• This gene is a member of the protein-tyrosine kinase oncogene family. (cancerindex.org)
  • BCR-ABL oncogene activates multiple cross-talking signal transduction pathways (STP), such as RAS/MEK/ERK, PI3K/Akt, Wnt and STAT5, contributing to abnormal proliferation of clonal cells. (oncotarget.com)
  • The c-Abl protein is inhibited by its SH3 domain, and deletion of this domain turns ABL1 into an oncogene. (enzolifesciences.com)
  • REALQUALITY RQ-BCR-ABL p210 One-Step is a CE-IVD kit for the identification and quantification of the t(9;22) (q34;q11) translocation, in the variant p210 (M-bcr b3a2 and b2a2 transcripts) , which involves the ABL proto-oncogene on chromosome 9 and part of the BCR gene on chromosome 22, by one-step Real-time RT-PCR of the BCR-ABL fusion gene. (web.app)
  • The proto-oncogene tyrosine-protein kinase (BCR-ABL1) oncogenic breakpoint cluster region-protein with enhanced tyrosine kinase action is encoded by this fusion gene. (inter-publishing.com)
  • Because cancer-driven by a single oncogene, such as leukemia driven by the BCR-ABL fusion gene, is amenable to treatment with inhibitors that target that very single causative agent, there is a lot of interest to develop therapies to treat the EHE. (oist.jp)
  • Chronic myeloid leukemia (CML) results from BCR-ABL oncogene, which blocks CML cells differentiation and protects these cells from apoptosis. (jcancer.org)
  • Chronic myeloid leukemia (CML) is a clonal expansion of the progenitor hematopoietic stem cells arising from the existence of the fusion BCR-ABL oncogene, that represents 15%-20% of the newly diagnosed cases of leukemia patients [ 1 - 2 ]. (jcancer.org)
  • BCR-ABL oncogene encodes a BCR-ABL tyrosine kinase (TK), which triggers different downstream targets including c-Myc, STAT5 and CrkL, which participated in the control of cell differentiation, proliferation, migration and other cellular behaviors [ 3 - 5 ]. (jcancer.org)
  • Hence, BCR-ABL oncogene has been the target for the treatment of patients with CML. (jcancer.org)
  • The c-Abl proto-oncogene encodes a nonreceptor type protein tyrosine kinase that is widely expressed and is distributed in both the nucleus and the cytoplasm of cells. (ecmbio.com)
  • Here we have analysed the relevance of NOX2 and NOX4 in the regulation of metabolism in chronic myeloid leukaemia (CML), a neoplasia driven by the expression of the breakpoint cluster region-Abelson fusion oncogene (BCR-ABL). (biomed.news)
  • BCR is one of the two genes in the BCR-ABL fusion protein, which is associated with the Philadelphia chromosome. (wikipedia.org)
  • His team has characterized more than 25 different translocations and found that the majority result in fusion genes encoding chimeric proteins with an N-terminal region derived from a partner gene fused in frame to the C-terminal region of tyrosine kinase such as ABL, PDGFRα, PDGFRß, JAK2, KIT or FGFR1. (cml-foundation.org)
  • Genes whose protein products stimulate or enhance the division and viability of cells. (cancerquest.org)
  • Genes whose protein products can directly or indirectly prevent cell division or lead to cell death. (cancerquest.org)
  • A chromosomal translocation results in the head-to-tail fusion of the BCR and ABL1 genes. (enzolifesciences.com)
  • In yet another coup for a research concept known as "big data," researchers at the Stanford University School of Medicine have developed a computerized algorithm to understand the complex and rapid choreography of hundreds of proteins that interact in mindboggling combinations to govern how genes are flipped on and off within a cell. (pharmaceuticalintelligence.com)
  • The ENCODE, for the Encyclopedia of DNA Elements , project was a five-year collaboration of more than 440 scientists in 32 labs around the world to reveal the complex interplay among regulatory regions, proteins and RNA molecules that governs when and how genes are expressed. (pharmaceuticalintelligence.com)
