The Role of Maintenance Chemotherapy, Immunotherapy, Induction Dose Reduction in Elderly Patients and Double Induction in the Treatment of Adult Acute Myeloid Leukemia. Four Randomized Studies of the AML Cooperative Group1

Author(s):  
Th. Büchner ◽  
W. Hiddemann ◽  
P. Koch ◽  
H. Pielken ◽  
D. Urbanitz ◽  
...  
2016 ◽  
Vol 33 (4) ◽  
pp. 273-280 ◽  
Author(s):  
Anıl Tombak ◽  
Mehmet Ali Uçar ◽  
Aydan Akdeniz ◽  
Eyüp Naci Tiftik ◽  
Deniz Gören Şahin ◽  
...  

2018 ◽  
Vol 25 (8) ◽  
pp. 2035-2037 ◽  
Author(s):  
Craig W Freyer ◽  
James K Mangan

We describe a case of dose-related periorbital edema in a patient with FLT3-mutated acute myeloid leukemia taking sorafenib and voriconazole that resolved following sorafenib dose reduction. We hypothesize that the mechanism of this adverse event may be related to the inhibition of platelet-derived growth factor receptor (PDGFR) by sorafenib. Clinicians should be aware of this possible dose-related adverse event and the potential role of sorafenib dose reduction when on concurrent voriconazole.


2019 ◽  
Vol XIV (1) ◽  
Author(s):  
A.M. Radzhabova ◽  
S.V. Voloshin ◽  
I.S. Martynkevich ◽  
A.A. Kuzyaeva ◽  
V.A. Shuvaev ◽  
...  

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Yiyi Yao ◽  
Fenglin Li ◽  
Jiansong Huang ◽  
Jie Jin ◽  
Huafeng Wang

AbstractDespite the advances in intensive chemotherapy regimens and targeted therapies, overall survival (OS) of acute myeloid leukemia (AML) remains unfavorable due to inevitable chemotherapy resistance and high relapse rate, which mainly caused by the persistence existence of leukemia stem cells (LSCs). Bone marrow microenvironment (BMM), the home of hematopoiesis, has been considered to play a crucial role in both hematopoiesis and leukemogenesis. When interrupted by the AML cells, a malignant BMM formed and thus provided a refuge for LSCs and protecting them from the cytotoxic effects of chemotherapy. In this review, we summarized the alterations in the bidirectional interplay between hematopoietic cells and BMM in the normal/AML hematopoietic environment, and pointed out the key role of these alterations in pathogenesis and chemotherapy resistance of AML. Finally, we focused on the current potential BMM-targeted strategies together with future prospects and challenges. Accordingly, while further research is necessary to elucidate the underlying mechanisms behind LSC–BMM interaction, targeting the interaction is perceived as a potential therapeutic strategy to eradicate LSCs and ultimately improve the outcome of AML.


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