ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Essay: Amersham Pharmacia Biotech & Science prize. Tantalizing transcriptomes--SAGE and its use in global gene expression analysis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Velculescu, V E -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1491-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231, USA. velculescu@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610550" target="_blank"〉PubMed〈/a〉
    Keywords: *Awards and Prizes ; Gene Expression ; *Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras ; *Genome ; History, 20th Century ; Humans ; Neoplasms/genetics ; RNA, Messenger/*genetics ; Saccharomyces cerevisiae/genetics ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Allelic variation in human gene expression (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, Hai -- Yuan, Weishi -- Velculescu, Victor E -- Vogelstein, Bert -- Kinzler, Kenneth W -- CA 62924/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 16;297(5584):1143.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sidney Kimmel Comprehensive Cancer Center and Howard Hughes Medical Institute, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12183620" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Calpain/genetics ; Female ; *Gene Expression ; Genetic Predisposition to Disease ; Genetic Techniques ; *Genetic Variation ; Genotype ; Haplotypes ; Humans ; Male ; Pedigree ; Polymorphism, Single Nucleotide ; Protein Kinases/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    A phosphatase associated with metastasis of colorectal cancer (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-13
    Description: To gain insights into the molecular basis for metastasis, we compared the global gene expression profile of metastatic colorectal cancer with that of primary cancers, benign colorectal tumors, and normal colorectal epithelium. Among the genes identified, the PRL-3 protein tyrosine phosphatase gene was of particular interest. It was expressed at high levels in each of 18 cancer metastases studied but at lower levels in nonmetastatic tumors and normal colorectal epithelium. In 3 of 12 metastases examined, multiple copies of the PRL-3 gene were found within a small amplicon located at chromosome 8q24.3. These data suggest that the PRL-3 gene is important for colorectal cancer metastasis and provide a new therapeutic target for these intractable lesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saha, S -- Bardelli, A -- Buckhaults, P -- Velculescu, V E -- Rago, C -- St Croix, B -- Romans, K E -- Choti, M A -- Lengauer, C -- Kinzler, K W -- Vogelstein, B -- CA 62924/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 9;294(5545):1343-6. Epub 2001 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Oncology Center, Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11598267" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/enzymology/genetics/pathology ; Chromosome Mapping ; Chromosomes, Human, Pair 8 ; Colon/enzymology ; Colorectal Neoplasms/*enzymology/*genetics/pathology ; Gene Amplification ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Library ; Humans ; Immediate-Early Proteins/*genetics/metabolism ; Intestinal Mucosa/enzymology ; Neoplasm Metastasis/*genetics ; Neoplasm Proteins ; Neoplasm Staging ; Polymerase Chain Reaction ; Protein Tyrosine Phosphatases/*genetics/metabolism ; Rectum/enzymology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Heteroplasmic mitochondrial DNA mutations in normal and tumour cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-05
    Description: The presence of hundreds of copies of mitochondrial DNA (mtDNA) in each human cell poses a challenge for the complete characterization of mtDNA genomes by conventional sequencing technologies. Here we describe digital sequencing of mtDNA genomes with the use of massively parallel sequencing-by-synthesis approaches. Although the mtDNA of human cells is considered to be homogeneous, we found widespread heterogeneity (heteroplasmy) in the mtDNA of normal human cells. Moreover, the frequency of heteroplasmic variants varied considerably between different tissues in the same individual. In addition to the variants identified in normal tissues, cancer cells harboured further homoplasmic and heteroplasmic mutations that could also be detected in patient plasma. These studies provide insights into the nature and variability of mtDNA sequences and have implications for mitochondrial processes during embryogenesis, cancer biomarker development and forensic analysis. In particular, they demonstrate that individual humans are characterized by a complex mixture of related mitochondrial genotypes rather than a single genotype.