scholarly journals Potential role of sorafenib in the treatment of acute myeloid leukemia

2008 ◽  
Vol 49 (12) ◽  
pp. 2246-2255 ◽  
Author(s):  
Shahram Mori ◽  
Jorge Cortes ◽  
Hagop Kantarjian ◽  
Weiguo Zhang ◽  
Michael Andreef ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Potential Role ◽  
Acute Myeloid

scholarly journals Cohesin-dependent regulation of gene expression during differentiation is lost in cohesin-mutated myeloid malignancies

Blood ◽  
2019 ◽  
Vol 134 (24) ◽  
pp. 2195-2208 ◽  
Author(s):  
Daniel Sasca ◽  
Haiyang Yun ◽  
George Giotopoulos ◽  
Jakub Szybinski ◽  
Theo Evan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Potential Role ◽  
Regulation Of Gene Expression ◽  
Specific Gene ◽  
Myeloid Malignancy ◽  
Erythroid Maturation ◽  
Acute Myeloid

Cohesin mutations are common in myeloid malignancy. Sasca et al elucidate the potential role of cohesin loss in myelodysplastic syndrome and acute myeloid leukemia (MDS/AML). They demonstrate that cohesin binding is critical for erythroid-specific gene expression and that reduction in cohesin impairs terminal erythroid maturation and promotes myeloid malignancy.

Potential role of CREB as a prognostic marker in acute myeloid leukemia

2007 ◽  
Vol 3 (4) ◽  
pp. 475-480 ◽  
Author(s):  
Jerry C Cheng ◽  
Samuel Esparza ◽  
Salemiz Sandoval ◽  
Deepa Shankar ◽  
Cecilia Fu ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Prognostic Marker ◽  
Myeloid Leukemia ◽  
Potential Role ◽  
Acute Myeloid

Dose-related periorbital edema following sorafenib in a patient with acute myeloid leukemia

2018 ◽  
Vol 25 (8) ◽  
pp. 2035-2037 ◽  
Author(s):  
Craig W Freyer ◽  
James K Mangan
Keyword(s):  
Acute Myeloid Leukemia ◽  
Adverse Event ◽  
Dose Reduction ◽  
Myeloid Leukemia ◽  
Potential Role ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Periorbital Edema ◽  
Acute Myeloid

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.

scholarly journals Persistence of Cytogenetic Abnormalities at Complete Remission After Induction in Patients With Acute Myeloid Leukemia: Prognostic Significance and the Potential Role of Allogeneic Stem-Cell Transplantation

2011 ◽  
Vol 29 (18) ◽  
pp. 2507-2513 ◽  
Author(s):  
Yiming Chen ◽  
Jorge Cortes ◽  
Zeev Estrov ◽  
Stefan Faderl ◽  
Wei Qiao ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Stem Cell ◽  
Complete Remission ◽  
Stem Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Myeloid Leukemia ◽  
Potential Role ◽  
Cytogenetic Abnormalities ◽  
Acute Myeloid

Purpose To determine the prognostic impact of persistent cytogenetic abnormalities at complete remission (CR) on relapse-free survival (RFS) and overall survival (OS) in patients with acute myeloid leukemia (AML) and to examine the potential role of allogeneic stem-cell transplantation (SCT) in this setting. Patients and Methods Data from 254 adult patients with AML (excluding acute promyelocytic leukemia) who achieved CR after induction chemotherapy on various first-line protocols were examined. Results Median follow-up for surviving patients was 43 months. Patients with cytogenetic abnormalities at CR (n = 71) had significantly shorter RFS (P = .001) and OS (P < .001) compared with patients with normal cytogenetics at CR (n = 183); 3-year RFS was 15% and 45%, and 3-year OS was 15% and 56%, respectively. Among the patients with persistent cytogenetic abnormalities at CR, those who underwent SCT in first CR (CR1; n = 15) had better RFS and OS compared to those without SCT (n = 56; P = .04 and .06, respectively). In multivariate analysis, persistent cytogenetic abnormalities at CR was an independent predictor for RFS (P < .001) and OS (P = .001), but among patients with persistent cytogenetic abnormalities at CR, no significant differences in OS (P = .25) was observed between those who did or did not receive SCT with a trend favoring SCT for RFS (P = .08). Conclusion Persistent cytogenetically abnormal cells at CR predict a significantly shorter RFS and OS. SCT in CR1 may improve the clinical outcome of patients lacking cytogenetic remission after induction although this depends on patient selection.

Role of FLT3 gene mutations in acute myeloid leukemia: effect on course of disease and results of therapy

2019 ◽  
Vol XIV (1) ◽  
Author(s):  
A.M. Radzhabova ◽  
S.V. Voloshin ◽  
I.S. Martynkevich ◽  
A.A. Kuzyaeva ◽  
V.A. Shuvaev ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Gene Mutations ◽  
Course Of Disease ◽  
Acute Myeloid

scholarly journals Leukemia stem cell-bone marrow microenvironment interplay in acute myeloid leukemia development

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Yiyi Yao ◽  
Fenglin Li ◽  
Jiansong Huang ◽  
Jie Jin ◽  
Huafeng Wang
Keyword(s):  
Bone Marrow ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Chemotherapy Resistance ◽  
Bone Marrow Microenvironment ◽  
Cytotoxic Effects ◽  
High Relapse Rate ◽  
Underlying Mechanisms ◽  
Acute Myeloid

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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