Secondary Leukemia or Myelodysplastic Syndrome After Treatment With Epipodophyllotoxins

Smith, Malcolm A.; Rubinstein, Larry; Anderson, James R.; Arthur, Diane C.; Catalano, Paul J.; Freidlin, Boris; Heyn, Ruth; Khayat, Anita; Krailo, Mark; Land, Vita J.; Miser, James S.; Shuster, Jonathan J.; Vena, Don

doi:10.1200/jco.1999.17.2.569

Cited by 270 publications

(159 citation statements)

References 45 publications

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“…Despite the importance of topoisomerase II as a target for cancer chemotherapy, considerable evidence suggests that the enzyme also initiates chromosomal translocations that lead to specific types of leukemia [84,86,94,[139][140][141]. For example, ~2-3% of patients treated with regimens that include etoposide ultimately develop acute myelocytic leukemia [84,86,94,139,140].…”

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

“…For example, ~2-3% of patients treated with regimens that include etoposide ultimately develop acute myelocytic leukemia [84,86,94,139,140]. Recently, correlations between the rising use of mitoxantrone to treat breast cancer and the development of secondary leukemias have been reported [142].…”

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

“…Recently, correlations between the rising use of mitoxantrone to treat breast cancer and the development of secondary leukemias have been reported [142]. Over 50% of these leukemias display translocations within an 8.3 kb breakpoint cluster region in the MLL gene at chromosomal band 11q23 [84,86,94,139,140,143]. DNA breakpoints found in these secondary leukemias are in close proximity to topoisomerase II cleavage sites [144][145][146].…”

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

“…DNA breakpoints found in these secondary leukemias are in close proximity to topoisomerase II cleavage sites [144][145][146]. It is notable that therapy-related leukemias with 11q23 rearrangements are unique to chemotherapeutic regimens that contain topoisomerase II-targeted drugs [84,86,94,139].…”

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

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DNA topoisomerase II, genotoxicity, and cancer

McClendon

Osheroff

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

363

466

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Type II topoisomerases are ubiquitous enzymes that play essential roles in a number of fundamental DNA processes. They regulate DNA under-and overwinding, and resolve knots and tangles in the genetic material by passing an intact double helix through a transient double-stranded break that they generate in a separate segment of DNA. Because type II topoisomerases generate DNA strand breaks as a requisite intermediate in their catalytic cycle, they have the potential to fragment the genome every time they function. Thus, while these enzymes are essential to the survival of proliferating cells, they also have significant genotoxic effects. This latter aspect of type II topoisomerase has been exploited for the development of several classes of anticancer drugs that are widely employed for the clinical treatment of human malignancies. However, considerable evidence indicates that these enzymes also trigger specific leukemic chromosomal translocations. In light of the impact, both positive and negative, of type II topoisomerases on human cells, it is important to understand how these enzymes function and how their actions can destablize the genome. This article discusses both aspects of human type II topoisomerases.

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Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

Section: Non-covalent Topoisomerase II Poisonsmentioning

confidence: 99%

See 2 more Smart Citations

DNA topoisomerase II, genotoxicity, and cancer

McClendon

Osheroff

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

363

466

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“…6,7 Childhood cancer survivors can also develop AML or MDS after treatment with growth factors (GFs), in combination with etoposide, anthracyclines, and radiotherapy. However, it is difficult to distinguish the contribution of GF versus intensified therapy and the effect of intensity 8 or cumulative doses of chemotherapy 9,10 in the development of secondary hematological malignancies.…”

mentioning

confidence: 99%

Secondary hematopoietic malignancies in survivors of childhood cancer

Rihani

Bazzeh

Faqih

et al. 2010

Cancer

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BACKGROUND: Studying secondary hematological malignancies in a large cohort of patients can help predict risks and trends associated with current therapies. METHODS: The authors analyzed data from the Surveillance, Epidemiology, and End Resultsecondary 9 (SEER-9) database on patients with a primary malignancy (diagnosed before the age of 20 years) between 1973 and 2005 who developed a secondary hematological malignancy. Primary cancer and histological subtype, incidence, risk factors, outcomes, and changes in risk patterns of secondary hematological malignancies were analyzed for 1973 to 1985, 1986 to 1995, and 1996 to 2005. Standardized incidence ratios (SIRs) of observed to expected cancers were calculated. RESULTS: Of 34,867 patients with a histology-confirmed primary malignancy, 111 developed secondary hematological malignancies (median, 44 months). Lymphoma was the commonest primary cancer (n ¼ 47). The main histological subtype of secondary hematological malignancy was acute myeloid leukemia (AML) (49%), which had the shortest median latency time and the worst 5-year survival (18% AE 5.3%; P ¼.044). Secondary Hodgkin lymphoma had the best 5-year survival (83% AE 15%). The 5-year overall survival for patients with secondary hematological malignancies was 31% AE 4.7%. The risk of secondary AML steadily increased from 1986 to 2005, whereas SIRs for acute lymphoblastic leukemia did not change over time. Non-Hodgkin lymphoma, the second most common secondary hematological malignancy, occurred at a median of 112 months, and its risk steadily increased over time periods. CONCLUSIONS: Childhood cancer survivors are at increased risk of developing secondary hematological malignancies, particularly secondary AML. This risk has continued to rise even in recent years, emphasizing the need to study other factors contributing to secondary hematological malignancies and closely monitor these patients. Cancer 2010;116:4385-94.

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The Adverse Events of Chemotherapy for Retinoblastoma

Rizzuti¹

2008

Arch Ophthalmol

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Secondary Leukemia or Myelodysplastic Syndrome After Treatment With Epipodophyllotoxins

Cited by 270 publications

References 45 publications

DNA topoisomerase II, genotoxicity, and cancer

DNA topoisomerase II, genotoxicity, and cancer

Secondary hematopoietic malignancies in survivors of childhood cancer

The Adverse Events of Chemotherapy for Retinoblastoma

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