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11位生命科学突破奖得主：6 - 11位科学家的学术影响力
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| 十一位科学家获生命科学巨奖 |
据《自然》网站消息，来自美国、荷兰和日本的11位科学家获得了首届生命科学大奖——“生命科学突破奖”（Breakthrough Prize in Life Sciences）。他们分别获得该奖的五个奖项，每个得奖人将获奖金300万美元，该数目是诺贝尔奖单项奖金（2012年为120万美元）的2.5倍。
1 美国普林斯顿大学教授David Botstein
2 美国哈佛大学教授Eric S. Lander 获基因组学奖
3 美国康奈尔大学教授Lewis C. Cantley
4 荷兰皇家艺术与科学学院Hubrecht研究所教授Hans Clevers
5 美国加州大学圣地亚哥分校教授Napoleone Ferrara
6 美国纪念斯隆•凯特林癌症中心教授Charles L. Sawyers
7 美国约翰•霍普金斯大学教授Bert Vogelstein
8 美国麻省理工学院教授Robert A. Weinberg 获癌症奖
9 美国洛克菲勒大学教授Titia de Lange 获端粒奖
10 日本京都大学山中伸弥Shinya Yamanaka 获干细胞奖
11 美国洛克菲勒大学教授Cornelia I. Bargmann 获神经生物学奖
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Brian J. Druker, Moshe Talpaz, Debra J. Resta, Bin Peng, Elisabeth Buchdunger, John M. Ford, Nicholas B. Lydon, Hagop Kantarjian, Renaud Capdeville, Sayuri Ohno-Jones,
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Published in 2002.
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Clinical studies with the Abl tyrosine kinase inhibitor STI-571 in chronic myeloid leukemia demonstrate that many patients with advanced stage disease respond initially but then relapse. Through biochemical and molecular analysis of clinical material, we find that drug resistance is associated with the reactivation of BCR-ABL signal transduction in all cases examined. In six of nine patients, resistance ...
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Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding. Crystallographic studies predict that most imatinib-resistant mutants should remain sensitive to inhibitors that bind ABL with less stringent conformational requirements. BMS-354825 is an orally bioavailable ...
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Through sequencing analysis of blood or bone marrow samples from patients with chronic myeloid leukemia, we identified BCR-ABL kinase domain mutations in 29 of 32 patients whose disease relapsed after an initial response to the tyrosine kinase inhibitor imatinib. Fifteen different amino acid substitutions affecting 13 residues in the kinase domain were found. Mutations fell into two groups—those ...
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Charlie D Chen, Derek S Welsbie, Chris Tran, Sung Hee Baek, Randy Chen, Robert Vessella, Michael G Rosenfeld,Using microarray-based profiling of isogenic prostate cancer xenograft models, we found that a modest increase in androgen receptor mRNA was the only change consistently associated with the development of resistance to antiandrogen therapy. This increase in androgen receptor mRNA and protein was both necessary and sufficient to convert prostate cancer growth from a hormone-sensitive to a hormone-refractory ...
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Moshe Talpaz, Neil P. Shah, Hagop Kantarjian, Nicholas Donato, John Nicoll, Ron Paquette, Jorge Cortes, Susan O'Brien, Claude Nicaise, Eric Bleickardt, M. Anne Blackwood-Chirchir, Vishwanath Iyerhttp://academic.research.microsoft.com/io.ashx?type=5&id=10210466&selfId1=23420138&selfId2=-1&maxNumber=12&query=Background The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromo- some-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations. We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR- ABL mutations, in patients with chronic myelogenous leukemia (CML) or ...
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Granulocyte–Macrophage Progenitors as Candidate Leukemic Stem Cells in Blast-Crisis CML (Citations: 468)
Catriona H. M. Jamieson, Laurie E. Ailles, Scott J. Dylla, Manja Muijtjens, Carol Jones, James L. Zehnder, Jason Gotlib, Kevin Li, Markus G. Manz, Armand Keating, , Irving L. Weissmanmethods We used fluorescence-activated cell sorting to isolate hematopoietic stem cells, common myeloid progenitors, granulocyte-macrophage progenitors, and megakaryocyte-eryth- roid progenitors from marrow during several phases of CML and from normal marrow. BCR-ABL, b -catenin , and LEF-1 transcripts were compared by means of a quantitative re- verse-transcriptase-polymerase-chain-reaction assay in normal and CML ... -
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One signal that is overactivated in a wide range of tumour types is the production of a phospholipid, phosphatidylinositol (3,4,5) trisphosphate, by phosphatidylinositol 3-kinase (PI3K). This lipid and the protein kinase that is activated by it — AKT — trigger a cascade of responses, from cell growth and proliferation to survival and motility, that drive tumour progression. Small-molecule ...
