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  • 1
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    Allelotype of colorectal carcinomas (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-14
    Description: To examine the extent and variation of allelic loss in a common adult tumor, polymorphic DNA markers were studied from every nonacrocentric autosomal arm in 56 paired colorectal carcinoma and adjacent normal colonic mucosa specimens. This analysis was termed an allelotype, in analogy with a karyotype. Three major conclusions were drawn from this analysis: (i) Allelic deletions were remarkably common; one of the alleles of each polymorphic marker tested was lost in at least some tumors, and some tumors lost more than half of their parental alleles. (ii) In addition to allelic deletions, new DNA fragments not present in normal tissue were identified in five carcinomas; these new fragments contained repeated sequences of the variable number of tandem repeat type. (iii) Patients with more than the median percentage of allelic deletions had a considerably worse prognosis than did the other patients, although the size and stage of the primary tumors were very similar in the two groups. In addition to its implications concerning the genetic events underlying tumorigenesis, tumor allelotype may provide a molecular tool for improved estimation of prognosis in patients with colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogelstein, B -- Fearon, E R -- Kern, S E -- Hamilton, S R -- Preisinger, A C -- Nakamura, Y -- White, R -- CA41183/CA/NCI NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 14;244(4901):207-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2565047" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Chromosome Aberrations/genetics ; Chromosome Disorders ; Colorectal Neoplasms/*genetics ; DNA, Neoplasm/genetics ; Humans ; *Karyotyping ; Polymorphism, Restriction Fragment Length
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Identification of a chromosome 18q gene that is altered in colorectal cancers (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-05
    Description: Allelic deletions involving chromosome 18q occur in more than 70 percent of colorectal cancers. Such deletions are thought to signal the existence of a tumor suppressor gene in the affected region, but until now a candidate suppressor gene on this chromosomal arm had not been identified. A contiguous stretch of DNA comprising 370 kilobase pairs (kb) has now been cloned from a region of chromosome 18q suspected to reside near this gene. Potential exons in the 370-kb region were defined by human-rodent sequence identities, and the expression of potential exons was assessed by an "exon-connection" strategy based on the polymerase chain reaction. Expressed exons were used as probes for cDNA screening to obtain clones that encoded a portion of a gene termed DCC; this cDNA was encoded by at least eight exons within the 370-kb genomic region. The predicted amino acid sequence of the cDNA specified a protein with sequence similarity to neural cell adhesion molecules and other related cell surface glycoproteins. While the DCC gene was expressed in most normal tissues, including colonic mucosa, its expression was greatly reduced or absent in most colorectal carcinomas tested. Somatic mutations within the DCC gene observed in colorectal cancers included a homozygous deletion of the 5' end of the gene, a point mutation within one of the introns, and ten examples of DNA insertions within a 0.17-kb fragment immediately downstream of one of the exons. The DCC gene may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fearon, E R -- Cho, K R -- Nigro, J M -- Kern, S E -- Simons, J W -- Ruppert, J M -- Hamilton, S R -- Preisinger, A C -- Thomas, G -- Kinzler, K W -- CA 09243/CA/NCI NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):49-56.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2294591" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Adhesion Molecules, Neuronal/genetics ; *Chromosome Deletion ; *Chromosomes, Human, Pair 18 ; Cloning, Molecular ; Colorectal Neoplasms/*genetics ; Cross Reactions ; DNA Probes ; DNA, Neoplasm/*genetics ; Exons ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Neoplasm/genetics ; Sequence Homology, Nucleic Acid ; *Suppression, Genetic ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Oncogenic forms of p53 inhibit p53-regulated gene expression (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Mutant forms of the gene encoding the tumor suppressor p53 are found in numerous human malignancies, but the physiologic function of p53 and the effects of mutations on this function are unknown. The p53 protein binds DNA in a sequence-specific manner and thus may regulate gene transcription. Cotransfection experiments showed that wild-type p53 activated the expression of genes adjacent to a p53 DNA binding site. The level of activation correlated with DNA binding in vitro. Oncogenic forms of p53 lost this activity. Moreover, all mutants inhibited the activity of coexpressed wild-type p53, providing a basis for the selection of such mutants during tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kern, S E -- Pietenpol, J A -- Thiagalingam, S -- Seymour, A -- Kinzler, K W -- Vogelstein, B -- CA06973/CA/NCI NIH HHS/ -- CA09243/CA/NCI NIH HHS/ -- CA35494/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):827-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589764" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; DNA-Binding Proteins/*genetics/*metabolism ; Exons ; *Gene Expression Regulation, Neoplastic ; *Genes, p53 ; Genetic Vectors ; Humans ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Recombinant Fusion Proteins/metabolism ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics/growth & development ; *Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/*genetics/*metabolism ; beta-Galactosidase/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Identification of p53 as a sequence-specific DNA-binding protein (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-21
