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Tytuł:
Overcoming the imatinib-resistant BCR-ABL mutants with new ureidobenzothiazole chemotypes endowed with potent and broad-spectrum anticancer activity.
Autorzy:
El-Damasy AK; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.; Department of Medicinal Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.
Jin H; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Park JW; Center for Supercomputing Applications, Div. of National Supercomputing R&D, Korea Institute of Science and Technology Information, Daejeon, Republic of Korea.
Kim HJ; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Khojah H; Department of Pharmacognosy, College of Pharmacy, Jouf University, Sakaka, Saudi Arabia.
Seo SH; Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Lee JH; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Bang EK; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Keum G; Center for Brain Technology, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.; Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology (UST), Seoul, Republic of Korea.
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Źródło:
Journal of enzyme inhibition and medicinal chemistry [J Enzyme Inhib Med Chem] 2023 Dec; Vol. 38 (1), pp. 2189097.
Typ publikacji:
Journal Article
MeSH Terms:
Fusion Proteins, bcr-abl*/genetics
Pyrimidines*/pharmacology
Imatinib Mesylate/pharmacology ; Piperazines/pharmacology ; Benzamides/pharmacology ; Apoptosis
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
Determination of a radotinib dosage regimen based on dose-response relationships for the treatment of newly diagnosed patients with chronic myeloid leukemia.
Autorzy:
Noh H; Department of Pharmacy, College of Pharmacy, Yonsei University, Incheon, Korea.
Jung SY; Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul, Korea.; Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Korea.
Kwak JY; Chonbuk National University Medical School & Hospital, Jeonju, Korea.
Kim SH; Department of Internal Medicine, Dong-A University College of Medicine, Busan, Korea.
Oh SJ; Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
Zang DY; Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea.
Lee S; Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul, Korea.; Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Korea.
Park HL; Central Research Institute, IL-YANG Pharmaceutical Co., Ltd., Yongin, Korea.
Jo DJ; Central Research Institute, IL-YANG Pharmaceutical Co., Ltd., Yongin, Korea.
Shin JS; Central Research Institute, IL-YANG Pharmaceutical Co., Ltd., Yongin, Korea.
Do YR; Department of Medicine, Dongsan Medical Center, Keimyung University, Daegu, Korea.
Kim DW; Seoul St. Mary's Hospital, Leukemia Research Institute, The Catholic University of Korea, Seoul, Korea.
Lee JI; Department of Pharmacy, College of Pharmacy, Seoul National University, Seoul, Korea.; Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Korea.
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Źródło:
Cancer medicine [Cancer Med] 2018 May; Vol. 7 (5), pp. 1766-1773. Date of Electronic Publication: 2018 Mar 25.
Typ publikacji:
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
MeSH Terms:
Benzamides/*administration & dosage
Fusion Proteins, bcr-abl/*genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Pyrazines/*administration & dosage
Adult ; Aged ; Aged, 80 and over ; Benzamides/adverse effects ; Dose-Response Relationship, Drug ; Drug Dosage Calculations ; Female ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Male ; Middle Aged ; Molecular Weight ; Pyrazines/adverse effects ; Treatment Outcome ; Young Adult
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition.
Autorzy:
Xiao X; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liu P; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Li D; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xia Z; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wang P; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhang X; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liu M; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liao L; Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China.
Jiao B; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. .
Ren R; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. .; Department of Biology, Brandeis University, Waltham, MA, USA. .
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Źródło:
Journal of hematology & oncology [J Hematol Oncol] 2020 Jun 18; Vol. 13 (1), pp. 80. Date of Electronic Publication: 2020 Jun 18.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Molecular Targeted Therapy*
Antineoplastic Combined Chemotherapy Protocols/*therapeutic use
Fusion Proteins, bcr-abl/*antagonists & inhibitors
JNK Mitogen-Activated Protein Kinases/*antagonists & inhibitors
Neoplasm Proteins/*antagonists & inhibitors
Adult ; Aged ; Aged, 80 and over ; Animals ; Anthracenes/administration & dosage ; Azepines/administration & dosage ; Benzamides/administration & dosage ; Cell Line, Tumor ; Dasatinib/administration & dosage ; Drug Screening Assays, Antitumor ; Female ; Humans ; Imatinib Mesylate/administration & dosage ; Male ; Mice ; Mice, Inbred BALB C ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; Protein Kinase Inhibitors/administration & dosage ; Proto-Oncogene Proteins c-myc/biosynthesis ; Pyridines/administration & dosage ; Pyrimidines/administration & dosage ; RNA Interference ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Radiation Chimera ; Random Allocation ; Signal Transduction/drug effects ; Triazoles/administration & dosage
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
Optimization of radotinib doses for the treatment of Asian patients with chronic myelogenous leukemia based on dose-response relationship analyses.
