Intestinal tumorigenesis in compound mutant mice of both dpc4 (smad4) and apc genes
Kazuaki Takaku,Masanobu Oshima,Hiroyuki Miyoshi,Minoru Matsui,Michael F. Seldin,Makoto Mark Taketo +5 more
TLDR
The authors showed that mutations in the DPC4 (SMAD4) gene play a significant role in the malignant progression of colorectal tumors in mice. But, their experiments were performed on Apc Δ 716 knockout mice, a model for human familial adenomatous polyposis.About:
This article is published in Cell.The article was published on 1998-03-06 and is currently open access. It has received 598 citations till now. The article focuses on the topics: Familial adenomatous polyposis & Compound heterozygosity.read more
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TGF-beta signal transduction.
TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
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TGFβ in Cancer
TL;DR: The mechanistic basis and clinical relevance of TGFbeta's role in cancer is becoming increasingly clear, paving the way for a better understanding of the complexity and therapeutic potential of this pathway.
Journal ArticleDOI
Cyclooxygenases: Structural, cellular, and molecular biology
TL;DR: This review examines how the structures of these enzymes relate mechanistically to cyclooxygenase and peroxidase catalysis, and how differences in the structure of PGHS-2 confer on this isozyme differential sensitivity to COX-2 inhibitors.
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Role of transforming growth factor beta in human disease.
TL;DR: In human tissues, normal homeostasis requires intricately balanced interactions between cells and the network of secreted proteins known as the extracellular matrix, which is clearly evident in the interactions mediated by the cytokine transforming growth factor β (TGF-β).
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Tgfbeta signaling in growth control, cancer, and heritable disorders
TL;DR: The author would like to thank S. H. Roan for all her help and members of the Massague laboratory for insightful discussions.
References
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Journal ArticleDOI
Genetic alterations during colorectal-tumor development.
Bert Vogelstein,Eric R. Fearon,Stanley R. Hamilton,Scott E. Kern,Ann C. Preisinger,Mark Leppert,A M Smits,Johannes L. Bos +7 more
TL;DR: It is found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas, which are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumors.
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Lessons from Hereditary Colorectal Cancer
TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
Journal ArticleDOI
Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease
Marcia M. Shull,Ilona Ormsby,Ann B. Kier,Sharon A. Pawlowski,Ronald J. Diebold,Moying Yin,Ruth D. Allen,Charles L. Sidman,Gabriele Proetzel,Dawn Calvin,Nikki Annunziata,Thomas Doetschman +11 more
TL;DR: TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
Journal ArticleDOI
Identification and characterization of the familial adenomatous polyposis coli gene
Joanna Groden,Andrew Thliveris,Andrew Thliveris,Wade S. Samowitz,M. Carlson,Lawrence Gelbert,Lawrence Gelbert,Hans Albertsen,Geoff Joslyn,Geoff Joslyn,Jeff Stevens,Jeff Stevens,Lisa Spirio,Margaret Robertson,Margaret Robertson,Leslie Sargeant,Leslie Sargeant,Karen Krapcho,Karen Krapcho,E. Wolff,E. Wolff,Randall W. Burt,John P. Hughes,Janet A. Warrington,John Douglas Mcpherson,John J. Wasmuth,Denis Le Paslier,Hadi Abderrahim,Daniel Cohen,Mark Leppert,Mark Leppert,Ray White,Ray White +32 more
TL;DR: DNA from 61 unrelated patients with adenomatous polyposis coli (APC) was examined for mutations in three genes located within a 100 kb region deleted in two of the patients, and data have established that DP2.5 is the APC gene.
Journal ArticleDOI
Suppression of Intestinal Polyposis in ApcΔ716 Knockout Mice by Inhibition of Cyclooxygenase 2 (COX-2)
Masanobu Oshima,Joseph E. Dinchuk,Stacia Kargman,Hiroko Oshima,Bruno C. Hancock,Elizabeth Kwong,James M. Trzaskos,Jilly F. Evans,Makoto Mark Taketo,Makoto Mark Taketo +9 more
TL;DR: Results provide direct genetic evidence that COX-2 plays a key role in tumorigenesis and indicate that COx-2-selective inhibitors can be a novel class of therapeutic agents for colorectal polyposis and cancer.