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Ingo K. Mellinghoff, Maria Y. Wang, Igor Vivanco, Daphne A. Haas-Kogan, Shaojun Zhu, Ederlyn Q. Dia, Kan V. Lu, Koji Yoshimoto, Julie H. Y. Huang, Dennis J. Chute, Bridget L. Riggs, Steve Horvathhttp://academic.research.microsoft.com/io.ashx?type=5&id=5518722&selfId1=23420138&selfId2=-1&maxNumber=12&query=background The epidermal growth factor receptor (EGFR) is frequently amplified, overexpressed, or mutated in glioblastomas, but only 10 to 20 percent of patients have a response to EGFR kinase inhibitors. The mechanism of responsiveness of glioblastomas to these inhibitors is unknown. methods We sequenced kinase domains in the EGFR and human EGFR type 2 ( Her2/neu ) genes and analyzed the ...
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, Andreas Hochhaus, Eric Feldman, John M. Goldman, Carole B. Miller, Oliver G. Ottmann, Charles A. Schiffer, Moshe Talpaz, Francois Guilhot, Michael W. N. Deininger, Thomas Fischer, Steve G. O'Brienhttp://academic.research.microsoft.com/io.ashx?type=5&id=11504747&selfId1=23420138&selfId2=-1&maxNumber=12&query=Blast crisis is the most advanced stage of chronic myelogenous leukemia (CML) and is highly refractory to therapy. CML is caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, the product of the t(9;22) Philadelphia translo- cation. Imatinib (Glivec, formerly STI571) is a rationally developed, orally adminis- tered inhibitor of the Bcr-Abl tyrosine kinase. A ...
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Katrina Podsypanina, Richard T. Lee, Chris Politis, Ian Hennessy, Allison Crane, Janusz Puc, Mehran Neshat, Hong Wang, Lin Yang, Jay Gibbons, Phil Frost, Valley Dreisbachhttp://academic.research.microsoft.com/io.ashx?type=5&id=15162754&selfId1=23420138&selfId2=-1&maxNumber=12&query=Journal: Proceedings of The National Academy of Sciences - PNAS , vol. 981, no. 18, pp. 10320-10325, 2001
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The clinical success of the ABL tyrosine kinase inhibitor imatinib in chronic myeloid leukaemia (CML) serves as a model for molecularly targeted therapy of cancer, but at least two critical questions remain. Can imatinib eradicate leukaemic stem cells? What are the dynamics of relapse due to imatinib resistance, which is caused by mutations in the ABL kinase domain? The precise ...
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The PTEN/MMAC1 phosphatase is a tumor suppressor gene implicated in a wide range of human cancers. Here we provide biochemical and functional evidence that PTEN/MMAC1 acts a negative regulator of the phosphoinositide 3-kinase (PI3-kinase)/Akt pathway. PTEN/MMAC1 impairs activation of endogenous Akt in cells and inhibits phosphorylation of 4E-BP1, a downstream target of the ...Journal: Proceedings of The National Academy of Sciences - PNAS , vol. 951, no. 26, pp. 15587-15591, 1998
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A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias (Citations: 160) Oliver G. Ottmann, Brian J. Druker, , John M. Goldman, Jose Reiffers, Richard T. Silver, Sante Tura, Thomas Fischer, Michael W. Deininger, Charles A. Schiffer, Michele Baccarani, Alois Gratwohlhttp://academic.research.microsoft.com/io.ashx?type=5&id=11350453&selfId1=23420138&selfId2=-1&maxNumber=12&query=induced complete hematologic responses (CHRs) and complete marrow responses (marrow-CRs) in 29% of ALL patients (CHR, 19%; marrow-CR, 10%), which were sus- tained for at least 4 weeks in 6% of patients. Median estimated time to progression and overall survival for ALL patients were 2.2 and 4.9 months, respectively. CHRs were reported for 3 (38%) of ...
