Increased incidence of acute nonlymphocytic leukemia following therapy in patients with small cell carcinoma of the lung.

Chak, Linda Y.; Šikić, Branimir I.; Tucker, Margaret A.; Horns, R. C.; Cox, Richard S.

doi:10.1200/jco.1984.2.5.385

Cited by 68 publications

(7 citation statements)

References 19 publications

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“…The median time between the previous cancer diagnosis and MDS in our study was considerably shorter for lung cancer (1.0 years) and somewhat shorter for lymphohematopoietic cancers (5.1 years) than for all cancer types combined (6.5 years), additionally suggesting that the specific treatments for these cancers may have resulted in more aggressive MDS. Very rapid onset of secondary MDS following chemotherapy for lung cancer has also been observed in clinical studies (1.7-2.7 years median latency) [25,26], in which the actuarial risk of secondary MDS was notably higher for lung cancer than that recorded for other primary malignancies. Whether the clinical course of MDS following lung cancer differs from that in MDS following other primary malignancies was not described in previous clinical studies.…”

Section: Discussionmentioning

confidence: 89%

A population-based study of survival in patients with secondary myelodysplastic syndromes (MDS): impact of type and treatment of primary cancers

Roos

Deeg

Davis

2007

Cancer Causes Control

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Section: Discussionmentioning

confidence: 89%

A population-based study of survival in patients with secondary myelodysplastic syndromes (MDS): impact of type and treatment of primary cancers

Roos

Deeg

Davis

2007

Cancer Causes Control

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“…Chak et al [124] Jackson et al [127] (lung cancer) Newcomer and Farber [128] (lung cancer) Volk et al [129] (lung cancer) h i et al [6] (acute lymphocytic leukemia) Winick et al [88] (acute lymphocytic leukemia) Amylon et al [89] (acute lymphocytic leukemia and lymphoma) (acute lymphocytic leukemia) (acute lymphocytic leukemia) (acute lymphocytic leukemia) (pediatric malignancies) Sugita et al [87] Rubin et al [130] Verdeguer et al [131] Hawkins et a]. [95] The relatively high frequency with which translocations involving chromosome 1 lq23 occur (both de novo and following chemotherapy) implies the presence of a leukemogenic gene at this locus.…”

Section: Clinical and Biologic Characteristics Of Aml Following Topo-mentioning

confidence: 98%

Therapy‐related acute myeloid leukemia following treatment with epipodophyllotoxins: Estimating the risks

Smith

Rubinstein

Ungerleider

1994

Med. Pediatr. Oncol.

165

102

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In the past decade, therapy-related acute myeloid leukemia (t-AML) following treatment with regimens that include inhibitors of topoisomerase-II (TOPO-II) has been reported with increasing frequency. These cases of t-AML generally have a shorter latency period than t-AML following alkylator therapy, are associated with chromosomal translocations (especially involving chromosome band 11q23), and usually present as M4 or M5 FAB subtype. Although the epipodophyllotoxins (etoposide and teniposide) have been most often implicated, similar cases of t-AML occur following therapy with other classes of Topo-II inhibitors (e.g., anthracyclines). There is wide variation in published studies in the estimates of risk of t-AML following epipodophyllotoxin therapy. These varying estimates may reflect a number of factors, including: small sample size leading to large confidence intervals around risk estimates; varying susceptibility of different patient populations; varying schedules of epipodophyllotoxin administration; different cumulative doses of epipodophyllotoxins; and administration of epopodophyllotoxins with additional agents that may alter the leukemogenic effect of the epipodophyllotoxins. Available data suggest that children with acute lymphocytic leukemia (ALL) treated with high cumulative doses of epipodophyllotoxins using either weekly or twice-weekly schedules of administration have a relatively high risk of developing t-AML (5-12% cumulative risk). On the other hand, germ cell patients treated with relatively low cumulative doses of etoposide (usually 1,500-2,500 mg/m2) appear to have a low risk for developing t-AML. There is inadequate experience at this time with higher cumulative doses of etoposide (e.g., 4,000-5,000 mg/m2 as used for pediatric solid tumors) given on a daily x 5 schedule to allow estimates of risk to be developed for this schedule and cumulative dose. The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan designed to obtain reliable estimates of the risk of t-AML following epipodophyllotoxin treatment. Twelve Cooperative Group clinical trials that use epipodophyllotoxins at either low (< 1,500 mg/m2), moderate (1,500-3,999 mg/m2), or higher cumulative doses (> 4,000 mg/m2) are being prospectively monitored for cases of t-AML occurring among patients entered onto the trials.

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“…Additionally, the pathological type and stage of LC were found to be important factors affecting the occurrence of t-AML. The cumulative risk of t-MDS/t-AML after intensive treatment targeting SCLC has been reported to be 14% at 4 years after diagnosis [ 20 ] and 25% at 3 years after diagnosis [ 21 ]. Unfortunately, neither of these studies compared NSCLC with SCLC.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological features, risk and survival in lung cancer survivors with therapy-related acute myeloid leukaemia

et al. 2020

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Background A secondary malignancy is the most serious complication in lung cancer (LC) survivors. This study aimed to evaluate the clinicopathological features, predictable risk factors and survival of patients with LC who developed therapy-related acute myeloid leukaemia (t-AML). Methods Patients from the Surveillance, Epidemiology, and End Results (SEER) database diagnosed with t-AML after LC between 1975 and 2015 were included. Standardized incidence ratios (SIRs) were used to perform multiple primary analyses. The risk of t-AML development among LC patients was assessed using a logistic regression model. Kaplan–Meier analysis was used to construct overall survival (OS) curves. Cox regression was used to assess the influence of various prognostic factors. Results A total of 104 patients with t-AML after LC-targeting chemotherapy were included. The median latency period to the development of t-AML was 35.5 months. The calculated SIR of t-AML was 4.00. Chemoradiotherapy, small cell lung cancer (SCLC), or localized/regional-stage LC was a risk factor for the development of t-AML. The median OS was only 1 month, and those younger than 65 years were predicted to have a better OS time. Conclusions t-AML is a rare but serious late complication in LC patients and is associated with a poor prognosis. It is necessary to carry out long-term follow-up and screen for t-AML in LC patients, especially among those undergoing both radiotherapy and chemotherapy, with SCLC or with localized/regional-stage LC.

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Increased incidence of acute nonlymphocytic leukemia following therapy in patients with small cell carcinoma of the lung.

Cited by 68 publications

References 19 publications

A population-based study of survival in patients with secondary myelodysplastic syndromes (MDS): impact of type and treatment of primary cancers

A population-based study of survival in patients with secondary myelodysplastic syndromes (MDS): impact of type and treatment of primary cancers

Therapy‐related acute myeloid leukemia following treatment with epipodophyllotoxins: Estimating the risks

Clinicopathological features, risk and survival in lung cancer survivors with therapy-related acute myeloid leukaemia

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