• The Tel-ARG fusion protein, resulting from reciprocal translocation between chromosomes 1 and 12, is associated with acute myeloid leukemia (AML). (umbc.edu)
  • 7 In CML and acute myeloid leukemia (AML), we and others have shown that IL-1 is a positive regulator of LSC, and blocking IL-1 signaling inhibits the LSC. (haematologica.org)
  • Runt-related transcription factor 1 (RUNX1), which is also known as acute myeloid leukemia 1 (AML1), has been frequently found with genomic aberrations in human leukemia. (bvsalud.org)
  • BloodSpot database analysis for TRAIL expression in patients with acute myeloid leukemia were performed. (bvsalud.org)
  • The therapeutic approach to the patient with acute myeloid leukemia (AML) currently evolves toward new frontiers. (ashpublications.org)
  • The term acute myeloid leukemia (AML) collectively refers to a mixture of distinct diseases that differ with regard to their pathogenetic evolution, genetic abnormalities, clinical features, response to therapy, and prognosis. (ashpublications.org)
  • The Ph is seen in acute lymphoblastic leukemia, acute myeloid leukemia, and motley-type acute leukemia, in addition to CML. (inter-publishing.com)
  • Acute myeloid leukemia (AML) patients with a high allelic burden of an internal tandem duplication ( ITD )-mutated FMS - like Tyrosine Kinase - 3 ( FLT3 ) have a dismal outcome. (biomedcentral.com)
  • Acute myeloid leukemia (AML) is mainly a fatal disease. (biomedcentral.com)
  • Imatinib mesylate (IM) is a tyrosine kinase inhibitor, which inhibits phosphorylation of downstream proteins involved in BCR-ABL signal transduction. (tau.ac.il)
  • Different inhibitors have been designed to target different kinases: Inhibition of BCR/ABl constitutes the basis of the functioning of drugs like imatinib Inhibition of FLT3 is carried out by drugs like lestaurtinib Inhibition of JAK2 is carried out by the drug CYT387, which was successful in preclinical trials and is currently undergoing clinical trials. (wikipedia.org)
  • As a result, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 (human wild‑type) or TCCY‑T315I (human imatinib‑resistant) and the Ba/F3‑(T315I/E279K/Y253H) (mouse BCR/ABL point mutation‑transfected cells). (spandidos-publications.com)
  • Interestingly, AVM appeared to be more sensitive to imatinib‑resistant (T315I, Y253H, and E279K) than wild‑type BCR/ABL cells, indicating its potential to overcome imatinib‑resistant severe issues in CML. (spandidos-publications.com)
  • Focusing on preventing BCR-ABL activation is quite efficient, as imatinib has demonstrated, but may not be the optimal option. (spandidos-publications.com)
  • Thus, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 [human wild-type (WT)] or TCCY-T315I [human imatinib-resistant (IR)] and the Ba/F3-(T315I/E279K/Y253H) (mouse BCR/ABL point mutation-tranfected cells). (spandidos-publications.com)
  • BCR-Abl is the target of selective inhibitors, such as imatinib (Gleevec), used in the treatment of CML. (umbc.edu)
  • Dasatinib (Sprycel): Indicated for the treatment of adult patients with chronic myeloid leukemia in chronic, accelerated, or myeloid or lymphoid blast phase who are resistant or intolerant to prior therapy including imatinib. (medscape.com)
  • Imatinib (Veenat) is a specific protein-tyrosine kinase inhibitor (TKI) which mainly works by inhibiting the bcr-abl (a tyrosine kinase), the constitutive abnormal tyrosine kinase formed by the Philadelphia chromosomes abnormality in the CML. (theindianpharma.com)
  • In the Vivo, imatinib inhibits the growth of tumor of bcr-abl transfected murine myeloid cells as well as bcr-abl positive leukemia lines derived from the CML patients in the blast crisis. (theindianpharma.com)
  • Bcr-Abl fusion protein has constitutively activated Abl tyrosine kinase activity which is responsible for the uncontrolled proliferation in CML The tyrosine kinase inhibitors (TKIs) such as Imatinib, Dasatinib, and Nilotinib are the current first-line treatments approved by the United States Food and Drug Administration (US FDA) for the treatment of the disease. (eurekaselect.com)
  • Prospective outcome data on 267 unselected adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia confirms superiority of allogeneic transplantation over chemotherapy in the pre-imatinib era: results from the International ALL Trial MRC UKALLXII/ECOG2993. (inter-publishing.com)
  • A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. (inter-publishing.com)
  • Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. (inter-publishing.com)
  • Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic phase chronic myeloid leukemia. (medscape.org)
  • Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. (medscape.org)
  • International randomized study of interferon vs STI571 (IRIS) 8-year follow up: sustained survival and low risk for progression or events in patients with newly diagnosed chronic myeloid leukemia in chronic phase treated with imatinib [abstract]. (medscape.org)
  • Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. (medscape.org)
  • A population study of imatinib in chronic myeloid leukaemia demonstrates lower efficacy than in clinical trials. (medscape.org)
  • Phase III, randomized, open-label study of daily imatinib mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid leukemia in chronic phase using molecular end points: tyrosine kinase inhibitor optimization and selectivity study. (medscape.org)
  • Tolerability-adapted imatinib 800 mg/d versus 400 mg/d versus 400 mg/d plus interferon-{alpha} in newly diagnosed chronic myeloid leukemia. (medscape.org)
  • Imatinib plus peginterferon alfa-2a in chronic myeloid leukemia. (medscape.org)
  • Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. (medscape.org)
  • Superior efficacy of nilotinib compared with imatinib in newly-diagnosed patients with chronic myeloid leukemia in chronic (CML-CP): ENESTnd minimum 24-month follow-up [abstract]. (medscape.org)
  • ENESTnd update: continued superiority of nilotinib versus imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) [abstract]. (medscape.org)
  • Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. (medscape.org)
  • Efficacy and safety of dasatinib compared with imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): minimum 24-month follow-up from the DASISION trial [abstract]. (medscape.org)
  • Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure. (medscape.org)
  • Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia. (medscape.org)
  • It is a targeted therapy whereby imatinib competes for the BCR-ABL1 tyrosine kinase site to prevent phosphorylation and inhibit proliferation [ 6 ]. (biomedcentral.com)
  • Imatinib, marketed by Novartis as Gleevec (U.S.) or Glivec (Europe/Australia/Latin America), and sometimes referred to by its investigational name STI-571, is a tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML). (keralapharmacist.com)
  • Because the BCR-Abl tyrosine kinase enzyme exists only in cancer cells and not in healthy cells, imatinib works as a form of targeted therapy-only cancer cells are killed through the drug's action. (keralapharmacist.com)
  • Imatinib is used to treat chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. (keralapharmacist.com)
  • Imatinib is specific for the TK domain in abl (the Abelson proto-oncogene), c-kit and PDGF-R (platelet-derived growth factor receptor). (keralapharmacist.com)
  • As this is now a constitutively active tyrosine kinase, imatinib is used to decrease bcr-abl activity. (keralapharmacist.com)
  • Imatinib works by binding close to the ATP binding site of bcr-abl, locking it in a closed or self-inhibited conformation, and therefore inhibiting the enzyme activity of the protein semi-competitively. (keralapharmacist.com)
  • This fact explains why many BCR-ABL mutations can cause resistance to imatinib by shifting its equilibrium toward the open or active conformation. (keralapharmacist.com)
  • Imatinib is quite selective for bcr-abl - it does also inhibit other targets mentioned above (c-kit and PDGF-R), but no other known tyrosine kinases. (keralapharmacist.com)
  • Imatinib also inhibits the abl protein of non-cancer cells but cells normally have additional redundant tyrosine kinases which allow them to continue to function even if abl tyrosine kinase is inhibited. (keralapharmacist.com)
  • Children with chronic myeloid leukemia treated with front-line imatinib have a slower molecular response and comparable survival compared with adults: a multicentre experience in Taiwan (Liu HC et al. (cml-foundation.org)
  • An abnormal chromosomal translocation known as t(9;22) results in the establishment of the Philadelphia chromosome, which contains the BCR-ABL gene, culminating in the development of this syndrome ( 1 ). (spandidos-publications.com)
  • In CML, a balanced (9;22) chromosomal translocation results in a chimeric BCR-ABL fusion gene. (medscape.com)
