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      Call for Papers: Artificial Intelligence in Gastroenterology

      Submit here before September 30, 2024

      About Digestion: 3.0 Impact Factor I 7.9 CiteScore I 0.891 Scimago Journal & Country Rank (SJR)

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      Basics of TGF-β and Pancreatic Cancer

      review-article
      Author(s): a , b
      Publication date (Electronic):
      Journal: Pancreatology
      Publisher: S. Karger AG
      Keywords: Pancreatic cancer, Transforming growth factor-β, Signaling system

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Pancreatic cancer is the 4th leading cause of cancer-related death in the United States. The number of diagnoses per year equals the number of deaths per year, making it the deadliest of all malignancies. Modern advances and breakthroughs in molecular oncology have allowed researchers to gain a better understanding of the mechanisms responsible for the pathogenesis of this disease. The transforming growth factor-β (TGF-β) pathway is one of the signaling systems that has been identified as a major contributor. TGF-β plays a paradoxical role as both a tumor suppressor and a tumor promoter in pancreatic cancer. The purpose of this review is to provide the practicing clinician a thorough review of this molecule and its associated signaling partners in the context of its duplicitous role and behavior in patients with pancreatic cancer.

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          TGF-beta signal transduction.

          J Massagué (1998)
          The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
          Article 0 comments Cited 693 times – based on 0 reviews     Review now
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            Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

            M Shull, I Ormsby, A Kier … (1992)
            Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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              Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

              Yigong Shi, Joan Massagué (2003)
              Article 0 comments Cited 439 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): PAN
                Journal ID (nlm-ta): Pancreatology
                Journal ID (doi): 10.1159/issn.1424-3903
                Title: Pancreatology
                Publisher: S. Karger AG
                ISSN (Print): 1424-3903
                ISSN (Electronic): 1424-3911
                Publication date Subscription-year: 2007
                Publication date (Print): October 2007
                Publication date (Electronic): 25 September 2007
                Volume: 7
                Issue: 5-6
                Pages: 423-435
                Affiliations
                aDepartment of Surgery, and bGastrointestinal Research Unit, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, Minn., USA
                Article
                Publisher ID: 108959 Other ID: Pancreatology 2007;7:423–435
                DOI: 10.1159/000108959
                PubMed ID: 17898532
                SO-VID: a93a9e52-eeee-4239-be67-4bb274e99c2d
                Copyright © © 2007 S. Karger AG, Basel and IAP
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 4, References: 108, Pages: 13
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy,Gastroenterology & Hepatology,Surgery,Nutrition & Dietetics,Internal medicine
                Keywords: Signaling system,Transforming growth factor-β,Pancreatic cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy, Gastroenterology & Hepatology, Surgery, Nutrition & Dietetics, Internal medicine
                Keywords: Signaling system, Transforming growth factor-β, Pancreatic cancer

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