The Biology of Alkylating-Agent Cellular Injury
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New strategies in microbial screening for novel chemotherapeutics
2022, Bioprospecting of Microbial Diversity: Challenges and Applications in Biochemical Industry, Agriculture and Environment ProtectionSelective sensitization of tumors to chemotherapy by marine-derived lipids: A review
2013, Cancer Treatment ReviewsCitation Excerpt :It is assumed that the toxicity of chemotherapy to normal tissues is due to its non-selective distribution to tissues, and is driven by mechanisms similar to those responsible for its toxicity to tumors. DHA or EPA enhance the antitumor activity of 15 anticancer drugs which represent six families of drugs: antimetabolites (5-FU and cytarabine),92,93 alkylating (cyclophosphamide, mitomycin-C and cisplatin)94–96 or intercalating agents (doxorubicin, epirubicin, irinotecan and mitoxantrone),97–99 microtubule stabilizers (vinorelbine, vincristine, docetaxel, paclitaxel),100–102 Abl tyrosine kinase inhibitor (imatinib)103 and arsenic trioxide.104 Most of these drugs have damaging effects on the DNA.
Impact of first- and second-line treatment for Hodgkin's lymphoma on the incidence of AML/MDS and NHL-experience of the German Hodgkin's lymphoma study group analyzed by a parametric model of carcinogenesis
2011, Annals of OncologyCitation Excerpt :Increased incidence of secondary AML/MDS is clearly related to the primary chemotherapy [10–14]. The AML/MDS-inducing effect of chemotherapy is assumed to be based on DNA-breaking alkylating agents (e.g. cyclophosphamide, procarbazine) and Topoisomerase II inhibitors (e.g. doxorubicin, etoposide) while the effect of RT is less clear [10, 11, 15–18]. Several study groups assessed the long-term incidence of AML/MDS for different primary therapies of Hodgkin's lymphoma (see [19, 20] for an overview and meta-analysis).
Cytogenetically defined myelodysplasia after melphalan-based autotransplantation for multiple myeloma linked to poor hematopoietic stem-cell mobilization: The Arkansas experience in more than 3000 patients treated since 1989
2008, BloodCitation Excerpt :Long-term sequelae are uncommon, so that even third and fourth transplants have been successfully applied.7,8 Myelodysplastic syndrome (MDS) is a well-recognized complication of cancer therapy, especially with hematopoietic stem cell–toxic therapies such as ionizing radiation and alkylating agent–based chemotherapy (melphalan, nitrosoureas), occurring a median of 4 to 5 years after treatment.9TTT–11 Whereas cytogenetic abnormalities typifying MDS (MDS-CAs) after alkylator-based therapy include partial or complete deletions of chromosomes 5, 7, and 20 as well as trisomy 8,12,13 topoisomerase inhibitors, etoposide and doxorubicin, target chromosome 11 and induce MDS with a shorter latency phase of 1 to 2 years.14TTT–16
Niacin deficiency delays DNA excision repair and increases spontaneous and nitrosourea-induced chromosomal instability in rat bone marrow
2007, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisDeletion of 5q31 and 7q31 in patients with stable melphalan treated multiple myeloma
2004, Cancer Genetics and Cytogenetics