  • This gene codes a fusion protein with high tyrosine kinase activity, resulting in growth factor-independent proliferation. (medscape.com)
  • BCR-ABL fusion gene levels are monitored to determine the treatment efficacy. (medscape.com)
  • Approximately 95% of all CML patients harbor the gene fusion, BCR-ABL, which is formed via a double stranded break (DSB) within both the Abelson oncogene 1 (ABL) on chromosome 9q, which codes for a non-receptor tyrosine kinase (ABL), and the breakpoint cluster region gene (BCR) on chromosome 22q. (ubc.ca)
  • The second provides for the highly sensitive detection of DSBs in the anaplastic lymphoma kinase (ALK) gene that result in a non-reciprocal (inversion) translocation (inv(2)(p21;p23)) associated with an ALK-positive non-small cell lung cancer (NSCLC). (ubc.ca)
  • In chronic myelogenous leukemia (CML) patients, an aberrant translocation results in the replacement of the first exon of Abl with the BCR (breakpoint cluster region) gene. (umbc.edu)
  • Abl2, also known as ARG (Abelson-related gene), is thought to play a cooperative role with Abl in the proper development of the nervous system. (umbc.edu)
  • The TEL gene is a frequent fusion partner of other tyr kinase oncogenes, including Tel/Abl, Tel/PDGFRbeta, and Tel/Jak2, found in patients with leukemia and myeloproliferative disorders. (umbc.edu)
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease caused due to translocation between chromosome 9 and 22 leading to a chimeric gene product known as Bcr-Abl. (eurekaselect.com)
  • 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)
  • During this translocation, a piece of chromosome 9 containing the oncogene ABL is translocated to chromosome 22 and fused to the BCR gene. (msdmanuals.com)
  • The chimeric fusion gene BCR-ABL is responsible for production of the oncoprotein bcr-abl tyrosine kinase. (msdmanuals.com)
  • Using in vitro cell lines derived in from conditional MYC, RAS, and BCR-ABL transgenic murine models and oncogene-driven human cell lines, we determined gene regulation, metabolic profiles, and sensitivity to inhibition of lipogenesis in lymphoid malignancies. (biomedcentral.com)
  • Outcome of pediatric chronic myeloid leukemia with management focusing on gene transcript levels (Al-Ghamblas I et al. (cml-foundation.org)
  • This translocation, written as t(9;22), fuses part of the ABL1 gene from chromosome 9 with part of the BCR gene from chromosome 22, creating an abnormal fusion gene called BCR-ABL1 . (medlineplus.gov)
  • The function of the protein produced from the normal BCR gene is not completely understood, although it has been shown to help control signaling in cells. (medlineplus.gov)
  • In 5 to 10 percent of cases of chronic myeloid leukemia, the BCR-ABL1 fusion gene is created by complex rearrangements that involve other chromosomes in addition to chromosomes 9 and 22. (medlineplus.gov)
  • Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. (jefferson.edu)
  • Chromosomal translocations can cause cancer, often through the formation of fusion genes that code for an unnatural tyrosine kinase that promotes constitutive activation of a signaling pathway controlling cell proliferation and differentiation. (ubc.ca)
  • It was initially found that the induction of TRAIL expression following the megakaryocytic differentiation of human leukemia cells was RUNX1-dependent. (bvsalud.org)
  • Although the molecular mechanisms that control MSC proliferation and differentiation are not well understood, the involvement of microRNAs has been reported. (embrapa.br)
  • The tyrosine kinases of the epidermal growth factor receptor (EGFR) constitute the beginning of one signal transduction cascade leading to AP-1 activation and are known to control cell proliferation and differentiation. (biomedcentral.com)
  • Cellular processes such as proliferation, differentiation, and death are regulated by signal transduction pathways which commonly exert their function through receptor mediated activation. (biomedcentral.com)
  • The phosphorylated tyrosines act as binding sites for signal transducers initiating a series of kinase actions resulting in cellular proliferation and differentiation [ 3 - 5 ]. (biomedcentral.com)
  • BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia. (jefferson.edu)
  • BCR-ABL encodes a constitutively active tyrosine kinase BCR-ABL responsible for the uncontrolled proliferation associated with chronic myelogenous leukemia. (ubc.ca)
  • 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)
