Results 71 to 80 of about 1,683,745 (416)

A phase I/II study of the combination of quizartinib with azacitidine or low-dose cytarabine for the treatment of patients with acute myeloid leukemia and myelodysplastic syndrome

open access: yesHaematologica, 2021
FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) mutation in acute myeloid leukemia (AML) is associated with poor prognosis. We hypothesized that quizartinib, a selective and potent FLT3 inhibitor, with azacitidine (AZA) or low-dose ...
Mahesh Swaminathan   +23 more
doaj   +1 more source

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]

open access: yes, 2012
Background: Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity.
Badura, Susanne   +8 more
core   +1 more source

Breaking Down the Hierarchy: A New Approach to Leukemia Classification [PDF]

open access: yesLecture Notes in Computer Science (LNCS,volume 14313) - 2023
The complexities inherent to leukemia, multifaceted cancer affecting white blood cells, pose considerable diagnostic and treatment challenges, primarily due to reliance on laborious morphological analyses and expert judgment that are susceptible to errors.
arxiv   +1 more source

Acute lymphoblastic leukemia: a comprehensive review and 2017 update

open access: yesBlood Cancer Journal, 2017
Acute lymphoblastic leukemia (ALL) is the second most common acute leukemia in adults, with an incidence of over 6500 cases per year in the United States alone.
T. Terwilliger, M. Abdul-Hay
semanticscholar   +1 more source

Circulating tumor cells: advancing personalized therapy in small cell lung cancer patients

open access: yesMolecular Oncology, EarlyView.
Small cell lung cancer (SCLC) is an aggressive form of lung cancer that spreads rapidly to secondary sites such as the brain and liver. Cancer cells circulating in the blood, “circulating tumor cells” (CTCs), have demonstrated prognostic value in SCLC, and evaluating biomarkers on CTCs could guide treatment decisions such as for PARP inhibitors ...
Prajwol Shrestha   +6 more
wiley   +1 more source

The clathrin-binding domain of CALM-AF10 alters the phenotype of myeloid neoplasms in mice. [PDF]

open access: yes, 2012
The PICALM (CALM) gene, whose product is involved in clathrin-mediated endocytosis, has been identified in two recurring chromosomal translocations, involving either MLL or MLLT10 (AF10). We developed a mouse model of CALM-AF10(+) leukemia to examine the
Anastasi, J   +5 more
core   +2 more sources

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

open access: yesMolecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy   +12 more
wiley   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

open access: yesMolecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita   +1 more
wiley   +1 more source

Patient Attitudes Toward Genetic Testing for Inherited Predispositions to Hematologic Malignancies [PDF]

open access: yes, 2018
Although inherited predispositions to hematologic malignancies have previously been considered extremely rare, approximately 12 causative genes have been implicated in the last decade.
Beecroft, Taylor
core   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

open access: yesMolecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi   +5 more
wiley   +1 more source

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