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Mechanisms of abnormal erythropoiesis in malignancy
Author(s) -
Dainiak Nicholas,
Kulkarni Vivek,
Howard Donald,
Kalmanti Maria,
Dewey Maureen C.,
Hoffman Ronald
Publication year - 1983
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19830315)51:6<1101::aid-cncr2820510622>3.0.co;2-g
Subject(s) - erythropoietin , erythropoiesis , bone marrow , medicine , progenitor cell , anemia , hemoglobin , in vitro , malignancy , endocrinology , cell culture , pathogenesis , immunology , cancer research , biology , stem cell , microbiology and biotechnology , biochemistry , genetics
Abstract In order the investigate mechanisms of diminished red cell production in malignancy, we assayed erythroid progenitor cell proliferative responses to erythropoietin in plasma cloth cultures of bone marrow cells from 34 cancer patients. Erythroid colony growht by marrow cells of 11 healthy donors (means of 58 CFU‐E and 19 BFU‐E derived colonies/6 × 10 4 cells) was similar to that in cultures of cells from patients either with (means of 44 CFU‐E and 22 BFU‐E derived colonies/6 × 10 4 cells) or without was normal at all erythropoietin concentrations tested, indicating that both the CFU‐E and BFU‐E retin normal erythropoietin sensitivity in vitro. CFU‐E proliferation correlated negatively (r = − 0.56; P < 0.001) with the level of hemoglobin. In contrast to marrow cell proliferative responses to erythropoeitin, serum erythropoietin levels were inappropriately reduced in all 19 patients in whom they were measured, a finding which may be important in the pathogenesis of anemia in patients with cancer.