  • Inhibition of TA was associated with 50% inhibition of proliferation. (tau.ac.il)
  • The inhibition of proliferation was associated with a decrease in the S-phase of the cell cycle and an accumulation of cells in the G2/M phase. (tau.ac.il)
  • This study demonstrates an additional cellular target of IM, not necessarily mediated via known tyrosine kinases, that causes inhibition of TA and cell proliferation. (tau.ac.il)
  • Binding mode and structural elements of Bcr-Abl inhibition are discussed with emphasis on pathways involved in this complex disease to determine alternative strategies and combination therapies. (eurekaselect.com)
  • The kinase movement is measurable for cell proliferation, diversity inhibition, and cell death confrontation. (inter-publishing.com)
  • Inhibition of the bcr-abl tyrosine kinase also stimulates its entry in to the nucleus, where it is unable to perform any of its normal anti-apoptopic functions. (keralapharmacist.com)
  • Using cell lines derived from conditional MYC, RAS, and BCR-ABL transgenic murine models, we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(tetradecloxy)-2-furic acid (TOFA), and other lipogenesis inhibitors. (biomedcentral.com)
  • Furthermore, TRAIL expression was reduced in leukemia cells carrying the t(8;21) translocation, where the RUNX1-ETO chimeric protein interfere with normal RUNX1 function. (bvsalud.org)
  • It may be a critical substrate for p210(bcr/abl), a chimeric protein whose presence is associated with CML. (novusbio.com)
  • For example, the diagnostic hallmark of chronic myelogenous leukemia (CML) is an oncogene fusion formed from a reciprocal translocation (t(9;22)(q34.1;q11.2)) between chromosomes 9 and 22 that results in an altered chromosome 22q known as the Philadelphia chromosome. (ubc.ca)
  • 3 Myelofibrosis (MF) refers to the Philadelphia chromosome ( BCR-ABL1 )-negative myeloproliferative neoplasm (MPN) originating at the level of the multipotent hematopoietic stem cell. (haematologica.org)
  • Specifically, it is used for chronic myelogenous leukemia treatment (CML) and acute lymphocytic leukemia (ALL) that are Philadelphia chromosome-positive (Ph+), certain types of gastrointestinal stromal tumors (GIST), hypereosinophilic syndrome (HES), chronic eosinophilic leukemia (CEL), systemic mastocytosis, and myelodysplastic syndrome. (theindianpharma.com)
  • Newly diagnosed adult patients with Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) in chronic phase. (theindianpharma.com)
  • BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (zju.edu.cn)
  • Stone, M. Translocation of C-Abl oncogene correlates with the presence of a philadelphia chromosome in chronic myelocytic leukaemia. (eurekaselect.com)
  • Iclusig® (ponatinib) MEDICARE Prior Authorization Form Complete Patient and Physician information (PLEASE PRINT) STEP 1 Member Name: Address: Physician Name: Address: Member ID: Member DOB: Member Phone: Phone #: Fax #: NPI Number: If Applicable: Pharmacy Name: ________________________________________ Pharmacy Phone: ________________________________________ Complete the Clinical Assessment: Diagnosis Chronic, Accelerated, or Blast Phase CML Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ALL) Other (please state): __________________________________________________________ Clinical Consideration Patient had resistance and/or intolerance to prior TKIs. (abcdocz.com)
  • q11) results in the Philadelphia chromosome (Ph), which is an ideal marker of chronic myeloid leukemia (CML). (inter-publishing.com)
  • A total of 180 patients with leukocytosis, 150 of them had Philadelphia chromosome-positive with a mean age of 52.86 ± 13.9 (range: 29-80) years were collected. (inter-publishing.com)
  • In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of abl with bcr (breakpoint cluster region), termed bcr-abl. (keralapharmacist.com)
  • The Philadelphia (Ph) chromosome is present in 90 to 95% of cases of chronic myeloid leukemia. (msdmanuals.com)
  • Alterations in cellular metabolism after TKI therapy for Philadelphia chromosome-positive leukemia in children: A review (Li C et al. (cml-foundation.org)
  • Dasatinib-related pleural effusion and lymphocytosis rates are different between adult and pediatrc pts with Philadelphia chromosome-positive leukemias: are age and comorbidities only to blame? (cml-foundation.org)
  • Ponatinib in pediatric patients with Philadelphia chromosome-positive leukemia: a retrospective survey of the Japan Children's Cancer Group (Kodama Y et al. (cml-foundation.org)