Autorzy:
Noh H; a Department of Pharmacy, College of Pharmacy , Yonsei University , Incheon , Republic of Korea ;; b Yonsei Institute of Pharmaceutical Sciences, College of Pharmacy , Yonsei University , Incheon , Republic of Korea ;
Park MS; c Department of Pharmaceutical Medicine and Regulatory Science, Colleges of Medicine and Pharmacy , Yonsei University , Incheon , Republic of Korea ;; d Department of Clinical Pharmacology, Severance Hospital , Yonsei University Health Systems , Seoul , Republic of Korea ;
Kim SH; e Department of Hematology and Oncology , Dong-A University Medical Center , Busan , Republic of Korea ;
Oh SJ; f Department of Internal Medicine, Kangbuk Samsung Hospital , Sungkyunkwan University School of Medicine , Seoul , Republic of Korea ;
Zang DY; g Department of Internal Medicine , Hallym University Sacred Heart Hospital , Anyang , Republic of Korea ;
Park HL; h Central Research Institute , IL-YANG Pharm. Co., Ltd. , Yongin , Republic of Korea ;
Cho DJ; h Central Research Institute , IL-YANG Pharm. Co., Ltd. , Yongin , Republic of Korea ;
Kim DW; i Cancer Research Institute , The Catholic University of Korea , Seoul , Republic of Korea ;; j Department of Hematology, Seoul St. Mary's Hospital , The Catholic University of Korea , Seoul , Republic of Korea.
Lee JI; a Department of Pharmacy, College of Pharmacy , Yonsei University , Incheon , Republic of Korea ;; b Yonsei Institute of Pharmaceutical Sciences, College of Pharmacy , Yonsei University , Incheon , Republic of Korea ;; c Department of Pharmaceutical Medicine and Regulatory Science, Colleges of Medicine and Pharmacy , Yonsei University , Incheon , Republic of Korea ;; d Department of Clinical Pharmacology, Severance Hospital , Yonsei University Health Systems , Seoul , Republic of Korea ;
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Źródło:
Leukemia & lymphoma [Leuk Lymphoma] 2016 Aug; Vol. 57 (8), pp. 1856-64. Date of Electronic Publication: 2015 Dec 15.
Typ publikacji:
Clinical Trial, Phase II; Journal Article; Multicenter Study
MeSH Terms:
Antineoplastic Agents/*pharmacology
Benzamides/*pharmacology
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Protein Kinase Inhibitors/*pharmacology
Pyrazines/*pharmacology
Adult ; Aged ; Antineoplastic Agents/therapeutic use ; Asian People ; Benzamides/therapeutic use ; Body Surface Area ; Body Weight ; Dose-Response Relationship, Drug ; Drug Dosage Calculations ; Drug Resistance, Neoplasm ; Female ; Humans ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Male ; Middle Aged ; Philadelphia Chromosome ; Protein Kinase Inhibitors/therapeutic use ; Pyrazines/therapeutic use ; Treatment Outcome ; Young Adult
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
Identification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemias.
Autorzy:
Kang Y; Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America.
Hodges A; Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America.
Ong E; Salgomed Inc., Del Mar, California, United States of America.
Roberts W; Rady Children's Hospital, Department of Pediatrics, University of California San Diego, San Diego, California, United States of America.
Piermarocchi C; Department of Physics and Astronomy, Michigan State University, East Lansing, Michigan, United States of America.
Paternostro G; Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America.