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176451/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176451/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yiping -- Wu, Jian -- Dressman, Devin C -- Iacobuzio-Donahue, Christine -- Markowitz, Sanford D -- Velculescu, Victor E -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Vogelstein, Bert -- Papadopoulos, Nickolas -- CA 43460/CA/NCI NIH HHS/ -- CA 62924/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-06/CA/NCI NIH HHS/ -- R01 CA057345/CA/NCI NIH HHS/ -- R01 CA057345-08/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-16/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Mar 25;464(7288):610-4. doi: 10.1038/nature08802. Epub 2010 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ludwig Center for Cancer Genetics and Therapeutics and The Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, Maryland 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20200521" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Child ; Colorectal Neoplasms/*pathology ; DNA, Mitochondrial/blood/*genetics ; Female ; Gene Frequency ; *Genetic Heterogeneity ; Genetic Variation ; Genotype ; Humans ; Intestinal Mucosa/cytology/pathology ; Male ; Middle Aged ; Mutation/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Distant metastasis occurs late during the genetic evolution of pancreatic cancer (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-29
    Description: Metastasis, the dissemination and growth of neoplastic cells in an organ distinct from that in which they originated, is the most common cause of death in cancer patients. This is particularly true for pancreatic cancers, where most patients are diagnosed with metastatic disease and few show a sustained response to chemotherapy or radiation therapy. Whether the dismal prognosis of patients with pancreatic cancer compared to patients with other types of cancer is a result of late diagnosis or early dissemination of disease to distant organs is not known. Here we rely on data generated by sequencing the genomes of seven pancreatic cancer metastases to evaluate the clonal relationships among primary and metastatic cancers. We find that clonal populations that give rise to distant metastases are represented within the primary carcinoma, but these clones are genetically evolved from the original parental, non-metastatic clone. Thus, genetic heterogeneity of metastases reflects that within the primary carcinoma. A quantitative analysis of the timing of the genetic evolution of pancreatic cancer was performed, indicating at least a decade between the occurrence of the initiating mutation and the birth of the parental, non-metastatic founder cell. At least five more years are required for the acquisition of metastatic ability and patients die an average of two years thereafter. These data provide novel insights into the genetic features underlying pancreatic cancer progression and define a broad time window of opportunity for early detection to prevent deaths from metastatic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148940/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148940/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yachida, Shinichi -- Jones, Sian -- Bozic, Ivana -- Antal, Tibor -- Leary, Rebecca -- Fu, Baojin -- Kamiyama, Mihoko -- Hruban, Ralph H -- Eshleman, James R -- Nowak, Martin A -- Velculescu, Victor E -- Kinzler, Kenneth W -- Vogelstein, Bert -- Iacobuzio-Donahue, Christine A -- A62924/PHS HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- GM078986/GM/NIGMS NIH HHS/ -- K08 CA106610/CA/NCI NIH HHS/ -- K08 CA106610-04/CA/NCI NIH HHS/ -- K08 CA106610-05/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-10/CA/NCI NIH HHS/ -- P50 CA062924-11/CA/NCI NIH HHS/ -- P50 CA062924-12/CA/NCI NIH HHS/ -- R01 CA057345/CA/NCI NIH HHS/ -- R01 CA057345-08/CA/NCI NIH HHS/ -- R01 CA057345-09/CA/NCI NIH HHS/ -- R01 CA057345-10/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-03/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA121113-05/CA/NCI NIH HHS/ -- R01 CA140599/CA/NCI NIH HHS/ -- R01 GM078986/GM/NIGMS NIH HHS/ -- R01 GM078986-02/GM/NIGMS NIH HHS/ -- R01 GM078986-03/GM/NIGMS NIH HHS/ -- R01 GM078986-04/GM/NIGMS NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-24/CA/NCI NIH HHS/ -- R37 CA043460-25/CA/NCI NIH HHS/ -- R37 CA043460-26/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Oct 28;467(7319):1114-7. doi: 10.1038/nature09515.