  • In this study, the researchers combined data from genomics (a field devoted to the study of genes) and proteomics (which focuses on proteins and their interactions). (pharmaceuticalintelligence.com)
  • The multifunctional regulator nuclear factor erythroid 2-related factor (Nrf2) is considered not only as a cytoprotective factor regulating the expression of genes coding for anti-oxidant, anti-inflammatory and detoxifying proteins, but it is also a powerful modulator of species longevity. (springer.com)
  • The major characteristics of Nrf2 are to some extent mimicked by Nrf2-dependent genes and their proteins including heme oxygenase-1 (HO-1), which besides removing toxic heme, produces biliverdin, iron ions and carbon monoxide. (springer.com)
  • Non-receptor tyrosine kinases encoded by the C-ABL GENES . (nih.gov)
  • Nonsense-mediated mRNA decay (NMD): a bifunctional mechanism… Proteins are the working-units of the cell, which are encoded by thousands of genes that pass their information into an intermediate molecule, the messenger RNA (mRNA). (atlasofscience.org)
  • Most of the patients exhibit BCR-ABL protein which forms the target to tyrosine kinase inhibitors that are the main stay of treatment in CML [4]. (waocp.com)
  • ABL allosteric inhibitors synergize with statins to enhance apoptosis of metastatic lung cancer cells. (inter-publishing.com)
  • Indolizine: In-Silico Identification of Inhibitors against Mutated BCR-ABL Protein of Chronic Myeloid Leukemia. (inter-publishing.com)
  • Knowledge of the molecular mechanisms behind imatinib resistance has led to the development of second-generation ABL kinase inhibitors. (touchoncology.com)
  • Imatinib mesylate (IM) and various other BCR-ABL tyrosine kinase inhibitors (TKIs), including dasatinib (DA) and nilotinib (NL), have already been introduced into scientific practice with exceptional therapeutic results on chronic-phase (CP) CML (10C13). (angiogenesis-blog.com)
  • JOA displayed the activity of inhibiting the BCR-ABL and promoted differentiation of not only imatinib -sensitive but also imatinib -resistant cells with BCR-ABL mutation, which could become a potent lead compound to overcome the imatinib -resistant induced by inhibitors of BCR-ABL tyrosine kinase in CML therapy. (jcancer.org)
  • For most patients with CML, BCR-ABL tyrosine kinase inhibitors (TKIs) have turned the an inevitably fatal disease into a manageable condition. (jcancer.org)
  • Food and Drug Administration (FDA)- approved BCR-ABL-specific kinase inhibitors (BCR-ABL-KIs) imatinib, dasatinib and nilotinib induce prolonged remissions in CML but poor leukemia-reduction and relapse-control in Ph+ ALL. (uthsc.edu)
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • 7 Secondary resistance to imatinib is thought to involve acquired evasion of BCR-ABL inhibition by various mechanisms such as mutations in the kinase domain that prevent imatinib binding, or genomic amplification and overexpression of BCR-ABL. (touchoncology.com)
  • We partition this multi-component review into different sections related to biochemical characteristics of BCR-ABL+ cells, underlying mechanism of generation of mutations and crosstalk of BCR-ABL with various intracellular signaling cascades. (yeditepe.edu.tr)
  • Nevertheless, early relapses as well as the introduction of IM-resistant disease at any correct period can cause main setbacks for a few sufferers (8,14,15), generally because of the selection and outgrowth of preexisting subclones of cells with mutations in the BCR-ABL kinase area (14,16). (angiogenesis-blog.com)
  • The relative primary BCR-ABL-KI-resistance in Ph+ ALL patients carrying predominantly BCR-ABLWT disease cannot be attributed to drug-resistant BCR-ABL mutations (BCR-ABLMUTANTS), and remains poorly understood. (uthsc.edu)
  • Our results showed that CP-CML CD34+ progenitors were characterized by significant lower phosphorylation of proteins involved in the regulation of growth and cell survival, such as tyrosine kinases of the Src family and members of STAT family, and by a significant higher phosphorylation of p53 (Ser15), compared to normal CD34+ cells from healthy donors. (oncotarget.com)
