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The combination of BCR-ABL1 transcript type and spleen size at diagnosis is significantly predictive for achieving an overall MMR and FFS. Incorporating these predictors could be important when making clinical decisions regarding changing therapy for CML patients treated initially with IM.
expression of WASP inversely correlates with BCR-ABL1 levels and the progression of the disease in Chronic myeloid leukemia patients. BCR-ABL1 downregulates WASP in part by epigenetic modification of its proximal promoter.
The imaging method achieved ultrasensitive detection of BCR/ABL (show ABL1 Proteins) fusion gene with a low detection limit down to 23 fM. And this method exhibited wide linear ranges over seven orders of magnitude and excellent discrimination ability toward target
This is the first report evaluating the role of SOD2 (show SOD2 Proteins) in native and T351-mutated BCR-ABL (show ABL1 Proteins)-expressing cells and in a large cohort of chronic myeloid leukemia (show BCL11A Proteins) patients. In leukemic cells silenced for SOD2 (show SOD2 Proteins) expression a specific down-regulation of the expression of PRDX2 (show PRDX2 Proteins) gene was found.
The compound missense mutations in BCR-ABL (show ABL1 Proteins) kinase domain responsible to elicit disease progression, drug resistance or disease relapse in chronic myeloid leukemia (show BCL11A Proteins).
JNJ-26854165, an inhibitor of MDM2 (show MDM2 Proteins), inhibits proliferation and triggers cell death in a p53 (show TP53 Proteins)-independent manner in various BCR/ABL (show ABL1 Proteins)-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL (show ABL1 Proteins) mutant.
Double inhibition of the N- and C-terminal termini can disrupt Hsp90 chaperone (show HSP90 Proteins) function synergistically, but not antagonistically, in Bcr-Abl (show ABL1 Proteins)-positive human leukemia cells.
this study identifies different BCR/Abl (show ABL1 Proteins) protein suppression patterns as a converging trait of chronic myeloid leukemia (show BCL11A Proteins) cell adaptation to energy restriction
BGB324 does not inhibit BCR-ABL1 and consequently inhibits chronic myeloid leukemia (CML)independent of BCR-ABL1 mutational status. Our data show that Axl inhibition has therapeutic potential in BCR-ABL TKI-sensitive as well as -resistant CML and support the need for clinical trials
BCR-ABL1 (show ABL1 Proteins)-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (show BBC3 Proteins) proteins; namely Bim (show BCL2L11 Proteins), Bik (show BIK Proteins), and Noxa (show PMAIP1 Proteins).
The resistance in BCR-ABL1 (show ABL1 Proteins) cells resulted either from the Y253H mutation in the BCR-ABL1 (show ABL1 Proteins) gene or incubation in increasing concentrations of imatinib.
PDZK1 (show PDZK1 Proteins) has novel SR-BI (show SCARB1 Proteins)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (show PDZK1 Proteins) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (show HAP1 Proteins) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (show GRB10 Proteins) is involved in BCR-ABL (show ABL1 Proteins)-positive leukemia in mice.
Bcr is an integral member of the Par (show AFG3L2 Proteins)-Tiam1 (show TIAM1 Proteins) complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (show PRKCZ Proteins) function.
Loss of Bcr expression causes defects in spine development.
Suggest that HS-438 may be a novel drug candidate with the therapeutic potential to target BCR-ABL (show ABL1 Proteins) and overcome imatinib resistance in patients with chronic myeloid leukemia (show BCL11A Proteins).
IRF8 (show IRF8 Proteins)-rescued BCR-ABL (show ABL1 Proteins)-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL (show ABL1 Proteins)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (show TP53 Proteins) at the K317/K320 residue, thus preventing the nuclear export of p53 (show TP53 Proteins) in response to DNA damage.
A reciprocal translocation between chromosomes 22 and 9 produces the Philadelphia chromosome, which is often found in patients with chronic myelogenous leukemia. The chromosome 22 breakpoint for this translocation is located within the BCR gene. The translocation produces a fusion protein which is encoded by sequence from both BCR and ABL, the gene at the chromosome 9 breakpoint. Although the BCR-ABL fusion protein has been extensively studied, the function of the normal BCR gene product is not clear. The protein has serine/threonine kinase activity and is a GTPase-activating protein for p21rac. Two transcript variants encoding different isoforms have been found for this gene.
breakpoint cluster region
, breakpoint cluster region protein-like
, BCR/FGFR1 chimera protein
, FGFR1/BCR chimera protein
, breakpoint cluster region protein
, renal carcinoma antigen NY-REN-26
, breakpoint cluster region homolog