Consensus on the Existence of Functional Erythropoietin Receptors on Cancer Cells

Consensus on the Existence of Functional Erythropoietin Receptors on Cancer Cells Even when the US Food and Drug Administration approved erythropoietin to treat chemotherapy-induced anemia in 1993, concern was raised that administration of erythropoietin may lead to tumor growth. This possibility was derived from concern that erythropoietin receptors or homologous receptors reside on cancer cells and respond to exogenous erythropoietin, inducing activation of the cell signaling pathway and cellular functional changes. There has been widespread disagreement on this topic. Before 2008, a review found that scientists without funding from manufacturers of erythropoiesis-stimulating agents (ESAs) were more likely than scientists with such funding or scientists employed by manufacturers of ESAs to report erythropoietin receptors on solid tumor cells, erythropoietin-induced signaling changes, or cellular function changes.1 Three studies have been published by scientists employed by manufacturers of ESAs, which was too small a number to allow for direct comparisons between findings of academic scientists and scientists employed by manufacturers of ESAs.1 In 2007, the National Cancer Institute convened a workshop seeking to facilitate consensus on this topic. Thirteen of 14 academic scientists without funding from manufacturers of ESAs reported that erythropoietin receptors were involved in cancer progression while all 6 scientists employed by manufacturers of ESAs reported the opposite (A. Mufson, PhD, written communication, August 2015) (Table). Review of subsequent studies provides opportunities to evaluate whether consensus was achieved after the workshop. Our hypothesis is that differences in findings regarding erythropoietin receptors between academic scientists and scientists employed by manufacturers of ESAs would persist after the workshop.