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Źródło:
PloS one [PLoS One] 2014 Jul 16; Vol. 9 (7), pp. e102221. Date of Electronic Publication: 2014 Jul 16 (Print Publication: 2014).
Typ publikacji:
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
MeSH Terms:
Antineoplastic Combined Chemotherapy Protocols*
Drug Discovery*
Benzamides/*administration & dosage
Benzamides/*pharmacology
Fusion Proteins, bcr-abl/*metabolism
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Piperazines/*administration & dosage
Piperazines/*pharmacology
Pyrimidines/*administration & dosage
Pyrimidines/*pharmacology
Algorithms ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Benzamides/therapeutic use ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Piperazines/therapeutic use ; Pyrimidines/therapeutic use
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Synthesis and identification of GZD856 as an orally bioavailable Bcr-Abl inhibitor overcoming acquired imatinib resistance.
Autorzy:
Lu X; a School of Pharmacy , Jinan University , Guangzhou , China.; b State Key Laboratory of Respiratory Diseases , Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou , China.
Zhang Z; a School of Pharmacy , Jinan University , Guangzhou , China.; b State Key Laboratory of Respiratory Diseases , Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou , China.
Ren X; b State Key Laboratory of Respiratory Diseases , Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou , China.
Wang D; b State Key Laboratory of Respiratory Diseases , Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou , China.
Ding K; a School of Pharmacy , Jinan University , Guangzhou , China.; b State Key Laboratory of Respiratory Diseases , Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou , China.
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Źródło:
Journal of enzyme inhibition and medicinal chemistry [J Enzyme Inhib Med Chem] 2017 Dec; Vol. 32 (1), pp. 331-336.
Typ publikacji:
Journal Article
MeSH Terms:
Benzamides/*chemical synthesis
Benzamides/*pharmacology
Drug Resistance, Neoplasm/*drug effects
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Administration, Oral ; Animals ; Cell Proliferation/drug effects ; Computer Simulation ; Enzyme Activation/drug effects ; Fusion Proteins, bcr-abl/metabolism ; Heterografts ; Humans ; Imatinib Mesylate/pharmacology ; K562 Cells ; Male ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Molecular Structure
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
AP24163 inhibits the gatekeeper mutant of BCR-ABL and suppresses in vitro resistance.
Autorzy:
Azam M; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, The Children's Hospital, Dana Farber Cancer Institute, Brigham and Women's Hospital, Boston, MA, USA.
Powers JT
Einhorn W
Huang WS
Shakespeare WC
Zhu X
Dalgarno D
Clackson T
Sawyer TK
Daley GQ
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Źródło:
Chemical biology & drug design [Chem Biol Drug Des] 2010 Feb; Vol. 75 (2), pp. 223-7. Date of Electronic Publication: 2009 Dec 17.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
Drug Resistance, Neoplasm*
Adenine/*analogs & derivatives
Benzamides/*chemistry
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Protein Kinase Inhibitors/*chemistry
Protein-Tyrosine Kinases/*antagonists & inhibitors
Adenine/chemistry ; Adenine/pharmacology ; Animals ; Benzamides/pharmacology ; Binding Sites ; Cell Line ; Computer Simulation ; Dasatinib ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Mice ; Mutation ; Piperazines/chemistry ; Piperazines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Pyrimidines/chemistry ; Pyrimidines/pharmacology ; Thiazoles/chemistry ; Thiazoles/pharmacology
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
A long noncoding RNA critically regulates Bcr-Abl-mediated cellular transformation by acting as a competitive endogenous RNA.
Autorzy:
Guo G; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Kang Q; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Zhu X; 1] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China [2] School of Life Sciences, Anhui University, Hefei, China.
Chen Q; College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, China.
Wang X; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Chen Y; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Ouyang J; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
Zhang L; Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medical Center, Peking Union Medical College, Beijing, China.
Tan H; Center of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Chen R; Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Huang S; Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, USA.
Chen JL; 1] CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China [2] College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, China.
