Outcome of azacitidine treatment in patients with therapy-related myeloid neoplasms with assessment of prognostic risk stratification models

Duong, Vu H.; Lancet, Jeffrey E.; Alrawi, E; Al-Ali, Najla; Perkins, Janelle; Field, Teresa; Epling-Burnette, Pearlie K.; Zhang, Ling; List, Alan F.; Komrokji, Rami S.

doi:10.1016/j.leukres.2012.12.012

Cited by 18 publications

(10 citation statements)

References 21 publications

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“…Azacitidine has emerged as an alternative of intensive chemotherapy, especially in poor-risk patients [29–30]. Azacitidine has already been evaluated in therapy-related myeloid neoplasms with 40% overall response rate and a median OS between 9 and 21 months [31–33], which is in line with our LD/t-AML series, although the number of patients treated in our study was very low.…”

Section: Discussionsupporting

confidence: 83%

Therapy-related acute myeloid leukemia following treatment of lymphoid malignancies

et al. 2016

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Therapy-related acute myeloid leukemia (t-AML) is a heterogeneous entity most frequently related to breast cancer or lymphoproliferative diseases (LD). Population-based studies have reported an increased risk of t-AML after treatment of lymphomas. The aim of this study was to describe the characteristics and outcome of 80 consecutive cases of t-AML following treatment of LD. t-AML accounted for 2.3% of all AML cases, occurred 60 months after LD diagnosis, and were characterized by a high frequency of FAB M6 AML and poor-risk cytogenetic abnormalities. Time to t-AML diagnosis was influenced by patient age, type of LD, and treatment. Among the 48 t-AML patients treated with intensive chemotherapy, median overall survival (OS) was 7.7 months compared to 26.1 months in de novo, 4.2 months in post-myeloproliferative neoplasm, 9.4 months in post-myelodysplastic syndrome, 8.6 months in post-chronic myelomonocytic leukemia AML, 13.4 months in t-AML secondary to the treatment of solid cancer, and 14.7 months in breast cancer only. OS of post-LD t-AML patients was significantly influenced by age, performance status, myelodysplastic syndrome prior to LD/t-AML, and treatment regimen for LD. Thus, t-AML following lymphoid malignancies treatment should be considered as very high-risk secondary AML. New treatment strategies in patients with LD/t-AML are needed urgently.

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Section: Discussionsupporting

confidence: 83%

Therapy-related acute myeloid leukemia following treatment of lymphoid malignancies

et al. 2016

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“…While at the time of treatment no data were available on the use of azacitidine for therapy of t-AML, meanwhile some smaller studies have been published on azacitidine for t-MN [14][15][16]. The median length of treatment in all studies was 4.0-4.5 cycles.…”

Section: Discussionmentioning

confidence: 99%

Potential impact of the hypomethylating agent 5-azacitidine on chronic lymphocytic leukemia with del(17)(p)/del(p53) and subsequent therapy-related acute myeloid leukemia without these aberrations: a case report

Pfeilstöcker

Weichselbaum

Mühlberger

et al. 2015

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The patient presented here had a very poor prognosis due to previous chronic lymphocytic leukemia with unfavourable cytogenetics (deleted 17p and p53), therapy-related acute myeloid leukemia (intact 17p/p53), multiple pre-treatments (fludarabine, rituximab-CHOP, rituximab-bendamustine), advanced age (71 years) and several comorbidities-circumstances that usually do not allow high-dose chemotherapy or stem cell transplantation. Due to this unfavourable condition and reportedly poorer outcome of therapy-related acute myeloid leukemia relative to de novo acute myeloid leukemia with chemotherapy, treatment with the hypomethylating agent 5-azacitidine (Vidaza®), 75 mg/m 2 /day, subcutaneously for 7 days of 28-day cycles was started. Therapy was well tolerated and yielded a good response not only by eradicating the therapy-related acute myeloid leukemia but also by keeping the chronic lymphocytic leukemia under control for a rather long period of time. The simultaneous suppression and re-appearance of both the therapyrelated acute myeloid leukemia with intact p53 and the chronic lymphocytic leukemia with deleted p53 suggests that hypomethylation by azacitidine attains tumour control by a mechanism that (i) is similar in the different tumours and (ii) acts independently of the p53 status. This case may serve as a model for disease progression mirrored in molecular and cytogenetic findings which are factored into treatment decisions.

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“…Data regarding the efficacy of HMAs in t-MN comes primarily from retrospective studies (Table 3). Overall response rate (ORR) to azacitidine ranges from 28 to 50% [110][111][112][113][114]115] and OS ranges from 9.6 months to 21 months. OS in t-MN treated with azacitidine was significantly less than their de novo counterpart (median 9.2 versus 15.3 months, p = 0.002) (2 year OS of 14% vs 33.9%, p = 0.0005) [113,116] .However in two other studies, there was no significant difference in OS between t-MDS and de novo MDS [113,115].…”

Section: Management Strategies For T-mdsmentioning

confidence: 99%

Therapy-related myelodysplastic syndromes, or are they?

et al. 2017

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Outcome of azacitidine treatment in patients with therapy-related myeloid neoplasms with assessment of prognostic risk stratification models

Cited by 18 publications

References 21 publications

Therapy-related acute myeloid leukemia following treatment of lymphoid malignancies

Therapy-related acute myeloid leukemia following treatment of lymphoid malignancies

Potential impact of the hypomethylating agent 5-azacitidine on chronic lymphocytic leukemia with del(17)(p)/del(p53) and subsequent therapy-related acute myeloid leukemia without these aberrations: a case report

Therapy-related myelodysplastic syndromes, or are they?

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