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981102" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/genetics/pathology ; Autopsy ; Cell Lineage/genetics ; Clone Cells/metabolism/pathology ; DNA Mutational Analysis ; *Disease Progression ; Early Detection of Cancer ; *Evolution, Molecular ; Humans ; Liver Neoplasms/genetics/secondary ; Lung Neoplasms/genetics/secondary ; Models, Biological ; Mutation/*genetics ; Neoplasm Metastasis/*genetics/pathology ; Pancreas/metabolism/pathology ; Pancreatic Neoplasms/*genetics/*pathology ; Peritoneal Neoplasms/genetics/secondary ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    International network of cancer genome projects (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-16
    Description: The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902243/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902243/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Cancer Genome Consortium -- Hudson, Thomas J -- Anderson, Warwick -- Artez, Axel -- Barker, Anna D -- Bell, Cindy -- Bernabe, Rosa R -- Bhan, M K -- Calvo, Fabien -- Eerola, Iiro -- Gerhard, Daniela S -- Guttmacher, Alan -- Guyer, Mark -- Hemsley, Fiona M -- Jennings, Jennifer L -- Kerr, David -- Klatt, Peter -- Kolar, Patrik -- Kusada, Jun -- Lane, David P -- Laplace, Frank -- Youyong, Lu -- Nettekoven, Gerd -- Ozenberger, Brad -- Peterson, Jane -- Rao, T S -- Remacle, Jacques -- Schafer, Alan J -- Shibata, Tatsuhiro -- Stratton, Michael R -- Vockley, Joseph G -- Watanabe, Koichi -- Yang, Huanming -- Yuen, Matthew M F -- Knoppers, Bartha M -- Bobrow, Martin -- Cambon-Thomsen, Anne -- Dressler, Lynn G -- Dyke, Stephanie O M -- Joly, Yann -- Kato, Kazuto -- Kennedy, Karen L -- Nicolas, Pilar -- Parker, Michael J -- Rial-Sebbag, Emmanuelle -- Romeo-Casabona, Carlos M -- Shaw, Kenna M -- Wallace, Susan -- Wiesner, Georgia L -- Zeps, Nikolajs -- Lichter, Peter -- Biankin, Andrew V -- Chabannon, Christian -- Chin, Lynda -- Clement, Bruno -- de Alava, Enrique -- Degos, Francoise -- Ferguson, Martin L -- Geary, Peter -- Hayes, D Neil -- Johns, Amber L -- Kasprzyk, Arek -- Nakagawa, Hidewaki -- Penny, Robert -- Piris, Miguel A -- Sarin, Rajiv -- Scarpa, Aldo -- van de Vijver, Marc -- Futreal, P Andrew -- Aburatani, Hiroyuki -- Bayes, Monica -- Botwell, David D L -- Campbell, Peter J -- Estivill, Xavier -- Grimmond, Sean M -- Gut, Ivo -- Hirst, Martin -- Lopez-Otin, Carlos -- Majumder, Partha -- Marra, Marco -- McPherson, John D -- Ning, Zemin -- Puente, Xose S -- Ruan, Yijun -- Stunnenberg, Hendrik G -- Swerdlow, Harold -- Velculescu, Victor E -- Wilson, Richard K -- Xue, Hong H -- Yang, Liu -- Spellman, Paul T -- Bader, Gary D -- Boutros, Paul C -- Flicek, Paul -- Getz, Gad -- Guigo, Roderic -- Guo, Guangwu -- Haussler, David -- Heath, Simon -- Hubbard, Tim J -- Jiang, Tao -- Jones, Steven M -- Li, Qibin -- Lopez-Bigas, Nuria -- Luo, Ruibang -- Muthuswamy, Lakshmi -- Ouellette, B F Francis -- Pearson, John V -- Quesada, Victor -- Raphael, Benjamin J -- Sander, Chris -- Speed, Terence P -- Stein, Lincoln D -- Stuart, Joshua M -- Teague, Jon W -- Totoki, Yasushi -- Tsunoda, Tatsuhiko -- Valencia, Alfonso -- Wheeler, David A -- Wu, Honglong -- Zhao, Shancen -- Zhou, Guangyu -- Lathrop, Mark -- Thomas, Gilles -- Yoshida, Teruhiko -- Axton, Myles -- Gunter, Chris -- Miller, Linda J -- Zhang, Junjun -- Haider, Syed A -- Wang, Jianxin -- Yung, Christina K -- Cros, Anthony -- Liang, Yong -- Gnaneshan, Saravanamuttu -- Guberman, Jonathan -- Hsu, Jack -- Chalmers, Don R C -- Hasel, Karl W -- Kaan, Terry S H -- Lowrance, William W -- Masui, Tohru -- Rodriguez, Laura Lyman -- Vergely, Catherine -- Bowtell, David D L -- Cloonan, Nicole -- deFazio, Anna -- Eshleman, James R -- Etemadmoghadam, Dariush -- Gardiner, Brooke B -- Kench, James G -- Sutherland, Robert L -- Tempero, Margaret A -- Waddell, Nicola J -- Wilson, Peter J -- Gallinger, Steve -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Mukhopadhyay, Debabrata -- DePinho, Ronald A -- Thayer, Sarah -- Shazand, Kamran -- Beck, Timothy -- Sam, Michelle -- Timms, Lee -- Ballin, Vanessa -- Lu, Youyong -- Ji, Jiafu -- Zhang, Xiuqing -- Chen, Feng -- Hu, Xueda -- Yang, Qi -- Tian, Geng -- Zhang, Lianhai -- Xing, Xiaofang -- Li, Xianghong -- Zhu, Zhenggang -- Yu, Yingyan -- Yu, Jun -- Tost, Jorg -- Brennan, Paul -- Holcatova, Ivana -- Zaridze, David -- Brazma, Alvis -- Egevard, Lars -- Prokhortchouk, Egor -- Banks, Rosamonde Elizabeth -- Uhlen, Mathias -- Viksna, Juris -- Ponten, Fredrik -- Skryabin, Konstantin -- Birney, Ewan -- Borg, Ake -- Borresen-Dale, Anne-Lise -- Caldas, Carlos -- Foekens, John A -- Martin, Sancha -- Reis-Filho, Jorge S -- Richardson, Andrea L -- Sotiriou, Christos -- Thoms, Giles -- van't Veer, Laura -- Birnbaum, Daniel -- Blanche, Helene -- Boucher, Pascal -- Boyault, Sandrine -- Masson-Jacquemier, Jocelyne D -- Pauporte, Iris -- Pivot, Xavier -- Vincent-Salomon, Anne -- Tabone, Eric -- Theillet, Charles -- Treilleux, Isabelle -- Bioulac-Sage, Paulette -- Decaens, Thomas -- Franco, Dominique -- Gut, Marta -- Samuel, Didier -- Zucman-Rossi, Jessica -- Eils, Roland -- Brors, Benedikt -- Korbel, Jan O -- Korshunov, Andrey -- Landgraf, Pablo -- Lehrach, Hans -- Pfister, Stefan -- Radlwimmer, Bernhard -- Reifenberger, Guido -- Taylor, Michael D -- von Kalle, Christof -- Majumder, Partha P -- Pederzoli, Paolo -- Lawlor, Rita A -- Delledonne, Massimo -- Bardelli, Alberto -- Gress, Thomas -- Klimstra, David -- Zamboni, Giuseppe -- Nakamura, Yusuke -- Miyano, Satoru -- Fujimoto, Akihiro -- Campo, Elias -- de Sanjose, Silvia -- Montserrat, Emili -- Gonzalez-Diaz, Marcos -- Jares, Pedro -- Himmelbauer, Heinz -- Bea, Silvia -- Aparicio, Samuel -- Easton, Douglas F -- Collins, Francis S -- Compton, Carolyn C -- Lander, Eric S -- Burke, Wylie -- Green, Anthony R -- Hamilton, Stanley R -- Kallioniemi, Olli P -- Ley, Timothy J -- Liu, Edison T -- Wainwright, Brandon J -- 077198/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- 6613/Cancer Research UK/United Kingdom -- K08 DK071329/DK/NIDDK NIH HHS/ -- K08 DK071329-04/DK/NIDDK NIH HHS/ -- K08 DK071329-05/DK/NIDDK NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- P01 CA117969-04S1/CA/NCI NIH HHS/ -- P01 CA117969-05/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50 CA102701-08/CA/NCI NIH HHS/ -- P50 CA127003/CA/NCI NIH HHS/ -- P50 CA127003-04/CA/NCI NIH HHS/ -- P50 CA127003-05/CA/NCI NIH HHS/ -- R01 HG001806-02/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Apr 15;464(7291):993-8. doi: 10.1038/nature08987.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393554" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Methylation ; DNA Mutational Analysis/trends ; Databases, Genetic ; Genes, Neoplasm/genetics ; Genetics, Medical/*organization & administration/trends ; Genome, Human/*genetics ; Genomics/*organization & administration/trends ; Humans ; Intellectual Property ; *International Cooperation ; Mutation ; Neoplasms/classification/*genetics/pathology/therapy
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    An integrated genomic analysis of human glioblastoma multiforme (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples. This comprehensive analysis led to the discovery of a variety of genes that were not known to be altered in GBMs. Most notably, we found recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) in 12% of GBM patients. Mutations in IDH1 occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival. These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Jones, Sian -- Zhang, Xiaosong -- Lin, Jimmy Cheng-Ho -- Leary, Rebecca J -- Angenendt, Philipp -- Mankoo, Parminder -- Carter, Hannah -- Siu, I-Mei -- Gallia, Gary L -- Olivi, Alessandro -- McLendon, Roger -- Rasheed, B Ahmed -- Keir, Stephen -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Busam, Dana A -- Tekleab, Hanna -- Diaz, Luis A Jr -- Hartigan, James -- Smith, Doug R -- Strausberg, Robert L -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Yan, Hai -- Riggins, Gregory J -- Bigner, Darell D -- Karchin, Rachel -- Papadopoulos, Nick -- Parmigiani, Giovanni -- Vogelstein, Bert -- Velculescu, Victor E -- Kinzler, Kenneth W -- 5P50-NS-20023/NS/NINDS NIH HHS/ -- CA09547/CA/NCI NIH HHS/ -- CA108786/CA/NCI NIH HHS/ -- CA11898/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- NS052507/NS/NINDS NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-160017/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA140316/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-27/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-13/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1807-12. doi: 10.1126/science.1164382. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772396" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/mortality ; Female ; Gene Amplification ; Gene Dosage ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Glioblastoma/*genetics/mortality ; Humans ; Isocitrate Dehydrogenase/chemistry/*genetics ; Male ; Middle Aged ; *Mutation ; Mutation, Missense ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Signal Transduction ; Survival Rate
