Case report: BCR-ABL-positive acute lymphoblastic leukemia with bone destruction: a treatment dilemma [PDF]
Frontiers in OncologyAlthough bone destruction and hypercalcemia without acute peripheral blast BCR-ABL-positive acute lymphoblastic leukemia (ALL) have been reported in children, they are rare in adults.
Shi Lijun+6 more
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Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha [PDF]
Journal of Hematology & Oncology, 2019Background Interferon alpha (IFNa) monotherapy is recommended as the standard therapy in polycythemia vera (PV) but not in chronic myeloid leukemia (CML). Here, we investigated the mechanisms of IFNa efficacy in JAK2V617F- vs.
Claudia Schubert+11 more
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Pterostilbene downregulates BCR/ABL and induces apoptosis of T315I-mutated BCR/ABL-positive leukemic cells [PDF]
Scientific Reports, 2022In this study, we examined the antileukemic effects of pterostilbene, a natural methylated polyphenol analog of resveratrol that is predominantly found in berries and nuts, using various human and murine leukemic cells, as well as bone marrow samples ...
Shohei Kawakami+11 more
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Tyrosine kinase inhibitors in BCR-ABL positive acute lymphoblastic leukemia. [PDF]
Haematologica, 2015Philadelphia chromosome (Ph)/BCR/ABL-positive acute lymphoblastic leukemia (ALL) is the most common genetic abnormality associated with adult ALL and has been shown to confer the worst prognosis to both children and adults.[1][1],[2][2] Approximately 3 ...
Leoni V, Biondi A.
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EPS8 regulates proliferation, apoptosis and chemosensitivity in BCR-ABL positive cells via the BCR-ABL/PI3K/AKT/mTOR pathway. [PDF]
Oncol Rep, 2018Although the introduction of tyrosine kinase inhibitors greatly improved the survival of patients with chronic myeloid leukemia (CML), drug resistance remains a problem. Thus, mechanism-based novel therapeutic targets warrant exploration.
Huang R+11 more
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The proteolytic activity of separase in BCR-ABL-positive cells is increased by imatinib. [PDF]
PLoS One, 2012Separase, an endopeptidase required for the separation of sister-chromatides in mitotic anaphase, triggers centriole disengagement during centrosome duplication. In cancer, separase is frequently overexpressed, pointing to a functional role as an aneuploidy promoter associated with centrosomal amplification and genomic instability.
Haaß W+7 more
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BCR/ABL positive thrombocythemia: a diagnostic dilemma
The Egyptian Journal of Internal Medicine, 2017Both chronic myeloid leukemia and essential thrombocythemia are part of the spectrum of myeloproliferative neoplasm. Therefore, considerable overlap may occur in the clinical manifestations, and hematological and molecular findings in some patients.
Lubna Zafar+3 more
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In Vivo Eradication of Human BCR/ABL-Positive Leukemia Cells With an ABL Kinase Inhibitor [PDF]
JNCI: Journal of the National Cancer Institute, 1999BACKGROUND The leukemia cells of approximately 95% of patients with chronic myeloid leukemia and 30%-50% of adult patients with acute lymphoblastic leukemia express the Bcr/Abl oncoprotein, which is the product of a fusion gene created by a chromosomal ...
Philipp le Coutre+7 more
semanticscholar +6 more sources
Aleukemic bcr-abl positive granulocytic sarcoma [PDF]
Leukemia Research, 2009Granulocytic sarcoma (GS) can occur de novo or in association with intramedullary myeloid disorders. With the advent of sophisticated molecular detection techniques to detect diagnostic genes such as bcr-abl, PML-RARA and CBFB/MYH11 in bone marrow or peripheral blood, many cases of the so called 'primary' GS are questionable.
Jew-Win Kuan+3 more
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Imatinib spells BAD news for Bcr/abl-positive leukemias [PDF]
Proceedings of the National Academy of Sciences, 2006One of the medical success stories of the past decade has been the development of new agents to treat chronic myelogenous leukemia (CML). Building on earlier studies that identified the t(9;22) chromosomal translocation in CML, cloned the BCR/ABL fusion gene, and demonstrated the ability of the resulting kinase to transform cells, investigators ...
Scott H. Kaufmann
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