Acute myeloid leukemia: Treatment and research outlook for 2021 and the MD Anderson approach

Cancer ◽  
2021 ◽  
Author(s):  
Hagop M. Kantarjian ◽  
Tapan M. Kadia ◽  
Courtney D. DiNardo ◽  
Mary Alma Welch ◽  
Farhad Ravandi
2016 ◽  
Vol 87 (6) ◽  
pp. 927-935 ◽  
Author(s):  
Sorina Suarasan ◽  
Timea Simon ◽  
Sanda Boca ◽  
Ciprian Tomuleasa ◽  
Simion Astilean

2021 ◽  
pp. 1-5
Author(s):  
Ali Amanati ◽  

Persistent marrow aplasia is a rare complication with poor prognosis after intensive chemotherapy for acute myeloid leukemia. We present a 14-year-old boy with acute myeloid leukemia (AML), was complicated by chemotherapy induced persistent aplasia and he was expired because of prolonged neutropenia and pulmonary Aspergilosis. In this review we explain causes of persistent post chemotherapy persistent aplasia and prevention of this phenomenon during treatment with consideration of minimal residual disease (MRD) and response to question about chemotherapy titration dose.


2021 ◽  
Author(s):  
Romy E. Weelderen ◽  
Festus Njuguna ◽  
Kim Klein ◽  
Saskia Mostert ◽  
Sandra Langat ◽  
...  

2021 ◽  
Vol 17 (11) ◽  
pp. 2165-2175
Author(s):  
Xi Xu ◽  
Jian Wang ◽  
Tong Tong ◽  
Shao-Fen Lin ◽  
Congmin Liu ◽  
...  

Despite the continuous improvement of leukemia treatment in the clinic, the overall 5-year disease-free survival of acute myeloid leukemia (AML) is only approximately 30%–60% due to relapse and the refractoriness of AML after traditional chemotherapy. Inhibition of poly(ADP-ribose) polymerase (PARP), a member of the DNA damage repair complex, has a strong antitumor effect in solid tumors. However, the role of PARP in AML remains unclear. We found that high levels of PARP1 and PARP2 were positively related to chemotherapy resistance and poor prognosis in patients with AML. Doxorubicin (DOX)-resistant AML cells highly expressed PAPR1 and PARP2. Knockdown of PARP1 and PARP2, or pharmaceutical inhibition of PARP by the PARP inhibitor (PARPi) BGB-290, significantly enhanced the cytotoxicity of DOX in AML cells due to increased DNA damage. PLGA-loading BGB-290 was properly self-assembled into stable BGB-290@PLGA nanoparticles (NPs), which is uniform particle size and good stability. BGB-290@PLGA is easily uptake by AML cell lines and stays for a long time. Combined with DOX, BGB-290@PLGA can significantly improve the chemosensitivity of AML cell lines. Furthermore, BGB-290 and DOX combination treatment dramatically repressed the onset of leukemia and prolonged the survival of THP-1 xenografted mice. Overall, this study demonstrated that PARPi with traditional chemotherapy could be an efficient therapeutic strategy for AML.


2019 ◽  
Vol 35 (11) ◽  
pp. 1965-1970 ◽  
Author(s):  
Norah L. Crossnohere ◽  
Daniel R. Richardson ◽  
Crystal Reinhart ◽  
Bernadette O’Donoghue ◽  
Susan M. Love ◽  
...  

2020 ◽  
Vol 21 (16) ◽  
pp. 5626
Author(s):  
Laurène Fenwarth ◽  
Elise Fournier ◽  
Meyling Cheok ◽  
Thomas Boyer ◽  
Fanny Gonzales ◽  
...  

Gemtuzumab ozogamicin (GO, Mylotarg®) consists of a humanized CD33-targeted antibody-drug conjugated to a calicheamicin derivative. Growing evidence of GO efficacy in acute myeloid leukemia (AML), demonstrated by improved outcomes in CD33-positive AML patients across phase I to III clinical trials, led to the Food and Drug Administration (FDA) approval on 1 September 2017 in CD33-positive AML patients aged 2 years and older. Discrepancies in GO recipients outcome have raised significant efforts to characterize biomarkers predictive of GO response and have refined the subset of patients that may strongly benefit from GO. Among them, CD33 expression levels, favorable cytogenetics (t(8;21), inv(16)/t(16;16), t(15;17)) and molecular alterations, such as NPM1, FLT3-internal tandem duplications and other signaling mutations, represent well-known candidates. Additionally, in depth analyses including minimal residual disease monitoring, stemness expression (LSC17 score), mutations or single nucleotide polymorphisms in GO pathway genes (CD33, ABCB1) and molecular-derived scores, such as the recently set up CD33_PGx6_Score, represent promising markers to enhance GO response prediction and improve patient management.


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