  • A recently available study further shows that the BCR-ABLCmediated signaling pathways in CML cells are managed by JAK2 through immediate phosphorylation of tyrosine 177 of BCR-ABL oncoprotein (9). (angiogenesis-blog.com)
  • Therefore, imatinib was a paradigm of targeted therapies, which due to that imatinib inhibits the phosphorylation of BCR-ABL then suppress the activation of BCR-ABL tyrosine kinase [ 6 ]. (jcancer.org)
  • Tyrosine phosphorylation is important for the regulation of c-Abl kinase activity. (ecmbio.com)
  • Phosphorylation of Tyr-245 is involved in activation of c-Abl kinase activity. (ecmbio.com)
  • Tyrosine 412 is located in the kinase activation loop of c-Abl, and phosphorylation of this residue is required for kinase activity. (ecmbio.com)
  • Thus, phosphorylation of Tyr-245 and Tyr-412 may be critical for activation of c-Abl in a variety of cell signaling pathways. (ecmbio.com)
  • Ph+ acute lymphoblastic leukemia (Ph+ ALL) is a high-risk acute leukemia with poor prognosis, in which the specific t(9;22)(q34;q11) translocation results in a chimeric bcr-abl (e1a2 breakpoint) and in a 190 KD protein (p190) with constitutive tyrosine kinase activity. (hindawi.com)
  • The hallmark of Philadelphia chromosome positive (Ph+) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. (bios-mep.info)
  • The presence of ABL/BCR changed the phenotype of the leukemia most likely due to its capacity CR2 to influence the stem cell population as shown by our data. (bios-mep.info)
  • In fact M-BCR p210is associated with primarily myeloid leukemia. (bios-mep.info)
  • These proteins being leukemogenic result in Chronic Myeloid leukemia (CML) and Acute lymphoid leukemia (ALL). (aku.edu)
  • Chronic Myeloid Leukemia (CML) is a myeloproliferative disorder characterized by the chromosomal translocation t(9;22) encoding for the Bcr/Abl fusion gene. (wcrj.net)
  • Secreted Frizzled Related Protein (sFRP) gene products are antagonists of Wnt signaling and their epigenetic silencing has been reported in different types of leukemia. (wcrj.net)
  • Chronic myeloid leukemia (CML) is characterized by the presence of BCR-ABL1 fusion gene. (cmleukemia.com)
  • The proportion of different BCR-ABL1 transcript types in chronic myeloid leukemia. (cmleukemia.com)
  • One hundred and forty-three patients with p210 BCR-ABL-positive leukemia were studied for coexpression of p190 BCR-ABL mRNA. (web.app)
  • BCR-ABL1 P210 + chronic myeloid leukemia (CML), it was found that 17,216 patients (37.9%) expressed only e13a2, with a proportion that varied with age, from 39.6% in The corresponding e13-a2 or e14-a2 BCR-ABL1 mRNAs produce a 210 kD protein (p210). (web.app)
  • The diagnostic and clinical success of standardization of BCR-ABL1 p210 monitoring in chronic myeloid leukemia patients could be seen as a good example for further standardization of molecular monitoring in other gene rearrangements. (web.app)
  • Every BCR-ABL1 transcription is concomittant with a specific leukemia phenotype that expects treatment clinical outcome and reaction prognosis. (inter-publishing.com)
  • This breakthrough revolutionized our knowledge related to leukemia biology and contemporary studies revealed that chromosomal translocation resulted in the fusion between the 5' segment of BCR gene and 3' segment of the ABL gene to form BCR/ABL fusion gene. (yeditepe.edu.tr)
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation. (stanford.edu)
  • The determining hallmark of persistent myeloid leukemia (CML) may be the fusion gene while it began with a hematopoietic stem cell (1C4). (angiogenesis-blog.com)
  • De Keersmaecker K, Porcu M, Cox L, Girardi T, Vandepoel R, Op de Beeck J, Gielen O, Mentens N, Bennett KL, Hantschel O. NUP214-ABL1 mediated cell proliferation in T-cell acute lymphoblastic leukemia is dependent on the LCK kinase and various interacting proteins. (cemm.at)
  • Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by an acquired 9;22-chromosomal translocation in a hematopoietic stem cell (HSC) resulting in the expression of the BCR-ABL1 fusion protein. (haematologica.org)
  • Oncogenic signaling by the Philadelphia chromosome-encoded BCR-ABL fusion kinase initiates and drives both Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) and chronic myelogenous leukemia (CML). (uthsc.edu)
  • This suggested that both cell-extrinsic IL7 and cell-intrinsic IKAROS loss converge on c-MYC, which may act as node of leukemia BCR-ABL-KI-refractoriness. (uthsc.edu)
  • Remarkably, DHA and dasatinib combination regimen eliminated host-protected dasatinib-refractory persistent leukemia and improved long-term survival from 0 to >90% in a murine model that faithfully captures the BCR-ABL-KI drug-refractoriness of human Ph+ ALL. (uthsc.edu)
  • An important early measure of treatment success is the disappearance of leukemia cells from blood and marrow as measured by cytogenetics (no Philadelphia (Ph) chromosomes detectable anymore) or molecular testing (BCR‐ABL fusion transcripts, the molecular correlate of the Ph‐chromosome, greatly reduced). (atlasofscience.org)
  • Native BCR acts as a negative regulator of proliferation and oncogenic transformation by a down-regulation of RAS-mediated signaling [18]. (bios-mep.info)
  • Oncogenic transformation of c-abl arises when specific N-terminal amino acids are deleted, releasing the kinase from negative regulation. (nih.gov)
  • Dr Cross has a long-standing career in the development of genetic tests and is particularly committed to the development and standardisation of molecular monitoring for CML patients worldwide by qRT-PCR for BCR-ABL mRNA. (cml-foundation.org)
  • Rare cases of CML are characterized by an e19-a2 type mRNA with a corresponding p230 protein. (web.app)
  • We also summarize how BCR-ABL encoding mRNA is negatively regulated by different miRNAs and the strategies which are currently being used to effectively target BCR-ABL protein. (yeditepe.edu.tr)
  • Both technologies have been primarily focused on measurement of protein epitopes, but have been used to measure nucleic acids such as targeted mRNA 11 , 12 . (nature.com)
  • The introduction of imatinib, a selective inhibitor of the ABL tyrosine kinase, has revolutionized the treatment and the outcome of this subset of patients [ 1 ]. (hindawi.com)
  • One such targeted therapy, imatinib mesylate (Gleevec®, Novartis), was found to be a relatively specific inhibitor of the BCR-ABL TK and effective in blocking the molecular signals contributing to the CML phenotype. (touchoncology.com)
  • T315I mutated BCR-ABL is the main cause of the resistance mediated by imatinib and second generation BCR-ABL inhibitor. (jcancer.org)
  • Nrf2 consists of six functional Neh domains (Neh1-Neh6), from which, the amino-terminal Neh2 domain controls binding Keap1-the inhibitor protein Kelch-like ECH-associated protein 1, that is responsible for the cytosolic sequestration of Nrf2 under physiological conditions (Fig. 2 a). (springer.com)
  • q11) resulting in a chimeric bcr-abl (e1a2 breakpoint) fusion gene that encodes a 190 KD protein (p190) with constitutively active tyrosine kinase activity that can alter multiple signaling pathways, contributing to tumor growth and proliferation. (hindawi.com)
  • These are frequently activated by fusion to other transcriptional proteins resulting in chimeric transcription factors. (stanford.edu)
  • The breakpoint cluster region protein (BCR) also known as renal carcinoma antigen NY-REN-26 is a protein that in humans is encoded by the BCR gene. (wikipedia.org)
  • These second-generation agents have significantly higher potency compared with imatinib and activity against most imatinib-resistant BCR-ABL kinase domain mutants. (touchoncology.com)
