Temozolomide-Induced Myelodysplasia
A patient who had received temozolomide (TMZ) as a single agent in treatment of malignant glioma developed therapy-induced myelodysplasia (T-MDS). TMZ is an orally active imidazotetrazine which methylates guanine residues in DNA, ultimately causing single and double-strand DNA breaks leading to apop...
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Wiley
2010-01-01
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Series: | Advances in Hematology |
Online Access: | http://dx.doi.org/10.1155/2010/760402 |
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author | Ethan A. Natelson David Pyatt |
author_facet | Ethan A. Natelson David Pyatt |
author_sort | Ethan A. Natelson |
collection | DOAJ |
description | A patient who had received temozolomide (TMZ) as a single agent in treatment of malignant glioma developed therapy-induced myelodysplasia (T-MDS). TMZ is an orally active imidazotetrazine which methylates guanine residues in DNA, ultimately causing single and double-strand DNA breaks leading to apoptotic cell death. TMZ does not chemically cross-link DNA and is considered a nonclassical alkylating agent, similar in structure and activity to dacarbazine. Observations on this patient, and on similarly treated others, suggest that the cumulative dose threshold (CDT) for TMZ that predisposes to T-MDS and which may potentially lead to acute myeloid leukemia (T-AML) is around 18000 to 20000 mg/sq m. Although the incidence of T-MDS and the predisposing CDT of TMZ may differ from that of other potentially leukemogenic compounds currently and formerly used as chemotherapeutic agents, all alkylating agents, including TMZ, should be considered potentially leukemogenic when administered long term. |
format | Article |
id | doaj-art-47109010266f4782b94fedf01df439cd |
institution | Kabale University |
issn | 1687-9104 1687-9112 |
language | English |
publishDate | 2010-01-01 |
publisher | Wiley |
record_format | Article |
series | Advances in Hematology |
spelling | doaj-art-47109010266f4782b94fedf01df439cd2025-02-03T06:43:54ZengWileyAdvances in Hematology1687-91041687-91122010-01-01201010.1155/2010/760402760402Temozolomide-Induced MyelodysplasiaEthan A. Natelson0David Pyatt1Department of Internal Medicine, The Methodist Hospital, Smith Tower 1001, 6550 Fannin Street, Houston, TX 77030, USASchool of Public Health, University of Colorado, Summit Toxicology, L.L.P., 1944 Cedaridge Circle, Superior, CO 80027, USAA patient who had received temozolomide (TMZ) as a single agent in treatment of malignant glioma developed therapy-induced myelodysplasia (T-MDS). TMZ is an orally active imidazotetrazine which methylates guanine residues in DNA, ultimately causing single and double-strand DNA breaks leading to apoptotic cell death. TMZ does not chemically cross-link DNA and is considered a nonclassical alkylating agent, similar in structure and activity to dacarbazine. Observations on this patient, and on similarly treated others, suggest that the cumulative dose threshold (CDT) for TMZ that predisposes to T-MDS and which may potentially lead to acute myeloid leukemia (T-AML) is around 18000 to 20000 mg/sq m. Although the incidence of T-MDS and the predisposing CDT of TMZ may differ from that of other potentially leukemogenic compounds currently and formerly used as chemotherapeutic agents, all alkylating agents, including TMZ, should be considered potentially leukemogenic when administered long term.http://dx.doi.org/10.1155/2010/760402 |
spellingShingle | Ethan A. Natelson David Pyatt Temozolomide-Induced Myelodysplasia Advances in Hematology |
title | Temozolomide-Induced Myelodysplasia |
title_full | Temozolomide-Induced Myelodysplasia |
title_fullStr | Temozolomide-Induced Myelodysplasia |
title_full_unstemmed | Temozolomide-Induced Myelodysplasia |
title_short | Temozolomide-Induced Myelodysplasia |
title_sort | temozolomide induced myelodysplasia |
url | http://dx.doi.org/10.1155/2010/760402 |
work_keys_str_mv | AT ethananatelson temozolomideinducedmyelodysplasia AT davidpyatt temozolomideinducedmyelodysplasia |