Acute promyelocytic leukemia current treatment algorithms

Yılmaz, Musa; Kantarjian, Hagop M.; Ravandi, Farhad

doi:10.1038/s41408-021-00514-3

Cited by 123 publications

(114 citation statements)

References 77 publications

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“… (A) Giemsa‐stained metaphase spread, acquired after 48 h of incubation in culture media. (B) Metaphase spread from a non‐stimulated culture of peripheral blood sample demonstrating 47, XY, +8, del [ 9 ] (q21.1q22.1); t (15;17) (q24; q21) …”

Section: Case Presentationmentioning

confidence: 99%

Rare additional chromosomal abnormalities in acute promyelocytic leukaemia resulting in rapidly fatal disease: report of a case

Haidary

Noor²,

Noor

et al. 2021

eJHaem

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Background: Acute promyelocytic leukaemia results from reciprocal translocation between the long arms of chromosomes 15 and 17. This translocation leads to the formation of chimeric gene, which is both the diagnostic marker as well as the therapeutic target of the disease. Additional chromosomal abnormalities are randomly encountered either at diagnosis or during therapy. Here, we present a case of acute promyelocytic leukaemia that had a rare cytogenetic profile at diagnosis. Case presentation:Our patient was a 14-year-old boy, who presented with characteristic clinical and morphological features of acute promyelocytic leukaemia. Karyotypic analysis revealed trisomy of chromosome 8 with deletion of 9p in addition to t(15;17).The patient passed away within the first 8 h of presentation while receiving conventional chemotherapy and haemodynamic resuscitation. Conclusion:Our patient presented with a rare cytogenetic profile and rapidly progressive disease. According to our extensive literature search, this was the first case of acute promyelocytic leukaemia having pathognomonic t(15;17) along with trisomy 8 and 9q deletion.

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Section: Case Presentationmentioning

confidence: 99%

Rare additional chromosomal abnormalities in acute promyelocytic leukaemia resulting in rapidly fatal disease: report of a case

Haidary

Noor²,

Noor

et al. 2021

eJHaem

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“…In some FLT3-ITD+ APL patients, it was observed that the presenting clone at relapse lost the FLT3-ITD mutations or other passenger mutations that were present at diagnosis, indicating the existence of a pre-leukemic PML-RARA-expressing clone that survived RA/chemotherapy and reinitiated APL [37]. The combination of ATRA and As 2 O 3 has greatly reduced the rate of relapse and improved the lives of APL patients [38], and represents one of the most successful targeted cancer therapies available today, second in line only to TKI treatment in CML.…”

Section: Pml-raramentioning

confidence: 99%

Genomic Abnormalities as Biomarkers and Therapeutic Targets in Acute Myeloid Leukemia

Ribeiro

Eiring

Khorashad

2021

Cancers

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Acute myeloid leukemia (AML) is a highly heterogeneous malignancy characterized by the clonal expansion of myeloid stem and progenitor cells in the bone marrow, peripheral blood, and other tissues. AML results from the acquisition of gene mutations or chromosomal abnormalities that induce proliferation or block differentiation of hematopoietic progenitors. A combination of cytogenetic profiling and gene mutation analyses are essential for the proper diagnosis, classification, prognosis, and treatment of AML. In the present review, we provide a summary of genomic abnormalities in AML that have emerged as both markers of disease and therapeutic targets. We discuss the abnormalities of RARA, FLT3, BCL2, IDH1, and IDH2, their significance as therapeutic targets in AML, and how various mechanisms cause resistance to the currently FDA-approved inhibitors. We also discuss the limitations of current genomic approaches for producing a comprehensive picture of the activated signaling pathways at diagnosis or at relapse in AML patients, and how innovative technologies combining genomic and functional methods will improve the discovery of novel therapeutic targets in AML. The ultimate goal is to optimize a personalized medicine approach for AML patients and possibly those with other types of cancers.

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“…Acute promyelocytic leukemia (APL) with PML‐RARA accounts for 10%–15% of the newly diagnosed acute myeloid leukemia (AML) cases (Arber et al, 2017; Yilmaz et al, 2021). The onset of APL is commonly associated with disseminated intravascular coagulation (DIC) and patients have a high mortality rate if not treated promptly.…”

Section: Introductionmentioning

confidence: 99%

“…The onset of APL is commonly associated with disseminated intravascular coagulation (DIC) and patients have a high mortality rate if not treated promptly. All‐trans retinoic acid (ATRA) has been used to induce the immediate improvement of APL and control DIC (Yilmaz et al, 2021). In earlier studies, others have shown that early administration of ATRA (<24 h) and vigorous correction of hemostatic imbalance are keys to reducing early death in APL patients (Gill et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Acute promyelocytic leukemia: Immunophenotype and differential diagnosis by flow cytometry

Fang

Wang

et al. 2022

Cytometry Part B Clinical

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Background: Prompt diagnosis of acute promyelocytic leukemia (APL) is critical for patient care. In this study, we aimed to characterize the immunophenotype of APL and explore immunophenotypic difference between APL and its mimics using flow cytometric analysis.Methods: Eighty-five cases were collected, including 47 APL, 26 NPM1-mutated acute myeloid leukemia (AML) and 12 KMT2A-rearranged AML with an APL-like immunophenotype. Immunophenotypes were analyzed using flow cytometric analysis. Results: APL showed four distinct patterns (designated a-d) based on CD45/SSC plots. Blasts in patterns a-c showed high side scatter, whereas blasts in pattern d had low side scatter and were located in the traditional blast gate. Compared with patterns a-c, pattern d of APL (APL-D) was more often positive for CD2 (p = 0.0005) and CD34 (p = 0.0002) in blasts. All NPM1-mutated AML and KMT2Arearranged AML cases with an APL-like immunophenotype had blasts in the traditional blast gate on CD45/SSC, mimicking APL-D. In comparison, uniform CD13 and positive CD64 were seen in 100% (n = 13) APL-D cases and in only 2 of 26 (8%) NPM1-mutated AML cases (p < 0.0001). In addition, APL-D cases were more likely to be positive for CD2 and/or CD34 than NPM1-mutated AML (p < 0.0001 and p = 0.0007, respectively). In comparison with APL-D, KMT2Arearranged AML cases were less often positive for myeloperoxidase (MPO) (p = 0.001), with none being strongly positive. Similar to NPM1-mutated AML and different from APL-D, KMT2A-rearranged AML cases were rarely positive for CD34 and all negative for CD2.Conclusions: APL and its immunophenotypic mimics share some immunophenotypic similarities but can be distinguished by CD2, CD13, CD34, CD64, and MPO.

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Acute promyelocytic leukemia current treatment algorithms

Cited by 123 publications

References 77 publications

Rare additional chromosomal abnormalities in acute promyelocytic leukaemia resulting in rapidly fatal disease: report of a case

Rare additional chromosomal abnormalities in acute promyelocytic leukaemia resulting in rapidly fatal disease: report of a case

Genomic Abnormalities as Biomarkers and Therapeutic Targets in Acute Myeloid Leukemia

Acute promyelocytic leukemia: Immunophenotype and differential diagnosis by flow cytometry

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