Results 71 to 80 of about 1,006,148 (403)

Comparative analysis of blood lymphocytes of patients with acute and chronic myeloid leukemia by surface and intracellular α1-acid glycoprotein and fibronectin

open access: yesБіологічні студії, 2014
The exposition of α1-acid glycoprotein and fibronectin on the surface and inside the lymphocytes of healthy donors and hematological patients with acute and chronic myeloid leukemia were studied.
G. S. Маslak
doaj   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells [PDF]

open access: yes, 2016
Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the ...
Agarwal, Puneet   +9 more
core   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]

open access: yes, 2011
Background: The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome.
Mahajna, Jamal   +5 more
core   +2 more sources

Treatment of Relapsed Acute Myeloid Leukemia

open access: yesCurrent Treatment Options in Oncology, 2020
Relapse is still a common scenario in acute myeloid leukemia (AML) treatment and occurs in 40–50% of younger and the great majority of elderly patients. The prognosis in relapsed AML patients is generally poor but depends largely on the timing of relapse
F. Thol, A. Ganser
semanticscholar   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Granulocytic Sarcoma as the First Sign of Acute Leukemia in Childhood [PDF]

open access: yes, 2012
Acute myeloid leukemia (AML) may rarely involve the orbit as a solid tumor termed granulocytic sarcoma. This report describes the case of a child who presented with rapidly progressive unilateral proptosis and was diagnosed as rhabdomyosarcoma.
Singh, T, Sufi, AR
core   +1 more source

FLT3 Length Mutations as Marker for Follow-Up Studies in Acute Myeloid Leukaemia [PDF]

open access: yes, 2004
Length mutations within the FLT3 gene (FLT3-LM) can be found in 23% of acute myeloid leukaemia (AML) and thus are the most frequent mutations in AML. FLT3-LM are highly correlated with AML with normal karyotype and other cytogenetic aberrations of the ...
Haferlach, Torsten   +4 more
core   +1 more source

Functional Genomic Landscape of Acute Myeloid Leukemia

open access: yesNature, 2018
The implementation of targeted therapies for acute myeloid leukaemia (AML) has been challenging because of the complex mutational patterns within and across patients as well as a dearth of pharmacologic agents for most mutational events.
J. Tyner   +87 more
semanticscholar   +1 more source

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