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Disruption of the normal regulation of cell-cycle progression and division lies at the heart of the events leading to cancer. Complex networks of regulatory factors, the tumour microenvironment and stress signals, such as those resulting from damaged DNA, dictate whether cancer cells proliferate or die. Recent progress in understanding the molecular changes that underlie cancer development offer the prospect ...
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Katharine Ellwood-Yen, Thomas G. Graeber, John Wongvipat, M. Luisa Iruela-Arispe, JianFeng Zhang, Robert Matusik, George V. Thomas,Increased Myc gene copy number is observed in human prostate cancer. To define Myc's functional role, we generated transgenic mice expressing human c-Myc in the mouse prostate. All mice developed murine prostatic intraepithelial neoplasia followed by invasive adenocarcinoma. Microarray-based expression profiling identified a Myc prostate cancer expression signature, which included the putative human tumor suppressor NXK3.1. ...
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Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment (Citations: 144) Ravi Bhatia, Melissa Holtz, Ning Niu, Rachel Gray, David S. Snyder, , Daniel A. Arber, Marilyn L. Slovak, Stephen J. FormanThe BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; No- vartis, Basel, Switzerland) has shown re- markable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achiev- ing complete cytogenetic responses (CCRs). However, it is not clear whether remissions will be durable and whether imatinib mesylate can eliminate the malig- nant primitive progenitors ...Published in 2003.
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Jerald P. Radich, Hongyue Dai, Mao Mao, Vivian Oehler, Jan Schelter, Brian Druker, , Neil Shah, Wendy Stock, Cheryl L. Willman, Stephen Friend, Peter S. LinsleyChronic myeloid leukemia (CML) is a hematopoietic stem cell disease with distinct biological and clinical features. The biologic basis of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood. We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases). ...Journal: Proceedings of The National Academy of Sciences - PNAS , vol. 103, no. 8, pp. 2794-2799, 2006
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Xinyi Wu, Karin Hepner, Shobha Castelino-Prabhu, Marc B. Kaye, Xiu-Juan Yuan, Jonathan Wood, Christopher Ross, , Young E. WhangPTEN is a tumor suppressor gene mutated in human cancers. Although many mutations target the phosphatase domain, others create a truncated protein lacking the C-terminal PDZ-binding motif or a protein that extends beyond the PDZ-binding motif. Using the yeast two-hybrid system, we isolated a membrane-associated guanylate kinase family protein with multiple PDZ domains [AIP-1 (...Journal: Proceedings of The National Academy of Sciences - PNAS , vol. 97, no. 8, pp. 4233-4238, 2000
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Sergei Roumiantsev, Neil P. Shah, Mercedes E. Gorre, John Nicoll, Bradley B. Brasher, , Richard A. van EttenThe Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse because of reactivation of Bcr-Abl signaling. Mutations of Thr-315 in the Abl kinase domain to Ile (T315I) were previously described in STI-571-resistant patients and ...Journal: Proceedings of The National Academy of Sciences - PNAS , vol. 991, no. 16, pp. 10700-10705, 2002
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Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (Citations: 104) Tim F. Cloughesy, Koji Yoshimoto, Phioanh Nghiemphu, Kevin Brown, Julie Dang, Shaojun Zhu, Teli Hsueh, Yinan Chen, Wei Wang, David Youngkin, Linda Liau, Neil Martinhttp://academic.research.microsoft.com/io.ashx?type=5&id=5387397&selfId1=23420138&selfId2=-1&maxNumber=12&query=Background There is much discussion in the cancer drug development community about how to incorporate molecular tools into early-stage clinical trials to assess target modulation, measure anti-tumor activity, and enrich the clinical trial population for patients who are more likely to benefit. Small, molecularly focused clinical studies offer the promise of the early definition of optimal biologic dose ...
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BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90 (Citations: 103) Clinical resistance to imatinib mesylate is commonly observed in patients with advanced Philadelphia chromosome- positive (Ph) leukemias. Acquired resis- tance is typically associated with reactiva- tion of BCR-ABL due to kinase domain mutations or gene amplification, indicat- ing that BCR-ABL remains a viable target for inhibition in these patients. Strategies for overcoming resistance can be envi- sioned through ...Published in 2002.
