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Eryptotic erythrocytes are rapidly cleared from circulating blood and may adhere to the vascular wall. Stimulation of eryptosis thus impairs microcirculation and leads to anemia as soon as the loss of erythrocytes cannot be fully compensated by enhanced erythropoiesis. Signaling stimulating eryptosis includes increase of cytosolic Ca<jats:sup>2+<\/jats:sup>\u2010activity, ceramide, caspases, calpain, p38\u2010kinase, protein\u2010kinase C, Janus\u2010activated kinase 3, casein\u2010kinase 1\u03b1, and cyclin\u2010dependent kinase 4. Eryptosis is inhibited by AMP\u2010activated kinase, p21\u2010activated kinase 2, cGMP\u2010dependent protein\u2010kinase, mitogen\u2010 and stress\u2010activated kinase, and sorafenib\u2010 and sunitinib\u2010sensitive tyrosine\u2010kinases. Eryptosis is triggered by complement, hyperosmotic shock, energy\u2010depletion, oxidative stress, multiple xenobiotics including diverse cytostatic drugs, diabetes, hepatic failure, iron\u2010deficiency, chronic kidney disease, hemolytic\u2010uremic\u2010syndrome, fever, systemic lupus erythematosus, infections, sepsis, sickle cell anemia, thalassemia, glucose\u20106\u2010phosphate\u2010dehydrogenase deficiency, and Wilson\u00b4s disease. Compelling evidence points to a decisive role of eryptosis in anemia of malignancy. As shown for lung cancer, eryptosis inducing plasma components accumulate in cancer patients and trigger oxidative stress and ceramide. The tumor\u2010induced eryptosis leads to anemia despite increased erythropoiesis. The stimulation of eryptosis in malignancy is compounded by cytostatic treatment, as a large number of cytostatic agents trigger eryptosis. Inhibiting eryptosis may be a useful strategy in reducing tumor\u2010induced anemia and impaired microcirculation. Inhibitors of eryptosis may, however, be harmful, if they similarly interfere with death of tumor cells. Clearly, additional experimental effort is required to achieve killing of tumor cells with simultaneous avoidance of stimulated eryptosis.<\/jats:p>","DOI":"10.1002\/ijc.30800","type":"journal-article","created":{"date-parts":[[2017,5,24]],"date-time":"2017-05-24T00:49:46Z","timestamp":1495586986000},"page":"1522-1528","source":"Crossref","is-referenced-by-count":75,"title":["Suicidal death of erythrocytes in cancer and its chemotherapy: A potential target in the treatment of tumor\u2010associated anemia"],"prefix":"10.1002","volume":"141","author":[{"given":"Elisabeth","family":"Lang","sequence":"first","affiliation":[{"name":"Department of Molecular Medicine II Heinrich Heine University of D\u00fcsseldorf D\u00fcsseldorf Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosi","family":"Bissinger","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III Eberhard\u2010Karls\u2010University of T\u00fcbingen T\u00fcbingen 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