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Źródło:
Oncogene [Oncogene] 2015 Apr 02; Vol. 34 (14), pp. 1768-79. Date of Electronic Publication: 2014 May 19.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Cell Transformation, Neoplastic/*genetics
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics
MicroRNAs/*genetics
RNA, Long Noncoding/*genetics
Animals ; Apoptosis/drug effects ; Benzamides/pharmacology ; Cell Line, Tumor ; DNA Methylation ; Fusion Proteins, bcr-abl/biosynthesis ; Fusion Proteins, bcr-abl/genetics ; Gene Expression Regulation, Leukemic/drug effects ; HEK293 Cells ; Hep G2 Cells ; Humans ; Imatinib Mesylate ; Jurkat Cells ; K562 Cells ; MCF-7 Cells ; Mice ; Mice, Nude ; Mice, Transgenic ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; PTEN Phosphohydrolase/antagonists & inhibitors ; PTEN Phosphohydrolase/genetics ; Piperazines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-myc/genetics ; Pyrimidines/pharmacology ; RNA, Long Noncoding/biosynthesis ; RNA, Messenger/genetics ; Transplantation, Heterologous
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Grb10 is involved in BCR-ABL-positive leukemia in mice.
Autorzy:
Illert AL; Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
Albers C; 1] Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany [2] Department of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.
Kreutmair S; Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
Leischner H; 1] Department of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany [2] Department of Hematology, Oncology, and Tumor Immunology, HELIOS Klinikum Berlin-Buch, Berlin, Germany.
Peschel C; Department of Internal Medicine III, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany.
Miething C; Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
Duyster J; Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany.
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Źródło:
Leukemia [Leukemia] 2015 Apr; Vol. 29 (4), pp. 858-68. Date of Electronic Publication: 2014 Sep 24.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Gene Expression Regulation, Leukemic*
Bone Marrow Cells/*pathology
Fusion Proteins, bcr-abl/*genetics
GRB10 Adaptor Protein/*genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics
Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Benzamides/pharmacology ; Bone Marrow Cells/metabolism ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Disease Models, Animal ; Female ; Fusion Proteins, bcr-abl/metabolism ; GRB10 Adaptor Protein/antagonists & inhibitors ; GRB10 Adaptor Protein/metabolism ; Humans ; Imatinib Mesylate ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Piperazines/pharmacology ; Primary Cell Culture ; Pyrimidines/pharmacology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia.
Autorzy:
Eiring AM; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Page BDG; Department of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Kraft IL; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Mason CC; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Vellore NA; Department of Medicinal Chemistry, College of Pharmacy, The University of Utah, Salt Lake City, Utah, USA.
Resetca D; York University Chemistry Department, Toronto, Ontario, Canada.
Zabriskie MS; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Zhang TY; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Khorashad JS; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Engar AJ; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Reynolds KR; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Anderson DJ; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Senina A; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Pomicter AD; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Arpin CC; Department of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Ahmad S; Department of Medicinal Chemistry, College of Pharmacy, The University of Utah, Salt Lake City, Utah, USA.
Heaton WL; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Tantravahi SK; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.
Todic A; Department of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Moriggl R; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Wilson DJ; York University Chemistry Department, Toronto, Ontario, Canada.; Center for Research in Mass Spectrometry, Department of Chemistry, York University, Toronto, Ontario, Canada.
Baron R; Department of Medicinal Chemistry, College of Pharmacy, The University of Utah, Salt Lake City, Utah, USA.
O'Hare T; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.; Division of Hematology and Hematologic Malignancies, The University of Utah, Salt Lake City, Utah, USA.
Gunning PT; Department of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Deininger MW; Huntsman Cancer Institute, The University of Utah, Salt Lake City, Utah, USA.; Division of Hematology and Hematologic Malignancies, The University of Utah, Salt Lake City, Utah, USA.