http://academic.research.microsoft.com/Detail?entitytype=2&searchtype=2&id=23420138&orderBy=1
11位生命科学突破奖得主：7 – 11位科学家
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十一位科学家获生命科学巨奖 |
据《自然》网站消息，来自美国、荷兰和日本的11位科学家获得了首届生命科学大奖——“生命科学突破奖”（Breakthrough Prize in Life Sciences）。他们分别获得该奖的五个奖项，每个得奖人将获奖金300万美元，该数目是诺贝尔奖单项奖金（2012年为120万美元）的2.5倍。
1 美国普林斯顿大学教授David Botstein
2 美国哈佛大学教授Eric S. Lander 获基因组学奖
3 美国康奈尔大学教授Lewis C. Cantley
4 荷兰皇家艺术与科学学院Hubrecht研究所教授Hans Clevers
5 美国加州大学圣地亚哥分校教授Napoleone Ferrara
6 美国纪念斯隆•凯特林癌症中心教授Charles L. Sawyers
7 美国约翰•霍普金斯大学教授Bert Vogelstein
8 美国麻省理工学院教授Robert A. Weinberg 获癌症奖
9 美国洛克菲勒大学教授Titia de Lange 获端粒奖
10 日本京都大学山中伸弥Shinya Yamanaka 获干细胞奖
11 美国洛克菲勒大学教授Cornelia I. Bargmann 获神经生物学奖
全文见 http://news.sciencenet.cn/htmlnews/2013/2/274939.shtm
我们对每位科学家的学术成就和影响力进行分析。
7 美国约翰•霍普金斯大学教授Bert Vogelstein
8 美国麻省理工学院教授Robert A. Weinberg 获癌症奖
9 美国洛克菲勒大学教授Titia de Lange 获端粒奖
10 日本京都大学山中伸弥Shinya Yamanaka 获干细胞奖
11 美国洛克菲勒大学教授Cornelia I. Bargmann 获神经生物学奖
7 美国约翰•霍普金斯大学教授Bert Vogelstein
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Publications (433)
· A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity (Citations: 9286)A. P. Feinberg, B. Vogelstein
Journal: Analytical Biochemistry - ANAL BIOCHEM , vol. 132, no. 1, pp. 6-13, 1983
· A genetic model for colorectal tumorigenesis (Citations: 3578)E. R. Fearon, B. Vogelstein
Journal: Cell , vol. 61, no. 5, pp. 759-767, 1990
· WAF1, a potential mediator of p53 tumor suppression (Citations: 2505)W. S. El-deiry, T. Tokino, V. E. Velculescu, D. B. Levy, R. Parsons, J. M. Trent, D. Lin, W. E. Mercer, K. W. Kinzler, B. Vogelstein
Journal: Cell , vol. 75, no. 4, pp. 817-825, 1993
· p53 Mutations in Human Cancers (Citations: 2416)Monica Hollstein, David Sidransky, Bert Vogelstein, Curtis C. Harris
Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific ...
Journal: Science , vol. 253, no. 5015, pp. 49-53, 1991
· Serial Analysis of Gene Expression (Citations: 2131)V. E. Velculescu, L. Zhang, B. Vogelstein, K. W. Kinzler
Journal: Science , vol. 270, no. 5235, pp. 484-487, 1995
· P53 Mutations in human can-cers (Citations: 1891)M Hollstein, D Sidransky, B Vogelstein, Cc Harris
Journal: Science , 1991
· Lessons from Hereditary Colorectal Cancer (Citations: 1819)Kenneth W Kinzler, Bert Vogelstein
Journal: Cell , vol. 87, no. 2, pp. 159-170, 1996
· Surfing the p53 network (Citations: 1529)Bert Vogelstein, Arnold J. Levine
Journal: Nature , vol. 408, pp. 307-310, 2000
· Genetic instabilities in human cancers (Citations: 1219)C. Lengauer, K. W. Kinzler, B. Vogelstein
Journal: Nature , 1998
· Participation of p53 protein in the cellular response to DNA damage (Citations: 1187)M. B. Kastan, O. Onyekwere, D. Sidransky, B. Vogelstein, R. W. Craig
Published in 1991.
http://academic.research.microsoft.com/Detail?entitytype=2&searchtype=2&id=22931656&orderBy=1
8 美国麻省理工学院教授Robert A. Weinberg 获癌症奖
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9 美国洛克菲勒大学教授Titia de Lange 获端粒奖
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10 日本京都大学山中伸弥Shinya Yamanaka 获干细胞奖
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11 美国洛克菲勒大学教授Cornelia I. Bargmann 获神经生物学奖
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