  • Here, we determined the effect of Jiyuan oridonin A (JOA), an ent -kaurene diterpenoid compound, on the differentiation blockade in imatinib-sensitive, particularly, imatinib-resistant CML cells with BCR-ABL-T315I mutation by cell proliferation assay, apoptosis analysis, cell differentiation analysis, cell cycle analysis and colony formation assay. (jcancer.org)
  • Due to bcr-abl fusion, the corresponding p190 joint region contains an amino acid sequence unique to the oncoprotein in addition to a novel amino acid, not belonging to either BCR or ABL sequences, created at the exact fusion point. (hindawi.com)
  • 2 , 3 , 4 Patients with the e19a2 transcript, which encodes P230, often present with prominent neutrophilic maturation or thrombocytosis, whereas patients with the e1a2 transcript, which encodes P190, often present with monocytosis, absence of basophilia and a tendency to progress to lymphoid blast phase (BP). (cmleukemia.com)
  • Tre kliniskt viktiga varianter kodade av fusionsgenen är p190-, p210- Både P190 och P210 BCR/ABL1-fusionstranskript har beskrivits i AML, som finns i t(9;22)-positiv ALL (P190 eller P210) och i KML (P210). (web.app)
  • Through the fusion to BCR, ABL constitutively activates its down-stream signaling pathways, including RAS, JAK/STAT and PI-3 kinase [1,12]. (bios-mep.info)
  • The translocation occurs in a primitive hematopoietic stem cell and the gene encodes a fusion protein (Bcr-Abl) that has deregulated tyrosine kinase (TK) activity and activates intracellular pathways that lead to increased cellular proliferation, resistance to apoptosis and genetic instability [1,3]. (rockstarsagainstliveearth.com)
  • The chromosome 22 breakpoint for this translocation is located within the BCR gene. (wikipedia.org)
  • The translocation produces a fusion protein that is encoded by sequence from both BCR and ABL, the gene at the chromosome 9 breakpoint. (wikipedia.org)
  • It is characterized by the translocation between chromosome 9 and 22 resulting in fusion gene BCR-ABL that forms the basis of pathogenecity of CML [2-3]. (waocp.com)
  • q11) chromosomal translocation , giving rise to BCR-ABL1 p210 fusion protein with constitutive activation of tyrosine kinase activity. (web.app)
  • Two principal breaks occur in the (breakpoint cluster region) gene locus on chromosome 22: the (major) M-BCR, between exons 12 and 16, and the (minor) m-BCR, in the first intron of and m-BCR to that of p185(Abelson tyrosin protein kinase 1) gene on chromosome 9 falls within the intron between the exons 1 and 2. (bios-mep.info)
  • Site of breakage in chromosome 22 (BCR gene) can occur in different regions within a 5.8kb region known as the major breakpoint cluster region (M-bcr), spanning 5 exons previously known as b1 to b5 but now as exon 12 to 16 [1]. (aku.edu)
  • Characteristics of BCR-ABL rearrangement variants in Pakistani patient" by Zeeshan Ansar Ahmed, Amna Nasir et al. (aku.edu)
  • Generally, chronic phase is characterized by leukocytosis, anemia and splenomegaly with detection of BCR-ABL fusion gene [6]. (waocp.com)
  • Styles of representation in isolate BCR-ABL1 transcripts change when CML progresses transitioning from a chronic to an expedited phase and ultimately to the blast phase. (inter-publishing.com)
  • What pathways are this gene/protein implicaed in? (cancerindex.org)
  • Its molecular counterpart, the resultant BCR-ABL fusion gene, encodes a constitutively active form of the ABL tyrosine kinase (TK) that induces malignancy through the activation of multiple signal transduction pathways involved in hematopoietic cell growth and survival. (touchoncology.com)
  • The BCR-ABL oncoprotein (p210BCR-ABL) encoded by this gene shows constitutively raised tyrosine kinase (TK) activity that drives the pathogenesis of the condition by perturbing multiple signaling pathways, like the RAS/MAPK, PI3K/AKT, and Janus kinase 2 (JAK2)/ sign transducer and activator of transcription 5 (STAT5) pathways (5,6). (angiogenesis-blog.com)
  • Mixture therapies to focus on various other pathways or proteins, furthermore to BCR-ABL, seem to be far better at inhibiting these cells (28C31). (angiogenesis-blog.com)