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Źródło:
Leukemia [Leukemia] 2015 Mar; Vol. 29 (3), pp. 586-597. Date of Electronic Publication: 2014 Aug 19.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
MeSH Terms:
Gene Expression Regulation, Leukemic*
Aminosalicylic Acids/*pharmacology
Fusion Proteins, bcr-abl/*genetics
Leukocytes, Mononuclear/*drug effects
Neoplastic Stem Cells/*drug effects
STAT3 Transcription Factor/*genetics
Small Molecule Libraries/*pharmacology
Sulfonamides/*pharmacology
Aminosalicylic Acids/chemical synthesis ; Aminosalicylic Acids/chemistry ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Benzamides/pharmacology ; Cell Line, Tumor ; Dasatinib ; Drug Discovery ; Drug Resistance, Neoplasm/drug effects ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/metabolism ; Genes, Reporter ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/pathology ; Luciferases/genetics ; Luciferases/metabolism ; Molecular Docking Simulation ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Phosphorylation ; Piperazines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Protein Structure, Tertiary ; Pyrimidines/pharmacology ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/chemistry ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Small Molecule Libraries/chemical synthesis ; Small Molecule Libraries/chemistry ; Sulfonamides/chemical synthesis ; Sulfonamides/chemistry ; Thiazoles/pharmacology
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Dasatinib induces fast and deep responses in newly diagnosed chronic myeloid leukaemia patients in chronic phase: clinical results from a randomised phase-2 study (NordCML006).
Autorzy:
Hjorth-Hansen H; Department of Hematology, St Olavs Hospital, Trondheim, Norway; Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Stenke L
Söderlund S
Dreimane A
Ehrencrona H
Gedde-Dahl T
Gjertsen BT
Höglund M
Koskenvesa P
Lotfi K
Majeed W
Markevärn B
Ohm L
Olsson-Strömberg U
Remes K
Suominen M
Simonsson B
Porkka K
Mustjoki S
Richter J
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Corporate Authors:
Nordic CML Study Group
Źródło:
European journal of haematology [Eur J Haematol] 2015 Mar; Vol. 94 (3), pp. 243-50. Date of Electronic Publication: 2014 Sep 13.
Typ publikacji:
Clinical Trial, Phase II; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
MeSH Terms:
Antineoplastic Agents/*therapeutic use
Benzamides/*therapeutic use
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Piperazines/*therapeutic use
Protein Kinase Inhibitors/*therapeutic use
Pyrimidines/*therapeutic use
Thiazoles/*therapeutic use
Adult ; Aged ; Dasatinib ; Drug Administration Schedule ; Female ; Follow-Up Studies ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Gene Expression ; Humans ; Hydroxyurea/therapeutic use ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/mortality ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Male ; Middle Aged ; Remission Induction ; Risk ; Survival Analysis
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
Inhibition of Aurora kinase B is important for biologic activity of the dual inhibitors of BCR-ABL and Aurora kinases R763/AS703569 and PHA-739358 in BCR-ABL transformed cells.
Autorzy:
Illert AL; Clinic for Internal Medicine 1, Hematology, Oncology and Stem Cell Transplantation, Freiburg University Medical Center, 79106 Freiburg, Germany.
Seitz AK; Department of Internal Medicine III, Technical University of Munich, 81675 Munich, Germany.
Rummelt C; Clinic for Internal Medicine 1, Hematology, Oncology and Stem Cell Transplantation, Freiburg University Medical Center, 79106 Freiburg, Germany.
Kreutmair S; Clinic for Internal Medicine 1, Hematology, Oncology and Stem Cell Transplantation, Freiburg University Medical Center, 79106 Freiburg, Germany.
Engh RA; The Norwegian Structural Biology Centre, Departments of Chemistry and Pharmacy, University of Tromsø, Tromsø, Norway.
Goodstal S; EMD-Serono Research and Development Institute, Inc., Billerica, Massachusetts, United States of America.
Peschel C; Department of Internal Medicine III, Technical University of Munich, 81675 Munich, Germany.
Duyster J; Clinic for Internal Medicine 1, Hematology, Oncology and Stem Cell Transplantation, Freiburg University Medical Center, 79106 Freiburg, Germany.
von Bubnoff N; Clinic for Internal Medicine 1, Hematology, Oncology and Stem Cell Transplantation, Freiburg University Medical Center, 79106 Freiburg, Germany.
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Źródło:
PloS one [PLoS One] 2014 Nov 26; Vol. 9 (11), pp. e112318. Date of Electronic Publication: 2014 Nov 26 (Print Publication: 2014).
