Results 51 to 60 of about 60,584 (224)

Imatinib and leptomycin B are effective in overcoming imatinib-resistance due to Bcr-Abl amplification and clonal evolution but not due to Bcr-Abl kinase domain mutation

Haematologica, 2008
Treatment with imatinib is very effective in Bcr-Abl positive leukemia. However, development of resistance to this drug is a common phenomenon in late stage disease.
Rama Krishna Kancha, Nikolas von Bubnoff, Cornelius Miething, Christian Peschel, Katharina S. Götze, Justus Duyster   +5 more
doaj   +1 more source

Aleukemic bcr-abl positive granulocytic sarcoma [PDF]

Leukemia Research, 2009
Granulocytic 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.
Kuan, Jew-Win, Pathmanathan, Rajadurai, Chang, Kian Meng, Tan, Sen Mui   +3 more
openaire   +3 more sources

Urokinase Plasminogen Activator Receptor‐Associated Protein (uPARAP) as a Potential Next Generation Molecular Target for Treatment of Gastrointestinal Stromal Tumors (GIST)

International Journal of Cancer, EarlyView.
A key component of the collagen internalization and lysosomal degradation cellular machinery, uPARAP may contribute to cancer progression. Here, the authors explored the expression of uPARAP in gastrointestinal stromal tumors using well‐annotated clinical patient samples and specimens from cell line‐ and patient‐derived xenografts.
Chao‐Chi Wang, Flavia Paternostro, Agnieszka Wozniak, Lore De Cock, Luna De Sutter, Kimberly Verbeeck, Ulla Vanleeuw, Daniël Gorgels, Che‐Jui Lee, Raf Sciot, Patrick Schöffski   +10 more
wiley   +1 more source

Activation of tyrosine kinases by mutation of the gatekeeper threonine. [PDF]

, 2008
Protein kinases targeted by small-molecule inhibitors develop resistance through mutation of the gatekeeper threonine residue of the active site. Here we show that the gatekeeper mutation in the cellular forms of c-ABL, c-SRC, platelet-derived growth ...
Azam, Mohammad, Daley, George, Gray, Nathanael, KURIYAN, John, Seeliger, Markus   +4 more
core   +1 more source

Oncogenic KRAS Rewires Stress Granule Dynamics: Mechanisms and Therapeutic Opportunities

The Kaohsiung Journal of Medical Sciences, EarlyView.
ABSTRACT Stress granules (SGs) are dynamic, membrane‐less structures that form in response to various cellular stresses, including metabolic, oxidative, and therapeutic challenges. They function as adaptive hubs and reorganize protein synthesis and signaling networks to help cells survive under stress. In cancer, these condensates are often hijacked to
Msimisi Ndzinisa, Birhanetensay Masresha Altaye, Yuh‐Pyng Sher   +2 more
wiley   +1 more source

Sphingomyelin synthase 1 activity is regulated by the BCR-ABL oncogene[S]

Journal of Lipid Research, 2013
Sphingomyelin synthase (SMS) produces sphingomyelin while consuming ceramide (a negative regulator of cell proliferation) and forming diacylglycerol (DAG) (a mitogenic factor). Therefore, enhanced SMS activity could favor cell proliferation.
Tara Ann Burns, Marimuthu Subathra, Paola Signorelli, Young Choi, Xiaofeng Yang, Yong Wang, Maristella Villani, Kapil Bhalla, Daohong Zhou, Chiara Luberto   +9 more
doaj   +1 more source

Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]

, 2013
The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype.
Beißert, Tim, Goldblum, Amiram, Mahajna, Jamal, Mian, Afsar Ali, Najajreh, Yousef, Oancea, Claudia, Ottmann, Oliver Gerhard, Ruthardt, Martin, Schüll, Marion   +8 more
core  

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

, 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, Bhatia, Ravi, Campbell, Victoria L., Chu, Su, Gaal, Karl, Holyoake, Tessa L., Hopcroft, Lisa, Jørgensen, Heather G., Lin, Allen, Zhang, Bin   +9 more
core   +1 more source

Update on Non‐Biological and RNA‐Based Therapeutics in Chronic Inflammatory Diseases: Precision Medicine Through Small Molecules: An EAACI Position Paper

Allergy, EarlyView.
ABSTRACT In the last decades, critical advancements in research technology and knowledge on disease mechanisms steered therapeutic approaches for chronic inflammatory diseases towards unprecedented target specificity. For allergic and chronic lung diseases, biologic drugs pioneered this goal, acquiring on the way—through the clinical use of monoclonal ...
F. Roth‐Walter, I. M. Adcock, C. Benito‐Villalvilla, R. Bianchini, L. Bjermer, G. Caramori, L. Cari, K. F. Chung, Z. Diamant, I. Eguiluz‐Gracia, E. F. Knol, M. Jesenak, F. Levi‐Schaffer, G. Nocentini, L. O'Mahony, O. Palomares, F. Redegeld, M. Sokolowska, B. Van Esch, M. Zurlo, C. Stellato   +20 more
wiley   +1 more source

Chemotherapy‐driven expression of WNT ligands in bone marrow stromal cells contributes to chemoresistance in acute lymphoblastic leukaemia

British Journal of Haematology, EarlyView.
Chemotherapy‐induced WNT ligand secretion by bone marrow (BM) stroma drives acute lymphoblastic leukaemia (ALL) chemoresistance. WNT pathway inhibition disrupts this cross‐talk and restores therapeutic response, highlighting WNT inhibitors as a promising strategy to prevent relapse in ALL.
Foteini Kalampalika, Amanda Jiménez‐Pompa, Raúl Sánchez‐Lanzas, Bela Patel, Miguel Ganuza   +4 more
wiley   +1 more source