WordNet

a nuclear reaction in which nuclei combine to form more massive nuclei with the simultaneous release of energy (同)nuclear_fusion, nuclear fusion reaction
the merging of adjacent sounds or syllables or words
correction of an unstable part of the spine by joining two or more vertebrae; usually done surgically but sometimes done by traction or immobilization (同)spinal_fusion
the act of fusing (or melting) together
an occurrence that involves the production of a union (同)merger, unification
the combining of images from the two eyes to form a single visual percept (同)optical fusion
the 2nd letter of the Roman alphabet (同)b
the blood group whose red cells carry the B antigen (同)type_B, group B
any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
the 1st letter of the Roman alphabet (同)a
the blood group whose red cells carry the A antigen (同)type_A, group A
the eleventh month of the civil year; the fifth month of the ecclesiastical year in the Jewish calendar (in July and August) (同)Av

PrepTutorEJDIC

〈U〉(金属などが)溶けること,融解,融合《+『of』+『名』》 / 〈C〉融合物 / 〈C〉(政党・党派などの)連合,合同;(民族などの)融合《+『of』+『名』》 / 〈U〉〈C〉核融合(nuclear fusion)
蛋白(たんばく)質
answer / ampere

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1. 慢性骨髄性白血病の分子遺伝学 molecular genetics of chronic myeloid leukemia
2. 慢性骨髄性白血病の細胞生物学および分子生物学 cellular and molecular biology of chronic myeloid leukemia
3. 慢性骨髄性白血病の臨床症状および診断 clinical manifestations and diagnosis of chronic myeloid leukemia
4. アントラサイクリン系以外の癌化学療法剤の心毒性 cardiotoxicity of nonanthracycline cancer chemotherapy agents
5. 血液悪性腫瘍およびリンパ悪性腫瘍の遺伝的異常 genetic abnormalities in hematologic and lymphoid malignancies

English Journal

Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation.

Lane AA1, Chapuy B1, Lin CY1, Tivey T1, Li H2, Townsend EC1, van Bodegom D1, Day TA1, Wu SC1, Liu H1, Yoda A1, Alexe G2, Schinzel AC3, Sullivan TJ4, Malinge S5, Taylor JE6, Stegmaier K7, Jaffe JD6, Bustin M8, Te Kronnie G9, Izraeli S10, Harris MH11, Stevenson KE12, Neuberg D12, Silverman LB2, Sallan SE2, Bradner JE1, Hahn WC3, Crispino JD13, Pellman D14, Weinstock DM3.Author information 1Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.2Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.31] Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA. [2] Broad Institute, Cambridge, Massachusetts, USA.4Microarray Core, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.5Institut National de la Santé et de la Recherche Médicale (INSERM) U985, Institut Gustave Roussy, Villejuif, France.6Broad Institute, Cambridge, Massachusetts, USA.71] Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA. [2] Broad Institute, Cambridge, Massachusetts, USA.8Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.9Department of Pediatrics, University of Padova, Padova, Italy.101] Department of Pediatric Hemato-Oncology, Sheba Medical Center, Tel Hashomer, Ramat Gan, Israel. [2] Department of Human Molecular Genetics and Biochemsitry, Tel Aviv University, Tel Aviv, Israel.11Department of Pathology, Children's Hospital Boston, Boston, Massachusetts, USA.12Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.13Division of Hematology/Oncology, Northwestern University, Chicago, Illinois, USA.141] Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA. [2] Howard Hughes Medical Institute, Chevy Chase, Maryland, USA.AbstractDown syndrome confers a 20-fold increased risk of B cell acute lymphoblastic leukemia (B-ALL), and polysomy 21 is the most frequent somatic aneuploidy among all B-ALLs. Yet the mechanistic links between chromosome 21 triplication and B-ALL remain undefined. Here we show that germline triplication of only 31 genes orthologous to human chromosome 21q22 confers mouse progenitor B cell self renewal in vitro, maturation defects in vivo and B-ALL with either the BCR-ABL fusion protein or CRLF2 with activated JAK2. Chromosome 21q22 triplication suppresses histone H3 Lys27 trimethylation (H3K27me3) in progenitor B cells and B-ALLs, and 'bivalent' genes with both H3K27me3 and H3K4me3 at their promoters in wild-type progenitor B cells are preferentially overexpressed in triplicated cells. Human B-ALLs with polysomy 21 are distinguished by their overexpression of genes marked with H3K27me3 in multiple cell types. Overexpression of HMGN1, a nucleosome remodeling protein encoded on chromosome 21q22 (refs. 3,4,5), suppresses H3K27me3 and promotes both B cell proliferation in vitro and B-ALL in vivo.
Nature genetics.Nat Genet.2014 Apr 20. doi: 10.1038/ng.2949. [Epub ahead of print]
Down syndrome confers a 20-fold increased risk of B cell acute lymphoblastic leukemia (B-ALL), and polysomy 21 is the most frequent somatic aneuploidy among all B-ALLs. Yet the mechanistic links between chromosome 21 triplication and B-ALL remain undefined. Here we show that germline triplication of
PMID 24747640

Omacetaxine: a protein translation inhibitor for treatment of chronic myelogenous leukemia.