  • The PI3K/Akt/mTOR signaling pathway is a key regulator of diverse physiological functions such as proliferation, global protein, and lipid synthesis as well as many metabolic pathways interacting to increase secretory capabilities. (go.jp)
  • 1 The BCR-ABL1 fusion protein is a constitutively active tyrosine kinase and triggers a cascade of aberrant downstream signaling pathways leading to clonal outgrowth of CML cells and subsequent disease manifestation. (haematologica.org)
  • Our results support the relevance of NOX2 to regulate metabolism-related signalling pathways downstream of BCR-ABL. (biomed.news)
  • Mechanistically, the cell differentiation mediated by JOA may be originated from the inhibition of BCR-ABL/c-MYC signaling in CML cells expressing wild-type BCR-ABL and BCR-ABL-T315I. (jcancer.org)
  • On the other hand about 30% of patients with Ph+ ALL harbor the M-BCR p210or p210[5,6,7]. (bios-mep.info)
  • The e13a2 and e14a2 transcripts encode P210 BCR-ABL1 proteins with slightly different sizes. (cmleukemia.com)
  • Följaktligen kallas hybrid BCR-ABL1-fusionsproteinet p210 eller p185. (web.app)
  • External quality assessment (EQA) is an essential tool for quality assurance of analytical testing processes of p210 BCR‐ABL1 transcripts by RT‐qPCR. (web.app)
  • As an EQA provider, the National Center for Clinical Laboratories organized an EQA scheme of p210 BCR‐ABL1 testing in China for the first time to identify existing problems and ensure the reliability of p210 BCR‐ABL1 testing. (web.app)
  • Recent studies revealed high ratios of loss of the BCR-ABL1, t(9;22), (p210) kvantitativ PCR. (web.app)
  • CONCLUSIONS: Various problems were found for p210 BCR-ABL1 detection in the EQA. (web.app)
  • By solving the existing problems, the performance of p210 BCR-ABL1 detection can be improved, ensuring robust laboratory diagnostic capacities in China. (web.app)
  • For the p210 transcript associated with CML, quantitation is further adjusted to the international scale (IS) to allow comparison with other IS-compliant BCR-ABL1 assays. (web.app)
  • 1 Different subtypes of BCR-ABL1 transcripts encode fusion proteins with different sizes that may lead to different disease phenotypes. (cmleukemia.com)
  • In CML, the breakpoint in the BCR gene mostly (95%) falls within the major break point cluster region with b2a2 at 40 % and b3a2 at 55% [1]. (aku.edu)
  • Two transcript variants encoding different isoforms have been found for this gene. (wikipedia.org)
  • Alternatively spliced transcript variants encoding distinct isoforms exist. (cancerindex.org)
  • We found that JOA at lower concentration significantly inhibited the proliferation of CML cells expressing mutant BCR-ABL (T315I mutation included) and wild-type BCR-ABL, which was due to that JOA induced the cell differentiation and the cell cycle arrest at G0/G1 phase. (jcancer.org)
  • The BCR-ABL oncoprotein oligomerisation domain found at the N-terminus of BCR is essential for the oncogenicity of the BCR-ABL fusion protein. (wikipedia.org)
  • The BCR-ABL oncoprotein oligomerisation domain consists of a short N-terminal helix (alpha-1), a flexible loop and a long C-terminal helix (alpha-2). (wikipedia.org)
  • Structure-based engineering starting from the antiparallel coiled coil domain of the BCR-ABL oncoprotein (BCR30-65) resulted in a new pH-sensitive homodimeric antiparallel coiled coil. (wikipedia.org)
  • The protein associates with the p85 subunit of phosphatidylinositol 3-kinase and interacts with the fyn-binding protein. (cancerindex.org)
  • Specifically, JAK2 bodily interacts using the C-terminal area of BCR-ABL and is among the most prominent goals of BCR-ABL (7,8). (angiogenesis-blog.com)
  • Significantly, AHI-1 bodily interacts with JAK2 and BCR-ABL in CML cells to mediate these natural results, although the type from the direct or indirect interaction between JAK2 and AHI-1 still continues to be uncharacterized. (angiogenesis-blog.com)