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Antineoplastic Agents/*pharmacology
Aurora Kinase B/*antagonists & inhibitors
Benzamides/*pharmacology
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Norbornanes/*pharmacology
Protein Kinase Inhibitors/*pharmacology
Pyrazoles/*pharmacology
Pyrimidines/*pharmacology
Animals ; Apoptosis/drug effects ; Aurora Kinase B/chemistry ; Aurora Kinase B/genetics ; Aurora Kinase B/metabolism ; B-Lymphocytes/drug effects ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Base Sequence ; Cell Cycle/drug effects ; Cell Line, Transformed ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Fusion Proteins, bcr-abl/chemistry ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Gene Expression ; Humans ; Mice ; Molecular Docking Simulation ; Molecular Sequence Data
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Velocity of early BCR-ABL transcript elimination as an optimized predictor of outcome in chronic myeloid leukemia (CML) patients in chronic phase on treatment with imatinib.
Autorzy:
Hanfstein B; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Shlyakhto V; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Lauseker M; Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, München, Germany.
Hehlmann R; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Saussele S; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Dietz C; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Erben P; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Fabarius A; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Proetel U; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Schnittger S; MLL Münchner Leukämielabor, München, Germany.
Krause SW; Medizinische Klinik 5, Universitätsklinikum Erlangen, Erlangen, Germany.
Schubert J; Klinik für Hämatologie, Onkologie und Palliativmedizin, Evangelisches Krankenhaus, Hamm, Germany.
Einsele H; Medizinischen Klinik und Poliklinik II, Universitätsklinikum Würzburg, Würzburg, Germany.
Hänel M; Klinik für Innere Medizin III, Klinikum Chemnitz, Chemnitz, Germany.
Dengler J; Medizinische Universitätsklinik, Abteilung Innere Medizin V, Ruprecht-Karls-Universität Heidelberg, Heidelberg, Germany.
Falge C; Medizinische Klinik 5, Klinikum Nürnberg Nord, Nürnberg, Germany.
Kanz L; Medizinische Klinik II, Universitätsklinikum Tübingen, Tübingen, Germany.
Neubauer A; Klinik für Innere Medizin, Schwerpunkt Hämatologie, Onkologie und Immunologie, Universitätsklinikum Gießen und Marburg, Marburg, Germany.
Kneba M; II. Medizinische Klinik und Poliklinik im Städtischen Krankenhaus, Universitätsklinikum Schleswig-Holstein, Kiel, Germany.
Stegelmann F; Klinik für Innere Medizin III, Universitätsklinikum Ulm, Ulm, Germany.
Pfreundschuh M; Innere Medizin I; Universitätsklinikum des Saarlandes, Homburg, Germany.
Waller CF; Klinik für Innere Medizin I, Universitätsklinikum Freiburg, Freiburg, Germany.
Spiekermann K; Medizinische Klinik und Poliklinik III, Ludwig-Maximilians-Universität München, München, Germany.
Baerlocher GM; Universitätsklinik für Hämatologie, Inselspital Bern, Bern, Switzerland.
Pfirrmann M; Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, München, Germany.
Hasford J; Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie der Ludwig-Maximilians-Universität München, München, Germany.
Hofmann WK; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
Hochhaus A; Abteilung für Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany.
Müller MC; III. Medizinische Universitätsklinik, Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany.
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Corporate Authors:
SAKK and the German CML Study Group
Źródło:
Leukemia [Leukemia] 2014 Oct; Vol. 28 (10), pp. 1988-92. Date of Electronic Publication: 2014 May 06.
Typ publikacji:
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
MeSH Terms:
Antineoplastic Agents/*therapeutic use
Benzamides/*therapeutic use
Fusion Proteins, bcr-abl/*metabolism
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics
Piperazines/*therapeutic use
Pyrimidines/*therapeutic use
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Disease-Free Survival ; Female ; Glucuronidase/metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Male ; Middle Aged ; Prognosis ; Proportional Hazards Models ; Risk ; Sensitivity and Specificity ; Treatment Outcome ; Young Adult
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Arsenic trioxide and bortezomib interact synergistically to induce apoptosis in chronic myelogenous leukemia cells resistant to imatinib mesylate through Bcr/Abl‑dependent mechanisms.
