Results 21 to 30 of about 21,002 (186)

Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL. [PDF]

PLoS ONE, 2011
The constitutively activated BCR-ABL tyrosine kinase of chronic myeloid leukemia (CML) is localized exclusively to the cytoplasm despite the three nuclear localization signals (NLS) in the ABL portion of this fusion protein.
Martin Preyer, Paolo Vigneri, Jean Y J Wang   +2 more
doaj   +1 more source

Spontaneous Soft Tissue Haematomas-A Rare Presentation of Chronic Myeloid Leukemia (CML) [PDF]

Journal of Clinical and Diagnostic Research, 2015
Spontaneous soft tissue haematomas are rarely found in haematological malignancies. Chronic myeloid leukemia (CML) is a myeloproliferative disorder which rarely present with thrombo-haemorrhagic phenomenon.
Manoj Lakhotia, Hans Raj Pahadiya, Gopal Raj Prajapati, Akanksha Choudhary, Ronak Gandhi   +4 more
doaj   +1 more source

Transforming and tumorigenic activity of JAK2 by fusion to BCR: molecular mechanisms of action of a novel BCR-JAK2 tyrosine-kinase. [PDF]

PLoS ONE, 2012
Chromosomal translocations in tumors frequently produce fusion genes coding for chimeric proteins with a key role in oncogenesis. Recent reports described a BCR-JAK2 fusion gene in fatal chronic and acute myeloid leukemia, but the functional behavior of ...
Álvaro Cuesta-Domínguez, Mara Ortega, Cristina Ormazábal, Matilde Santos-Roncero, Marta Galán-Díez, Juan Luis Steegmann, Ángela Figuera, Eva Arranz, José Luis Vizmanos, Juan A Bueren, Paula Río, Elena Fernández-Ruiz   +11 more
doaj   +1 more source

Light-Activating PROTACs in Cancer: Chemical Design, Challenges, and Applications

Applied Sciences, 2022
Nonselective cell damage remains a significant limitation of radiation therapies in cancer. Decades of successful integration of radiation therapies with other medicinal chemistry strategies significantly improved therapeutic benefits in cancer ...
Arvind Negi, Kavindra Kumar Kesari, Anne Sophie Voisin-Chiret   +2 more
doaj   +1 more source

Oncogenic fusion protein BCR-FGFR1 requires the breakpoint cluster region-mediated oligomerization and chaperonin Hsp90 for activation. [PDF]

, 2020
Mutation and translocation of fibroblast growth factor receptors often lead to aberrant signaling and cancer. This work focuses on the t(8;22)(p11;q11) chromosomal translocation which creates the breakpoint cluster region (BCR) fibroblast growth factor ...
Bisom-Rapp, Ezra W, Donoghue, Daniel J, Meyer, April N, Nelson, Katelyn N, Peiris, Malalage N   +4 more
core   +2 more sources

Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis [PDF]

Biomarker Research, 2014
Chronic myelogenous leukemia (CML) results from the neoplastic transformation of a hematopoietic stem cell. CML is cytogenetically characterized by the presence of the Philadelphia chromosome (Ph'). Most patients with CML express e13a2 or e14a2 mRNAs that result from a rearrangement of the major breakpoint cluster regions (M-BCR) generating the 210-kDa
Martinez-Serra, Jordi, del Campo Garcia, Raquel, Gutierrez, Antonio, Antich, Jose Luis, Ginard, Magdalena, Duran Pastor, Maria Antonia, Bento, Leyre, Ros, Teresa, Amat, Juan C, Vidal, Carmen, Iglesias, Julio F, Orlinska, Izabela, Besalduch Vidal, Juan   +12 more
openaire   +3 more sources

Influence of BCR/ABL fusion proteins on the course of Ph leukemias.

Acta Biochimica Polonica, 2004
The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase.
Gennady D, Telegeev, Anna N, Dubrovska, Mykhaylo V, Dybkov, Stanislav S, Maliuta   +3 more
openaire   +3 more sources

A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein [PDF]

Communications Biology, 2020
AbstractDrug resistance is of increasing concern, especially during the treatments of infectious diseases and cancer. To accelerate the drug discovery process in combating issues of drug resistance, here we developed a computational and experimental strategy to predict drug resistance mutations. Using BCR-ABL as a case study, we successfully recaptured
Jinxin Liu, Jianfeng Pei, Luhua Lai
openaire   +2 more sources

Flow Cytometric Detection of BCR-ABL Fusion Proteins in Leukemia Patients Via An Immunobead Assay [PDF]

Blood, 2008
Abstract The BCR-ABL fusion gene results from the translocation t(9;22). It is the hallmark of chronic myeloid leukemia (CML) and is present in a poor-risk subgroup of precursor B cell acute lymphoblastic leukemia (ALL), which represents 25–30% of adult ALL and 3–5% of childhood ALL.
Jacques JM van Dongen, Frank J.T. Staal, Elizabeth Macintyre, Tomas Kalina, Lukasz Sedek, Paulo Lucio, Juan Flores Montero, Elisabeth R. Van Wering, Nancy Boeckx, Sebastian Böttcher, Vincent H.J. Van der Velden, E. Dekking, Floor Weerkamp   +12 more
openaire   +1 more source

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

, 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, Khateb, Mamduh, Mahajna, Jamal, Metodieva, Anna, Mian, Afsar Ali, Najajreh, Yousef, Ottmann, Oliver Gerhard, Ruimi, Nili, Ruthardt, Martin   +8 more
core   +1 more source