PATHOGENESIS OF ANEMIA IN RATS WITH WALKER-256 CARCINOSARCOMA

  • 1 January 1977
    • journal article
    • research article
    • Vol. 90  (3) , 502-511
Abstract
The purpose of this study was to further clarify the pathophysiology of anemia in malignancy. A total of 210 normal or splenectomized rats with or without the solid form of Walker 256 carcinosarcoma was studied. In vivo studies demonstrated that in stage I cancer (tumor weight < 10% of body weight) a slightly shortened red cell survival resulted in a mild degree of anemia. With increasing tumor size, 51Cr body red cell mass decreased further, in spite of extramedullary erythropoiesis and a slightly increased incorporation of transferrin-bound Fe into red cells. Splenectomized rats with stage II cancer developed a more profound degree of anemia associated with a significantly decreased incorporation of 59Fe into red cells. Marrow cell culture studies demonstrated that heme synthesis in response to erythropoietin in stage I cancer was not significantly different from normal, but in rats with stage II cancer (tumor weight was > 10% of body weight) heme synthesis in response to erythropoietin was markedly decreased. In vitro studies demonstrated that plasma erythropoietin levels were appropriately increased in most rats with transplanted malignancy. These studies indicate that bone marrow heme synthesis in response to erythropoietin is impaired in rats with the anemia of advanced malignancy.