  • The myeloproliferative neoplasms (MPNs) are a heterogeneous group of chronic hematological malignancies that are generally divided into the Philadelphia chromosome-positive (Ph-positive) MPNs, which refers to chronic myelogenous leukemia (CML) and the Philadelphia chromosome-negative (Ph-negative) MPNs. (cancernetwork.com)
  • The presence of the Philadelphia chromosome provides a target for molecular therapies in people with chronic myeloid leukemia. (medlineplus.gov)
  • Chronic myeloid leukemia (CML) is a malignancy of the blood and bone marrow that affects children and adults. (spandidos-publications.com)
  • A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. (curehunter.com)
  • Bone marrow fibrosis is also detected in the spent phase of chronic myelogenous leukemia and polycythemia vera. (medscape.com)
  • In normal bone marrow cultures grown in the presence of either granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3), IL-4 suppresses granulocyte-macrophage colony-forming unit (CFU-GM) proliferation but it enhances the colony-stimulatory effect of granulocyte colony-stimulating factor (G-CSF). (utmb.edu)
  • We studied the effect of IL-4 on chronic myelogenous leukemia (CML) bone marrow or peripheral blood cells from 30 patients using the CFU-granulocyte-erythrocyte-monocyte-megakaryocyte colony culture assay. (utmb.edu)
  • Chronic myeloid leukemia is a slow-growing cancer of the blood-forming tissue (bone marrow). (medlineplus.gov)
  • In chronic myeloid leukemia, the bone marrow produces too many white blood cells. (medlineplus.gov)
  • The resulting BCR-Abl fusion protein is constitutively active and associates into tetramers, resulting in a hyperactive kinase sending a continuous signal. (umbc.edu)
  • 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)
  • Protein tyrosine kinase Abl promotes hepatitis C virus particle assembly via interaction with viral substrate activator NS5A.Miyamoto D, et al. (inter-publishing.com)
  • Indolizine: In-Silico Identification of Inhibitors against Mutated BCR-ABL Protein of Chronic Myeloid Leukemia. (inter-publishing.com)
  • The Bcr-Abl protein induces the upregulation of proto-oncogene c-Jun, which is involved in Bcr-Abl transforming activity in Bcr-Abl positive cells. (tmu.edu.tw)
  • The constantly active BCR-ABL1 protein signals cells to continue dividing abnormally and prevents them from self-destructing, which leads to overproduction of the abnormal cells and, eventually, a shortage of normal blood cells. (medlineplus.gov)
  • 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)
  • Docking protein 1 is constitutively tyrosine phosphorylated in hematopoietic progenitors isolated from chronic myelogenous leukemia (CML) patients in the chronic phase. (novusbio.com)
  • Sphingolipids are modified in multiple cancers and are responsible for tumor proliferation, progression, and metastasis. (frontiersin.org)
  • thus, tumors with a high cell turnover are most susceptible (certain leukemias and lymphomas, small proliferating tumors, "recruited" tumor cells, and micrometastases). (doctorlib.info)
  • Some tumor cells, however, have a dependence on bcr-abl. (keralapharmacist.com)
  • right), the default state of the cell is proliferation, and a disruption of the tissue architecture leads to the diffusion of various mutations within the tumor and to the activation of the tumor microenvironment (TME). (elifesciences.org)
  • Exogenous treatment of recombinant TRAIL proteins was found to induce leukemia cell death. (bvsalud.org)
  • Fusion Proteins, bcr-abl" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (jefferson.edu)
  • Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. (jefferson.edu)
  • This graph shows the total number of publications written about "Fusion Proteins, bcr-abl" by people in this website by year, and whether "Fusion Proteins, bcr-abl" was a major or minor topic of these publications. (jefferson.edu)
  • Below are the most recent publications written about "Fusion Proteins, bcr-abl" by people in Profiles. (jefferson.edu)
  • This review outlines the Bcr-Abl dependent and independent mechanism of TKIs resistance development and the strategies used to overcome drug resistance, such as the development of ATP site and allosteric site inhibitors. (eurekaselect.com)
  • Tyrosine kinase inhibitors (TKIs) as first-line therapy for Chronic Myeloid Leukemia (CML) show a high success rate. (biomedcentral.com)
