Inhibition of TGFβ signaling in cancer therapy

Research output: Contribution to journalReview article

101 Citations (Scopus)

Abstract

Recent evidence continues to support a central role for TGFβ in tumor maintenance and progression. Although this may involve TGFβ-mediated paracrine effects that modulate the tumor microenvironment and the host immune system, some studies causally implicate autocrine TGFβ in cancer cell motility and survival. Other recent evidence indicates synergy between oncogene and TGFβ signaling in epithelial cell transformation. This suggests opportunities for dissecting molecular mechanisms of cross-talk as well as providing insights into possible combinatorial molecular anticancer therapies that will include TGFβ inhibitors.

Original languageEnglish (US)
Pages (from-to)30-37
Number of pages8
JournalCurrent Opinion in Genetics and Development
Volume16
Issue number1
DOIs
StatePublished - Feb 1 2006

Fingerprint

Tumor Microenvironment
Oncogenes
Cell Movement
Immune System
Neoplasms
Cell Survival
Epithelial Cells
Maintenance
Therapeutics

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

Cite this

Inhibition of TGFβ signaling in cancer therapy. / Arteaga, Carlos L.

In: Current Opinion in Genetics and Development, Vol. 16, No. 1, 01.02.2006, p. 30-37.

Research output: Contribution to journalReview article

@article{39da772e9c844ef5970058da526d00b8,
title = "Inhibition of TGFβ signaling in cancer therapy",
abstract = "Recent evidence continues to support a central role for TGFβ in tumor maintenance and progression. Although this may involve TGFβ-mediated paracrine effects that modulate the tumor microenvironment and the host immune system, some studies causally implicate autocrine TGFβ in cancer cell motility and survival. Other recent evidence indicates synergy between oncogene and TGFβ signaling in epithelial cell transformation. This suggests opportunities for dissecting molecular mechanisms of cross-talk as well as providing insights into possible combinatorial molecular anticancer therapies that will include TGFβ inhibitors.",
author = "Arteaga, {Carlos L.}",
year = "2006",
month = "2",
day = "1",
doi = "10.1016/j.gde.2005.12.009",
language = "English (US)",
volume = "16",
pages = "30--37",
journal = "Current Opinion in Genetics and Development",
issn = "0959-437X",
publisher = "Elsevier Limited",
number = "1",

}

TY - JOUR

T1 - Inhibition of TGFβ signaling in cancer therapy

AU - Arteaga, Carlos L.

PY - 2006/2/1

Y1 - 2006/2/1

N2 - Recent evidence continues to support a central role for TGFβ in tumor maintenance and progression. Although this may involve TGFβ-mediated paracrine effects that modulate the tumor microenvironment and the host immune system, some studies causally implicate autocrine TGFβ in cancer cell motility and survival. Other recent evidence indicates synergy between oncogene and TGFβ signaling in epithelial cell transformation. This suggests opportunities for dissecting molecular mechanisms of cross-talk as well as providing insights into possible combinatorial molecular anticancer therapies that will include TGFβ inhibitors.

AB - Recent evidence continues to support a central role for TGFβ in tumor maintenance and progression. Although this may involve TGFβ-mediated paracrine effects that modulate the tumor microenvironment and the host immune system, some studies causally implicate autocrine TGFβ in cancer cell motility and survival. Other recent evidence indicates synergy between oncogene and TGFβ signaling in epithelial cell transformation. This suggests opportunities for dissecting molecular mechanisms of cross-talk as well as providing insights into possible combinatorial molecular anticancer therapies that will include TGFβ inhibitors.

UR - http://www.scopus.com/inward/record.url?scp=30644467227&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=30644467227&partnerID=8YFLogxK

U2 - 10.1016/j.gde.2005.12.009

DO - 10.1016/j.gde.2005.12.009

M3 - Review article

C2 - 16377175

AN - SCOPUS:30644467227

VL - 16

SP - 30

EP - 37

JO - Current Opinion in Genetics and Development

JF - Current Opinion in Genetics and Development

SN - 0959-437X

IS - 1

ER -