Gynecologic Oncology and Reproductive Medicine at MD Anderson, led a study that identified the cell receptor EphB4 as a catalyst for a chain of cell-signaling events leading to tumor growth. EphB4 is linked to the cancer-anemia therapy known as recombinant human erythropoietin (rhEPO). Erythropoietins (Epos) are protein molecules crucial for red blood cell production.
The study results were published last month in Cancer Cell.
Based on earlier studies, including work done by Molecular Health of Heidelberg, Germany, scientists wondered whether the cell receptor known as EpoR, which is normally associated with the anemia drug rhEPO, might be the cause. However, studies showed that EpoR “largely failed” to explain the effects of rhEPO on tumor growth.
“Evidence from other therapeutic areas has also suggested the existence of an alternative Epo receptor,” said Sood. “Such observations, combined with a lack of convincing molecular explanation underlying the effects of rhEpo on cancer growth, prompted us to consider the existence of an alternative Epo receptor.”
Sood’s team revealed EphB4 as a trigger for downstream cell signaling that promotes rhEpo-induced tumor growth and progression. The researchers found that EphB4 enhanced tumor growth via STAT3, a protein or transcription factor vital to gene regulation. The investigation employed both in vivo and in vitro samples.
Read more about this study on MD Anderson’s website.