  • Current and emerging tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia in young adults (Mersin S et al. (cml-foundation.org)
  • Impact of tyrosine kinase inhibitors applied for first-line chronic myeloid leukemia treatment on platelet function in whole blood of healthy volunteers in vitro (Eckart F et al. (cml-foundation.org)
  • Outcomes of adolescents and young adults with chronic-phase chronic myeloid leukemia treated with tyrosine kinase inhibitors (Nishiyam-Fujita Y et al. (cml-foundation.org)
  • Discontinuation of tyrosine kinase inhibitors based on BCR-ABL1 monitoring by digital droplet PCR in pediatric chronic myeloid leukemia (Kim Y et al. (cml-foundation.org)
  • Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia. (jefferson.edu)
  • The down-regulation was consistent with decreased amounts of BCR-ABL1 in patients taking TKIs regardless of molecular responses. (biomedcentral.com)
  • The up-regulation was consistent with the substantial presence of BCR-ABL1 in CML patients treated with TKIs at the molecular response. (biomedcentral.com)
  • Therefore, these miRNAs have potential as new therapeutic biomarkers for BCR-ABL1 status in adult CML patients treated with TKIs at molecular responses. (biomedcentral.com)
  • A molecular response is the major treatment endpoint with the optimal molecular response at BCR-ABL1 transcript level ≤ 10% by 3 months, ≤1% by 6 months is similar to CCyR and ≤ 0.1% by 12 months, known as Major Molecular Response (MMR). (biomedcentral.com)
  • Perrotti D, Silvestri G, Stramucci L, Yu J, Trotta R. Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay. (jefferson.edu)
  • Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. (curehunter.com)
  • Myeloproliferative diseases are a heterogeneous group of disorders characterized by cellular proliferation of one or more hematologic cell lines in the peripheral blood, distinct from acute leukemia. (medscape.com)
  • Aberrant NFAT signaling is causally involved in the development of chronic lymphocytic leukemia, non-Hodgkin lymphoma, pancreatic cancer, and several other malignancies. (biomedcentral.com)
  • We utilize preclinical murine models and transgenic primary model of T-ALL to determine the effect of lipogenesis blockade across BCR-ABL-, RAS-, and c-MYC-driven lymphoid malignancies. (biomedcentral.com)
  • Patients with Kit (CD117) positive unresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST). (theindianpharma.com)
  • This structure was designed with intentions of targeting the T315L mutation that occurs in up to 20% of patients that have resistance to the other TKIs in the treatment of chronic myelogenous leukemia (CML). (abcdocz.com)
  • In large cell lymphoma and leukemia cells involvement of body fluid this concept becomes less challenging. (cytojournal.com)
  • Large cell lymphoma and leukemia cells tend to have large size nuclei, less mature chromatin, and visible nucleoli with and without cytoplasmic vacuoles. (cytojournal.com)
  • In the cytoplasm, Abl plays a role in cell proliferation and survival. (umbc.edu)
  • Focusing on novel positive regulators of primitive CML cells, the myostatin antagonist myostatin propeptide gave the largest increase in cell expansion and was chosen for further studies. (haematologica.org)
  • Hematopoietic stem cell transplantation can be considered in young patients with chronic myelogenous leukemia in chronic phase if a human leukocyte antigen (HLA)-matched donor is available. (medscape.com)
  • Pediatric patients with Ph+ CML in chronic phase who are newly diagnosed or whose disease has recurred after stem cell transplant or who are resistant to interferon-alpha therapy. (theindianpharma.com)
  • Objective: The cytotoxic effect of berbamine on chronic myeloid leukemia (CML) cell line KU812 was evaluated, and the mechanisms of its action were explored. (zju.edu.cn)
  • berbamine inhibited KU812 cell proliferation in a dose- and time-dependent manner, and the half maximal inhibitory concentration (IC 50 ) values for treatments of 24, 48, and 72 h were 5.83, 3.43, and 0.75 μg/ml, respectively. (zju.edu.cn)
  • Holyoake, T.L. A comparison of normal and leukemic stem cell biology in chronic myeloid leukemia. (eurekaselect.com)
  • Many of these genes are responsible for providing the positive signals that lead to cell division. (cancerquest.org)
  • Sphingolipids are an extensive class of lipids with different functions in the cell, ranging from proliferation to cell death. (frontiersin.org)