Autorzy:
Xu W; Exclusive Medical Care Center, Rui‑Jin Hospital, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Wei W; Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Yu Q; Exclusive Medical Care Center, Rui‑Jin Hospital, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Wu C; Exclusive Medical Care Center, Rui‑Jin Hospital, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Ye C; Exclusive Medical Care Center, Rui‑Jin Hospital, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Wu Y; Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
Yan H; Exclusive Medical Care Center, Rui‑Jin Hospital, Shanghai Jiao‑Tong University School of Medicine, Shanghai 200025, P.R. China.
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Źródło:
Molecular medicine reports [Mol Med Rep] 2014 Sep; Vol. 10 (3), pp. 1519-24. Date of Electronic Publication: 2014 Jun 16.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Gene Expression Regulation, Leukemic*
Apoptosis/*drug effects
Arsenicals/*pharmacology
Benzamides/*pharmacology
Boronic Acids/*pharmacology
Fusion Proteins, bcr-abl/*metabolism
Oxides/*pharmacology
Piperazines/*pharmacology
Pyrazines/*pharmacology
Pyrimidines/*pharmacology
Arsenic Trioxide ; Bortezomib ; Caspase 3/genetics ; Caspase 3/metabolism ; Cell Line, Tumor ; Down-Regulation ; Drug Resistance, Neoplasm ; Drug Synergism ; Fusion Proteins, bcr-abl/genetics ; Humans ; Imatinib Mesylate ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Poly(ADP-ribose) Polymerases/genetics ; Poly(ADP-ribose) Polymerases/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reactive Oxygen Species/metabolism
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
BCR-ABL inhibitors: updates in the management of patients with chronic-phase chronic myeloid leukemia.
Autorzy:
Khan AM
Bixby DL
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Źródło:
Hematology (Amsterdam, Netherlands) [Hematology] 2014 Jul; Vol. 19 (5), pp. 249-58. Date of Electronic Publication: 2013 Dec 02.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't; Review
MeSH Terms:
Antineoplastic Agents/*therapeutic use
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Leukemia, Myeloid, Chronic-Phase/*drug therapy
Protein Kinase Inhibitors/*therapeutic use
Algorithms ; Benzamides/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; Imatinib Mesylate ; Leukemia, Myeloid, Chronic-Phase/mortality ; Piperazines/therapeutic use ; Practice Guidelines as Topic ; Pyrimidines/therapeutic use ; Risk Factors ; Treatment Outcome
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
Tytuł:
ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistance.
Autorzy:
Wang Z; Department of Cancer Biology, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Liu Z; Department of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Wu X; Department of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Chu S; Division of Hematopoietic Stem Cell and Leukemia Research, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Wang J; Department of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Yuan H; Department of Cancer Biology, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Roth M; Department of Cancer Biology, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Yuan YC; Department of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Bhatia R; Division of Hematopoietic Stem Cell and Leukemia Research, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
Chen W; Department of Cancer Biology, Beckman Research Institute, City of Hope, Duarte, California, United States of America.
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Źródło:
PLoS genetics [PLoS Genet] 2014 Jun 26; Vol. 10 (6), pp. e1004414. Date of Electronic Publication: 2014 Jun 26 (Print Publication: 2014).
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
ADP-ribosyl Cyclase 1/*biosynthesis
Fusion Proteins, bcr-abl/*genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics
Tretinoin/*administration & dosage
ADP-ribosyl Cyclase 1/genetics ; Apoptosis/drug effects ; Benzamides/administration & dosage ; Cell Differentiation/drug effects ; Cell Line, Tumor ; DNA Damage/drug effects ; Dasatinib ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Flow Cytometry ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Piperazines/administration & dosage ; Point Mutation ; Protein Kinase Inhibitors/administration & dosage ; Pyrimidines/administration & dosage ; Sirtuin 1/genetics ; Thiazoles/administration & dosage
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
BCR-ABL affects STAT5A and STAT5B differentially.
