Therapy-Related Acute Myeloid Leukemia after Concurrent Chemoradiotherapy for Esophageal Cancer: Report of Two Cases

2009 ◽  
Vol 95 (3) ◽  
pp. 371-373 ◽  
Author(s):  
Hung Chang ◽  
Chuang Chi Liaw ◽  
Hsien Kun Chang
Keyword(s):  
Esophageal Cancer ◽  
Acute Myeloid Leukemia ◽  
Cancer Treatment ◽  
Cancer Patients ◽  
Myeloid Leukemia ◽  
Concurrent Chemoradiotherapy ◽  
Late Complication ◽  
Definitive Therapy ◽  
Complex Chromosome ◽  
Acute Myeloid

Concurrent chemoradiotherapy (CCRT) has become an important part of esophageal cancer treatment. Its efficacy has been proved and its acute adverse effects are well understood. Leukemogenesis is a potential late complication of ionizing irradiation and chemotherapy. Therapy-related acute myeloid leukemia (AML), however, has been rarely reported in esophageal cancer patients receiving CCRT. We here report two such cases. One patient received neoadjuvant CCRT and developed AML with a complex chromosome aberration 55 months after exposure to radiation- and cisplatin-based chemotherapy. The other had AML with t(8;21) twenty months following CCRT as definitive therapy. Such a severe complication of CCRT is a serious concern in esophageal cancer treatment. In the wake of the prolonged survival of some esophageal cancer patients, the treatment intensity may need to be reconsidered according to such experience.

Acute Myeloid Leukemia Secondary to Oxaliplatin Treatment for Esophageal Cancer

2012 ◽  
Vol 11 (2) ◽  
pp. 151-154 ◽  
Author(s):  
Senthilkumar Damodaran ◽  
Tanya Bellavia ◽  
Sheila N.J. Sait ◽  
Eunice S. Wang ◽  
Meir Wetzler ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Oxaliplatin Treatment ◽  
Acute Myeloid

scholarly journals NRIP3: a novel translocation partner of MLL detected in a pediatric acute myeloid leukemia with complex chromosome 11 rearrangements

Haematologica ◽  
2009 ◽  
Vol 94 (7) ◽  
pp. 1033-1033 ◽  
Author(s):  
B. V. Balgobind ◽  
C. M. Zwaan ◽  
C. Meyer ◽  
R. Marschalek ◽  
R. Pieters ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Chromosome 11 ◽  
Pediatric Acute Myeloid Leukemia ◽  
Complex Chromosome ◽  
Acute Myeloid

scholarly journals How I treat acute myeloid leukemia presenting with preexisting comorbidities

Blood ◽  
2016 ◽  
Vol 128 (4) ◽  
pp. 488-496 ◽  
Author(s):  
Yishai Ofran ◽  
Martin S. Tallman ◽  
Jacob M. Rowe
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Pulmonary Insufficiency ◽  
Curative Intent ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Clinical Scenarios ◽  
Definitive Therapy ◽  
Acute Myeloid

Abstract Acute myeloid leukemia (AML) is a devastating disease with an incidence that progressively increases with advancing age. Currently, only ∼40% of younger and 10% of older adults are long-term survivors. If untreated, the overall prognosis of AML remains dismal. Initiation of therapy at diagnosis is usually urgent. Barriers to successful therapy for AML are the attendant toxicities directly related to chemotherapy or those associated with inevitable aplasia. Organ dysfunction often further complicates such toxicities and may even be prohibitive. There are few guidelines to manage such patients and the fear of crossing the medico-legal abyss may dominate. Such clinical scenarios provide particular challenges and require experience for optimal management. Herein, we discuss select examples of common pretreatment comorbidities, including cardiomyopathy, ischemic heart disease; chronic renal failure, with and without dialysis; hepatitis and cirrhosis; chronic pulmonary insufficiency; and cerebral vascular disease. These comorbidities usually render patients ineligible for clinical trials and enormous uncertainty regarding management reigns, often to the point of withholding definitive therapy. The scenarios described herein emphasize that with appropriate subspecialty support, many AML patients with comorbidities can undergo therapy with curative intent and achieve successful long-term outcome.

scholarly journals Biallelic TET2 mutation sensitizes to 5-azacitidine in acute myeloid leukemia