  • FLT3 ITD triggers the proliferation of the quiescent hematopoietic stem cell (HSC) pool but fails to directly transform HSCs. (biomedcentral.com)
  • These clones have the same proliferation rate as the parental cell line in general culture medium. (tmu.edu.tw)
  • Chronic myeloid leukemia (CML) occurs when a pluripotent stem cell undergoes malignant transformation and clonal myeloproliferation, leading to a striking overproduction of mature and immature granulocytes. (msdmanuals.com)
  • In a panel of human cell lines, we demonstrate sensitivity to TOFA treatment as a metabolic liability due to the general convergence on de novo lipogenesis in lymphoid malignancies driven by MYC, RAS, or BCR-ABL. (biomedcentral.com)
  • Patient-reported long-term outcome following allogeneic hematopoietic stem cell transplantation in pediatric chronic myeloid leukemia (Schleicher O et al. (cml-foundation.org)
  • It accounts for about 10 percent of all blood cell cancers (leukemias). (medlineplus.gov)
  • In summary, we identify myostatin propeptide as a novel positive regulator of primitive CML cells and corresponding normal hematopoietic cells. (haematologica.org)
  • Rowley, J.D. A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and giemsa staining. (eurekaselect.com)
  • We examined cells from mouse models of MYC-, RAS-, and BCR-ABL-driven lymphoid malignancies and find a convergence on de novo lipogenesis. (biomedcentral.com)
  • It has proved beneficial in treating patients with chronic myeloid leukaemia (CML). (tau.ac.il)
  • Chronic myeloid leukaemia. (inter-publishing.com)
  • Höglund M, Sandin F, Simonsson B. Epidemiology of chronic myeloid leukaemia: an update. (inter-publishing.com)
  • Additionally, several resistance mechanisms, such as BCR-ABL genomic amplification, are considered ( 4 ). (spandidos-publications.com)
  • In contrast to the stimulatory effect exerted by IL-4 on G-CSF-dependent CFU-GM progenitor proliferation in normal marrow, the addition of IL-4 to CML cultures grown in the presence of G-CSF resulted in a divergent effect: suppression of CML CFU-GM in two, stimulation in three, and no significant effect in two CML patients' samples. (utmb.edu)
  • 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)
  • The blast phase leads to fulminant complications resembling those of acute leukemia, including sepsis and bleeding. (msdmanuals.com)
  • Some patients progress directly from the chronic to the blast phase. (msdmanuals.com)
  • Management of children and adolescents with chronic myeloid leukemia in blast phase: International pediatric CML expert panel recommendations - Review (Sembill S et al. (cml-foundation.org)
  • The condition consists of three phases: the chronic phase, the accelerated phase, and the blast phase (or blast crisis). (medlineplus.gov)
  • Pleural effusion in patients with chronic-phase chronic myeloid leukemia (CML-CP) who received first-line dasatinib in the DASISION trial: patient characteristics, management, and outcomes [abstract]. (medscape.org)
  • abstract = "The constitutively active Bcr-Abl tyrosine kinase plays a crucial role in chronic myelogenous leukemia (CML) pathogenesis. (tmu.edu.tw)
  • The Bcr-Abl point mutations, including the gatekeeper T315I mutations, are the principal cause for the development of resistance to TKIs. (eurekaselect.com)
  • Novel BCR-ABL1 fusion identified by targeted next-generation sequencing in a patient with an atypical myeloproliferative neoplasm. (jefferson.edu)
  • Around the same time, and building on the observation that the vitamin folic acid could stimulate acute lymphoblastic leukemia (ALL) cells, Farber used folate analogs such as aminopterin and then amethopterin (methotrexate) to treat ALL, in what is often heralded as the first 'rational' drug development approach [ 4 ]. (biomedcentral.com)
  • chronic leukemias are composed of more mature cells. (curehunter.com)
  • To identify regulators of primitive chronic myeloid leukemia (CML) cells, we performed a high-content cytokine screen using primary CD34 + CD38 low chronic phase CML cells. (haematologica.org)
  • These genes are deleted or inactivated in cancer cells, allowing unregulated proliferation. (doctorlib.info)
  • Cancer cells can be defined by their constant and uncontrolled proliferation. (biomedcentral.com)
  • In the chronic phase, the number of mature white blood cells is elevated, and myeloblasts account for less than 10 percent of blood cells. (medlineplus.gov)