    Description: The tumor-suppressor gene p53 is altered by missense mutation in numerous human malignancies. However, the biochemical properties of p53 and the effect of mutation on these properties are unclear. A human DNA sequence was identified that binds specifically to wild-type human p53 protein in vitro. As few as 33 base pairs were sufficient to confer specific binding. Certain guanines within this 33-base pair region were critical, as methylation of these guanines or their substitution with thymine-abrogated binding. Human p53 proteins containing either of two missense mutations commonly found in human tumors were unable to bind significantly to this sequence. These data suggest that a function of p53 may be mediated by its ability to bind to specific DNA sequences in the human genome, and that this activity is altered by mutations that occur in human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kern, S E -- Kinzler, K W -- Bruskin, A -- Jarosz, D -- Friedman, P -- Prives, C -- Vogelstein, B -- CA06973/CA/NCI NIH HHS/ -- CA33620/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1708-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2047879" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; DNA Mutational Analysis ; DNA Replication ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Humans ; In Vitro Techniques ; Methylation ; Molecular Sequence Data ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship ; Tumor Suppressor Protein p53/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    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
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  • 6
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    Gene expression profiles in normal and cancer cells (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-05-23
    Description: As a step toward understanding the complex differences between normal and cancer cells in humans, gene expression patterns were examined in gastrointestinal tumors. More than 300,000 transcripts derived from at least 45,000 different genes were analyzed. Although extensive similarity was noted between the expression profiles, more than 500 transcripts that were expressed at significantly different levels in normal and neoplastic cells were identified. These data provide insight into the extent of expression differences underlying malignancy and reveal genes that may prove useful as diagnostic or prognostic markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, L -- Zhou, W -- Velculescu, V E -- Kern, S E -- Hruban, R H -- Hamilton, S R -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 May 23;276(5316):1268-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157888" target="_blank"〉PubMed〈/a〉
    Keywords: Colorectal Neoplasms/genetics ; Computer Simulation ; *Digestive System Physiological Phenomena ; Gastrointestinal Neoplasms/*genetics ; *Gene Expression ; Humans ; Reference Values ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-07-08
    Description: Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer. Normally, ROS levels are tightly controlled by an inducible antioxidant program that responds to cellular stressors and is predominantly regulated by the transcription factor Nrf2 (also known as Nfe2l2) and its repressor protein Keap1 (refs 2-5). In contrast to the acute physiological regulation of Nrf2, in neoplasia there is evidence for increased basal activation of Nrf2. Indeed, somatic mutations that disrupt the Nrf2-Keap1 interaction to stabilize Nrf2 and increase the constitutive transcription of Nrf2 target genes were recently identified, indicating that enhanced ROS detoxification and additional Nrf2 functions may in fact be pro-tumorigenic. Here, we investigated ROS metabolism in primary murine cells following the expression of endogenous oncogenic alleles of Kras, Braf and Myc, and found that ROS are actively suppressed by these oncogenes. K-Ras(G12D), B-Raf(V619E) and Myc(ERT2) each increased the transcription of Nrf2 to stably elevate the basal Nrf2 antioxidant program and thereby lower intracellular ROS and confer a more reduced intracellular environment. Oncogene-directed increased expression of Nrf2 is a new mechanism for the activation of the Nrf2 antioxidant program, and is evident in primary cells and tissues of mice expressing K-Ras(G12D) and B-Raf(V619E), and in human pancreatic cancer. Furthermore, genetic targeting of the Nrf2 pathway impairs K-Ras(G12D)-induced proliferation and tumorigenesis in vivo. Thus, the Nrf2 antioxidant and cellular detoxification program represents a previously unappreciated mediator of oncogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404470/" 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/PMC3404470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeNicola, Gina M -- Karreth, Florian A -- Humpton, Timothy J -- Gopinathan, Aarthi -- Wei, Cong -- Frese, Kristopher -- Mangal, Dipti -- Yu, Kenneth H -- Yeo, Charles J -- Calhoun, Eric S -- Scrimieri, Francesca -- Winter, Jordan M -- Hruban, Ralph H -- Iacobuzio-Donahue, Christine -- Kern, Scott E -- Blair, Ian A -- Tuveson, David