Gandhi V1, Plunkett W, Cortes JE.Author information 1Authors' Affiliations: Departments of Experimental Therapeutics and Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.AbstractChronic myelogenous leukemia (CML) is driven by the Bcr-Abl fusion protein, which is a result of a (9;22) chromosomal translocation. Imatinib, dasatinib, and nilotinib (tyrosine kinase inhibitors, TKI) have revolutionized how CML is treated. Although the majority of patients respond to these kinase inhibitors, a subset becomes resistant to these therapeutics. Synribo (omacetaxine mepesuccinate) was recently approved by the U.S. Food and Drug Administration for Philadelphia-positive CML either in the chronic or the accelerated phase whose disease failed two prior TKIs. With omacetaxine 1.25 mg/m(2) twice daily for 14 days during induction and for 7 days during maintenance, a major cytogenetic response occurred in 20% of patients in the chronic phase and major hematologic response in 27% of patients in the accelerated phase. Laboratory investigations unraveled the mechanism of action and effectiveness of this agent. Bcr-Abl protein is intrinsically programmed to turn over with a short half-life that makes it susceptible to protein translation inhibitors. Omacetaxine (homoharringtonine) inhibits total protein biosynthesis by binding to A-site cleft of ribosomes. As a corollary to this action, there is a diminution of short-lived proteins, such as Bcr-Abl, followed by cell death. Approval of this first-in-class protein translation inhibitor opens up new avenues for its use in other diseases as well as mechanism-based combinations. Clin Cancer Res; 20(7); 1735-40. ©2014 AACR.
Clinical cancer research : an official journal of the American Association for Cancer Research.Clin Cancer Res.2014 Apr 1;20(7):1735-40. doi: 10.1158/1078-0432.CCR-13-1283. Epub 2014 Feb 5.
Chronic myelogenous leukemia (CML) is driven by the Bcr-Abl fusion protein, which is a result of a (9;22) chromosomal translocation. Imatinib, dasatinib, and nilotinib (tyrosine kinase inhibitors, TKI) have revolutionized how CML is treated. Although the majority of patients respond to these kinase
PMID 24501394

Bosutinib : a review of preclinical and clinical studies in chronic myelogenous leukemia.

Rusconi F1, Piazza R, Vagge E, Gambacorti-Passerini C.Author information 1University of Milano-Bicocca, Department of Health Sciences , Via Cadore 48, 20900 Monza , Italy carlo.gambacorti@unimib.it.AbstractINTRODUCTION: Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease. It is characterized by a Bcr-Abl (breakpoint cluster region-Abelson leukemia virus) tyrosine kinase fusion protein produced from the Philadelphia (Ph) chromosome. The tyrosine kinase inhibitor (TKI) imatinib was the first targeted therapy licensed for patients with chronic-phase CML. In recent years, many other TKIs have been approved for the treatment of patients with CML. For this reason, the choice of the best strategy treatment has become increasingly complex.
Expert opinion on pharmacotherapy.Expert Opin Pharmacother.2014 Apr;15(5):701-10. doi: 10.1517/14656566.2014.882898. Epub 2014 Jan 30.
INTRODUCTION: Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease. It is characterized by a Bcr-Abl (breakpoint cluster region-Abelson leukemia virus) tyrosine kinase fusion protein produced from the Philadelphia (Ph) chromosome. The tyrosine kinase inhibitor (TKI) imatinib was the f
PMID 24479382

Japanese Journal

STAP-2 interacts with and modulates BCR-ABL-mediated tumorigenesis

Sekine Y.,Ikeda O.,Mizushima A.,Ueno Y.,Muromoto R.,Yoshimura A.,Kanakura Y.,Oritani K.,Matsuda T.
Oncogene 31(40), 4384-4396, 2012-10-04
… In chronic myeloid leukemia (CML), the BCR-ABL fusion oncoprotein activates multiple pathways involved in cell survival, growth promotion and disease progression. … In this report, we show that the signal transducing adaptor protein-2 (STAP-2) is involved in BCR-ABL activity. …
NAID 120005228623

Monitoring Twenty-Six Chronic Myeloid Leukemia Patients by BCR-ABL mRNA Level in Bone Marrow: A Single Hospital Experience

Sakamoto Yuichi,Mariya Yasushi,Oshikiri Toshiyuki,Sasaki Sumiko,Segawa Megumi,Teshiromori Ryuichi,Ogura Kazuto,Akagi Tomoaki,Kaimori Mitsuomi,Kubo Kohmei
Acta Medica Okayama 65(5), 335-342, 2011-10
… Chronic myeloid leukemia (CML) is caused by the BCR-ABL oncogene. … The Philadelphia chromosome (Ph) from a reciprocal translocation, t(9;22) (q34;q11) causes a fusion gene, BCR-ABL, that encodes a constitutively active tyrosine kinase. … Treatment of CML by imatinib is effective to control the tyrosyl phosphorylation of the protein related to the cell signaling. …
NAID 80022078065

Breakthrough in the treatment of chronic myeloid leukemia

YAMADA Yoshihiro
Aino journal 10, 17-21, 2011
… The resulting fusion protein BCR-ABL shows constantly activated ABL tyrosine kinase activity which is essential for growth of leukemic cells. … Imatinib is designed to inhibit the binding of ATP to the ABL tyrosine kinase so as to abolish the phosphorylation of the downstream signal proteins. …
NAID 110009493610