2021 ◽  
Author(s):  
Friedrich Stolzel ◽  
Sarah Fordham ◽  
Wei-Yu Lin ◽  
Helen Blair ◽  
Claire Elstob ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Precision Medicine ◽  
Cancer Patients ◽  
Myeloid Leukemia ◽  
Cell Model ◽  
Performance Status ◽  
Single Agent ◽  
Poor Performance Status ◽  
Allele Dosage ◽  
Acute Myeloid

Precision medicine can significantly improve outcomes for cancer patients, but implementation requires comprehensive characterization of tumor cells to identify therapeutically exploitable vulnerabilities. Here we describe somatic biallelic TET2 mutation (focal deletion and nonsense mutation) in an elderly patient with acute myeloid leukemia (AML) that was chemoresistant to anthracycline and cytarabine, but acutely sensitive to 5-azacitidine (5-Aza) hypomethylating monotherapy, resulting in long-term morphological remission (overall survival (OS) 850 days). Given the role of TET2 as a regulator of genomic methylation, we hypothesized that mutant TET2 allele dosage affects response to 5-Aza. Using an isogenic cell model system and an orthotopic mouse xenograft, we demonstrate that biallelic TET2 mutations confer sensitivity to 5-Aza compared to cells with monoallelic mutation. We subsequently identified 29 additional patients from the Study Alliance Leukemia biobank with chromosome 4 abnormalities and identified two further patients with complex biallelic TET2 mutations, including one with trisomy 4, homozygosity across the long arm and an inactivating point mutation. We also screened patients recruited to the PETHEMA FLUGAZA phase 3 clinical trial and identified three patients with biallelic TET2 mutations, two of whom had responded very well to single agent 5-Aza (OS 767 and 579 days) despite having adverse risk AML and poor performance status. Our data argue in favor of using hypomethylating agents for chemoresistant disease or as first line therapy in patients with biallelic TET2-mutated AML and demonstrate the importance of considering mutant allele dosage in the implementation of precision medicine for cancer patients.

Dexrazoxane exposure and risk of secondary acute myeloid leukemia in pediatric cancer patients.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 1504-1504
Author(s):  
Dana Marie Walker ◽  
Yimei Li ◽  
Yuan-Shung Huang ◽  
Alix Eden Seif ◽  
Marko Kavcic ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cancer Patients ◽  
Pediatric Cancer ◽  
Myeloid Leukemia ◽  
Administrative Database ◽  
Secondary Aml ◽  
Secondary Acute Myeloid Leukemia ◽  
Increased Risk ◽  
Pediatric Cancer Patients ◽  
Acute Myeloid

1504 Background: Dexrazoxane (DXZ) is an effective cardioprotectant in children with leukemia and solid tumors. However, the potential risk of secondary acute myeloid leukemia (AML) limits DXZ use. We compared the incidence of secondary AML in pediatric cancer patients with and without DXZ exposure to estimate the risk of DXZ-associated secondary AML. Methods: We conducted a retrospective cohort study of anthracycline exposed pediatric cancer patients (excluding de novo AML) hospitalized from January 1999 to March 2011 in 43 freestanding children’s hospitals in the Pediatric Health Information System (PHIS) database. Secondary AML was defined as an ICD9 code for AML that occurred at least 90 days after first anthracycline exposure. Proportions of patients with secondary AML were compared between patients with and without an exposure to DXZ after the initial anthracycline exposure. Results: During the study period of interest, 15,532 pediatric cancer patients were exposed to anthracycline, of which 1404 (9.04%) subsequently received DXZ. Secondary AML was identified in 235 (1.51%) patients. Patients ≥ 10 years of age, black patients, patients in New England and the Midatlantic regions, and those with bone tumors were significantly more likely to have received DXZ. The unadjusted incidence of secondary AML in the DXZ exposed and unexposed patients did not differ significantly (1.21% v. 1.54%, p=0.3308). After adjusting for these variations in demographics, the incidence of secondary AML still did not significantly differ between DXZ exposed and unexposed patients (p=0.6224). Conclusions: Our findings suggest that DXZ exposure does not lead to an increased risk of secondary AML in children. These data are important given the conflicting results from individual clinical trials about the risk of DXZ-associated secondary AML. While subject to well-known limitations of administrative database analyses, these data represent the largest cohort of DXZ exposed patients with available data on the occurrence of secondary AML. Additional multivariate analyses of chemotherapeutic covariates and time to secondary AML are ongoing.

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