Autorzy:
Schaller-Schönitz M; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Barzan D; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Williamson AJ; Faculty of Medical and Human Sciences, Manchester Academic Health Science Centre, University of Manchester, Wolfson Molecular Imaging Centre, Manchester, United Kingdom.
Griffiths JR; Faculty of Medical and Human Sciences, Manchester Academic Health Science Centre, University of Manchester, Wolfson Molecular Imaging Centre, Manchester, United Kingdom.
Dallmann I; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Battmer K; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Ganser A; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Whetton AD; Faculty of Medical and Human Sciences, Manchester Academic Health Science Centre, University of Manchester, Wolfson Molecular Imaging Centre, Manchester, United Kingdom.
Scherr M; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
Eder M; Hannover Medical School, Department of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover, Germany.
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Źródło:
PloS one [PLoS One] 2014 May 16; Vol. 9 (5), pp. e97243. Date of Electronic Publication: 2014 May 16 (Print Publication: 2014).
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Fusion Proteins, bcr-abl/*metabolism
STAT5 Transcription Factor/*metabolism
Signal Transduction/*physiology
Tumor Suppressor Proteins/*metabolism
Benzamides ; Cell Line ; Cell Proliferation/physiology ; Dimerization ; Fluorescent Antibody Technique ; Genetic Vectors/genetics ; Humans ; Imatinib Mesylate ; Immunoblotting ; Immunoprecipitation ; Interleukin-3/metabolism ; Lentivirus ; Mass Spectrometry ; Phosphorylation ; Piperazines ; Pyrimidines ; RNA Interference ; Signal Transduction/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Elucidation of the structural basis of interaction of the BCR-ABL kinase inhibitor, nilotinib (Tasigna) with the human ABC drug transporter P-glycoprotein.
Autorzy:
Shukla S; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Chufan EE; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Singh S; Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St John's University, Queens, NY, USA.
Skoumbourdis AP; NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, Rockville, MD, USA.
Kapoor K; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Boxer MB; NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, Rockville, MD, USA.
Duveau DY; NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, Rockville, MD, USA.
Thomas CJ; NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, Rockville, MD, USA.
Talele TT; Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St John's University, Queens, NY, USA.
Ambudkar SV; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
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Źródło:
Leukemia [Leukemia] 2014 Apr; Vol. 28 (4), pp. 961-4. Date of Electronic Publication: 2014 Jan 14.
Typ publikacji:
Letter; Research Support, N.I.H., Intramural
MeSH Terms:
ATP Binding Cassette Transporter, Subfamily B, Member 1/*chemistry
Fusion Proteins, bcr-abl/*antagonists & inhibitors
Protein Kinase Inhibitors/*metabolism
Pyrimidines/*metabolism
ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism ; Benzamides/metabolism ; Binding Sites ; Humans ; Imatinib Mesylate ; Piperazines/metabolism
Raport
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
BCR-ABL/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia.
Autorzy:
Xu C; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Fu H; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China.
Gao L; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Wang L; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Wang W; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Li J; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Li Y; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Dou L; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Gao X; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Luo X; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Jing Y; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
Chim CS; Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China.
Zheng X; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China.
Yu L; Department of Hematology, Chinese PLA General Hospital, Beijing, China.
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Źródło:
Oncogene [Oncogene] 2014 Jan 02; Vol. 33 (1), pp. 44-54. Date of Electronic Publication: 2012 Dec 03.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Gene Expression Regulation, Neoplastic*
Carcinogenesis/*genetics
Fusion Proteins, bcr-abl/*metabolism
GATA1 Transcription Factor/*metabolism
MicroRNAs/*genetics
Antineoplastic Agents/pharmacology ; Apoptosis ; Base Sequence ; Benzamides/pharmacology ; Binding Sites ; Carcinogenesis/metabolism ; Cell Proliferation ; Down-Regulation ; Fusion Proteins, bcr-abl/genetics ; G1 Phase Cell Cycle Checkpoints ; Gene Expression ; HEK293 Cells ; Humans ; Imatinib Mesylate ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; MicroRNAs/metabolism ; Open Reading Frames ; Piperazines/pharmacology ; Promoter Regions, Genetic ; Pyrimidines/pharmacology ; RNA Interference
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
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