A -- CA084291/CA/NCI NIH HHS/ -- CA101973/CA/NCI NIH HHS/ -- CA105490/CA/NCI NIH HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA111294/CA/NCI NIH HHS/ -- CA128920/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- R01 CA101973/CA/NCI NIH HHS/ -- R01 CA101973-05/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jul 6;475(7354):106-9. doi: 10.1038/nature10189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Li Ka Shing Centre, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734707" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/metabolism ; Alleles ; Animals ; Antioxidants/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics/*metabolism/*pathology ; Cells, Cultured ; Cytoskeletal Proteins/genetics/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/metabolism ; Genes, myc/genetics ; Humans ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase Kinases/metabolism ; NF-E2-Related Factor 2/deficiency/genetics/*metabolism ; NIH 3T3 Cells ; Oncogenes/*genetics ; Oxidation-Reduction ; Pancreatic Neoplasms/genetics/*metabolism/*pathology ; Proto-Oncogene Proteins B-raf/genetics/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; Reactive Oxygen Species/*metabolism
    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)
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  • 8
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    DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-19
    Description: About 90 percent of human pancreatic carcinomas show allelic loss at chromosome 18q. To identify candidate tumor suppressor genes on 18q, a panel of pancreatic carcinomas were analyzed for convergent sites of homozygous deletion. Twenty-five of 84 tumors had homozygous deletions at 18q21.1, a site that excludes DCC (a candidate suppressor gene for colorectal cancer) and includes DPC4, a gene similar in sequence to a Drosophila melanogaster gene (Mad) implicated in a transforming growth factor-beta (TGF-beta)-like signaling pathway. Potentially inactivating mutations in DPC4 were identified in six of 27 pancreatic carcinomas that did not have homozygous deletions at 18q21.1. These results identify DPC4 as a candidate tumor suppressor gene whose inactivation may play a role in pancreatic and possibly other human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, S A -- Schutte, M -- Hoque, A T -- Moskaluk, C A -- da Costa, L T -- Rozenblum, E -- Weinstein, C L -- Fischer, A -- Yeo, C J -- Hruban, R H -- Kern, S E -- CA62924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):350-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553070" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division ; Chromosome Mapping ; *Chromosomes, Human, Pair 18 ; *DNA-Binding Proteins ; Gene Deletion ; Gene Expression ; *Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Pancreatic Neoplasms/*genetics/pathology ; Proteins/chemistry/*genetics/physiology ; Signal Transduction ; Smad4 Protein ; *Trans-Activators ; Transforming Growth Factor beta/physiology ; Transplantation, Heterologous ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-07
    Description: Through complete sequencing of the protein-coding genes in a patient with familial pancreatic cancer, we identified a germline, truncating mutation in PALB2 that appeared responsible for this patient's predisposition to the disease. Analysis of 96 additional patients with familial pancreatic cancer revealed three distinct protein-truncating mutations, thereby validating the role of PALB2 as a susceptibility gene for pancreatic cancer. PALB2 mutations have been previously reported in patients with familial breast cancer, and the PALB2 protein is a binding partner for BRCA2. These results illustrate that complete, unbiased sequencing of protein-coding genes can lead to the identification of a gene responsible for a hereditary disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684332/" 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/PMC2684332/" 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 -- Hruban, Ralph H -- Kamiyama, Mihoko -- Borges, Michael -- Zhang, Xiaosong -- Parsons, D Williams -- Lin, Jimmy Cheng-Ho -- Palmisano, Emily -- Brune, Kieran -- Jaffee, Elizabeth M -- Iacobuzio-Donahue, Christine A -- Maitra, Anirban -- Parmigiani, Giovanni -- Kern, Scott E -- Velculescu, Victor E -- Kinzler, Kenneth W -- Vogelstein, Bert -- Eshleman, James R -- Goggins, Michael -- Klein, Alison P -- CA123483/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-150011/CA/NCI NIH HHS/ -- P50 CA062924-150012/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA097075-06A1/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA123483/CA/NCI NIH HHS/ -- R01 CA123483-01A2/CA/NCI NIH HHS/ -- R01CA97075/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-26/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):217. doi: 10.1126/science.1171202. Epub 2009 Mar 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19264984" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics ; Codon, Terminator ; Female ; *Genetic Predisposition to Disease ; *Germ-Line Mutation ; Humans ; Male ; Nuclear Proteins/*genetics ; Pancreatic Neoplasms/*genetics ; Pedigree ; Sequence Analysis, DNA ; Sequence Deletion ; Tumor Suppressor Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Targeted deletion of Smad4 shows it is required for transforming growth factor   and activin signaling in colorectal cancer cells (1998)
    National Academy of Sciences
    Details
    Publication Date: 1998-03-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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