89 research outputs found
Clinical practice guidelines for the prevention and treatment of EGFR inhibitor-associated dermatologic toxicities
Background Epidermal growth factor receptor inhibitors (EGFRI) produce various dermatologic side effects in the majority of patients, and guidelines are crucial for the prevention and treatment of these untoward events. The purpose of this panel was to develop evidence-based recommendations for EGFRI-associated dermatologic toxicities. Methods A multinational, interdisciplinary panel of experts in supportive care in cancer reviewed pertinent studies using established criteria in order to develop first-generation recommendations for EGFRI-associated dermatologic toxicities. Results Prophylactic and reactive recommendations for papulopustular (acneiform) rash, hair changes, radiation dermatitis, pruritus, mucositis, xerosis/fissures, and paronychia are presented, as well as general dermatologic recommendations when possible. Conclusion Prevention and management of EGFRI-related dermatologic toxicities is critical to maintain patients’ health-related quality of life and dose intensity of antineoplastic regimens. More rigorous investigation of these toxicities is warranted to improve preventive and treatment strategies
A comparative study of the effects of anti-tumour and immunosuppressive drugs on antibody-forming and erythropoietic cells
Immunosuppressive and erythroid cell line depressing activities of various agents used in cancer chemotherapy were investigated simultaneously in the same mice and compared to X-Rays. Vincristine, vinblastine, mitomycin C and actinomycin D had greater effects on erythropoiesis than on antibody-forming cells. By contrast, the immunosuppressive effects of cyclophosphamide, demecolcine and methotrexate exceeded markedly their erythropoietic toxicity. The Vinca alkaloids stimulated the secondary immune response, whereas X-Rays, antilymphocytic serum and the methylhydrazine derivatives inhibited the anamnestic response to a greater extent than the primary immune response
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