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    The antisense transcriptomes of human cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the plus or minus strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here, we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript, and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was nonrandom across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, which suggests that they are a fundamental component of gene regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824178/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824178/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yiping -- Vogelstein, Bert -- Velculescu, Victor E -- Papadopoulos, Nickolas -- Kinzler, Kenneth W -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1855-7. doi: 10.1126/science.1163853. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056939" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Line, Tumor ; Exons ; Gene Expression ; *Gene Expression Profiling ; *Genome, Human ; Humans ; Introns ; Leukocytes, Mononuclear/metabolism ; Promoter Regions, Genetic ; RNA, Antisense/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Core signaling pathways in human pancreatic cancers revealed by global genomic analyses (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: There are currently few therapeutic options for patients with pancreatic cancer, and new insights into the pathogenesis of this lethal disease are urgently needed. Toward this end, we performed a comprehensive genetic analysis of 24 pancreatic cancers. We first determined the sequences of 23,219 transcripts, representing 20,661 protein-coding genes, in these samples. Then, we searched for homozygous deletions and amplifications in the tumor DNA by using microarrays containing probes for approximately 10(6) single-nucleotide polymorphisms. We found that pancreatic cancers contain an average of 63 genetic alterations, the majority of which are point mutations. These alterations defined a core set of 12 cellular signaling pathways and processes that were each genetically altered in 67 to 100% of the tumors. Analysis of these tumors' transcriptomes with next-generation sequencing-by-synthesis technologies provided independent evidence for the importance of these pathways and processes. Our data indicate that genetically altered core pathways and regulatory processes only become evident once the coding regions of the genome are analyzed in depth. Dysregulation of these core pathways and processes through mutation can explain the major features of pancreatic tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848990/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Sian -- Zhang, Xiaosong -- Parsons, D Williams -- Lin, Jimmy Cheng-Ho -- Leary, Rebecca J -- Angenendt, Philipp -- Mankoo, Parminder -- Carter, Hannah -- Kamiyama, Hirohiko -- Jimeno, Antonio -- Hong, Seung-Mo -- Fu, Baojin -- Lin, Ming-Tseh -- Calhoun, Eric S -- Kamiyama, Mihoko -- Walter, Kimberly -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Hartigan, James -- Smith, Douglas R -- Hidalgo, Manuel -- Leach, Steven D -- Klein, Alison P -- Jaffee, Elizabeth M -- Goggins, Michael -- Maitra, Anirban -- Iacobuzio-Donahue, Christine -- Eshleman, James R -- Kern, Scott E -- Hruban, Ralph H -- Karchin, Rachel -- Papadopoulos, Nickolas -- Parmigiani, Giovanni -- Vogelstein, Bert -- Velculescu, Victor E -- Kinzler, Kenneth W -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-130011/CA/NCI NIH HHS/ -- P50 CA062924-140011/CA/NCI NIH HHS/ -- P50 CA062924-160017/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-27/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1801-6. doi: 10.1126/science.1164368. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sol Goldman Pancreatic Cancer Research Center, Ludwig Center and Howard Hughes Medical Institute at the Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772397" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/etiology/*genetics/*metabolism ; Algorithms ; Carcinoma, Pancreatic Ductal/etiology/genetics/metabolism ; Computational Biology ; Gene Amplification ; Gene Expression Profiling ; Genome, Human ; Humans ; Models, Molecular ; *Mutation ; Mutation, Missense ; Oligonucleotide Array Sequence Analysis ; Pancreatic Neoplasms/etiology/*genetics/*metabolism ; Point Mutation ; Polymorphism, Single Nucleotide ; Sequence Deletion ; Signal Transduction/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...