  • In models of Ph+ ALL we show that the functional interplay between ABL/BCR and BCR/ABL not only increases the transformation potential of BCR/ABL but is also indispensable for the growth and survival of Ph+ ALL leukemic cells. (bios-mep.info)
  • Recently "natural" bcr-abl breakpoint-specific cytotoxic T lymphocytes (CTLs) were found in the bone marrow of Ph+ ALL patients treated with imatinib correlating with a better response to this TKI [ 6 ]. (hindawi.com)
  • The fusion gene on der9 differs between m-BCR-p185and M-BCR-p210gene encodes a small ABL/BCR with an approximate molecular mass of 40 kDa (p40transcript is detectable in 65% of the CML patients [15] and the p96transcript is present in 100% of examined patients with m-BCR Ph+ ALL [16]. (bios-mep.info)
  • We conclude that the distribution of BCR/ABL transcript types in patients with CML and ALL differs from most, but not all other populations studied. (aku.edu)
  • Second, this MAP infection triggers a specific humoral response, as Sardinian T1D Olcegepant hydrochloride patients display high frequencies of antibodies (Abs) against mycobacterial proteins (heparin-binding hemagglutinin, glycosyl transferase) [17], whole MAP lysates (70% Ab+ T1D patients vs 7.6% Ab+ healthy controls) [16] and. (healthweblognews.info)
  • This study: 1) Uncovers novel mechanisms of clinical drug-resistance against BCR-ABL-KIs, 2) Identifies increased levels of IL7, pSTAT5 and c-MYC protein, and IKAROS haploinsufficiency as potential biomarkers of BCR-ABL-targeted drug-resistance, 3) Strongly supports clinical exploration of the BCR-ABL-KI and DHA combinations for treating patients with Ph+ ALL, and 4) Establishes a paradigm for investigating frequently overlooked host-tumor-drug interactions. (uthsc.edu)
  • Imatinib binds to the inactive conformation of the Bcr-Abl TK, occluding its ATP-binding pocket and preventing its switch to the active conformation [10]. (rockstarsagainstliveearth.com)
  • Imatinib binds the ABL domain at the ATP-binding site and traps the protein in an inactive conformation to inhibit the kinase activity. (touchoncology.com)
  • The underlying mechanism and causes for the sex-depending distribution of the BCR/ABL transcript types remains open to speculation. (aku.edu)
  • Conclusions Concurrently concentrating on BCR-ABL and JAK2 actions in CML WP1130 (Degrasyn) stem/progenitor cells may improve final results in sufferers destined to build up IM level of resistance. (angiogenesis-blog.com)
  • encoded by Nfe2l2 gene) is a transcription factor responsible for the regulation of cellular redox balance and protective antioxidant and phase II detoxification responses in mammals [ 1 , 2 ]. (springer.com)
  • BCR-ABL fusion gene leads to proliferation of myeloid elements by encoding a protein with tyrosine kinase activity [5]. (waocp.com)
  • The overexpression of a membrane protein designated P-glycoprotein (P-gp) is a typical phenotypic marker of pleiotropic drug resistance. (ashpublications.org)
  • Our studies have demonstrated that several of the proteins encoded by cellular oncogenes function in fundamental aspects of gene regulation. (stanford.edu)
  • Targeting BCR/ABL by selective ATP competitors, such as imatinib or nilotinib, is a well validated therapeutic concept, but unable to definitively eradicate the disease. (bios-mep.info)
  • We also provide an overview of the natural products which have been used for targeting of BCR-ABL protein. (yeditepe.edu.tr)
  • Phospho-c-Abl (Tyr-412) synthetic peptide (coupled to KLH) corresponding to amino acid residues around tyrosine 412 of human c-Abl. (ecmbio.com)
  • Like tyrosine, serine and threonine are amino acid building blocks for protein. (callaix.com)
  • The mutant proteins often retain some of their capabilities but are no longer sensitive to the controls that regulate the normal form of the protein. (cancerquest.org)
  • The protein has serine/threonine kinase activity and is a guanine nucleotide exchange factor for the Rho family of GTPases including RhoA. (wikipedia.org)