Author
Listed:
- Zhihu Ding
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Chang-Jiun Wu
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Gerald C. Chu
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Brigham and Women’s Hospital)
- Yonghong Xiao
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- Dennis Ho
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Jingfang Zhang
(McArdle Lab for Cancer Research, University of Wisconsin)
- Samuel R. Perry
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- Emma S. Labrot
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- Xiaoqiu Wu
(Dana-Farber Cancer Institute
Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute)
- Rosina Lis
(Dana-Farber Cancer Institute
Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute)
- Yujin Hoshida
(Pediatric Oncology, Dana-Farber Cancer Institute
The Eli and Edythe L. Broad Institute, Massachusetts Institute of Technology and Harvard University)
- David Hiller
(Stanford University)
- Baoli Hu
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- Shan Jiang
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- Hongwu Zheng
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Alexander H. Stegh
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Kenneth L. Scott
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Sabina Signoretti
(Renal Cancer Program, Dana-Farber/Harvard Cancer Center)
- Nabeel Bardeesy
(Massachusetts General Hospital Cancer Center)
- Y. Alan Wang
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute)
- David E. Hill
(Harvard Medical School
Dana-Farber Cancer Institute)
- Todd R. Golub
(Pediatric Oncology, Dana-Farber Cancer Institute
The Eli and Edythe L. Broad Institute, Massachusetts Institute of Technology and Harvard University)
- Meir J. Stampfer
(Harvard School of Public Health
Harvard School of Public Health
Channing Laboratory, Brigham and Women’s Hospital)
- Wing H. Wong
(Stanford University)
- Massimo Loda
(Dana-Farber Cancer Institute
Brigham and Women’s Hospital
Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute)
- Lorelei Mucci
(Harvard School of Public Health
Channing Laboratory, Brigham and Women’s Hospital)
- Lynda Chin
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
- Ronald A. DePinho
(Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute
Dana-Farber Cancer Institute
Harvard Medical School
Harvard Medical School)
Abstract
Four-gene marker in prostate cancer Using a Smad4/Pten null transgenic mouse model of prostate cancer, Ding et al. show that the transforming growth factor-β (TGFβ) signalling pathway limits tumour progression and metastasis. By utilizing markers of this pathway and other biologically relevant factors, they develop a four-gene signature that is associated with poorer clinical outcome and metastatic progression in several prostate cancer cohorts, especially in combination with other clinical parameters. This signature may prove useful as a basis for an improved prognostic test for those cases of prostate cancer in which deciding on the right treatment regime while avoiding over-treatment is an important clinical challenge.
Suggested Citation
Zhihu Ding & Chang-Jiun Wu & Gerald C. Chu & Yonghong Xiao & Dennis Ho & Jingfang Zhang & Samuel R. Perry & Emma S. Labrot & Xiaoqiu Wu & Rosina Lis & Yujin Hoshida & David Hiller & Baoli Hu & Shan Ji, 2011.
"SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression,"
Nature, Nature, vol. 470(7333), pages 269-273, February.
Handle:
RePEc:nat:nature:v:470:y:2011:i:7333:d:10.1038_nature09677
DOI: 10.1038/nature09677
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Cited by:
- Michael Fraser & Julie Livingstone & Jeffrey L. Wrana & Antonio Finelli & Housheng Hansen He & Theodorus van der Kwast & Alexandre R. Zlotta & Robert G. Bristow & Paul C. Boutros, 2021.
"Somatic driver mutation prevalence in 1844 prostate cancers identifies ZNRF3 loss as a predictor of metastatic relapse,"
Nature Communications, Nature, vol. 12(1), pages 1-15, December.
- Ni Li & Qiuli Liu & Ying Han & Siyu Pei & Bisheng Cheng & Junyu Xu & Xiang Miao & Qiang Pan & Hanling Wang & Jiacheng Guo & Xuege Wang & Guoying Zhang & Yannan Lian & Wei Zhang & Yi Zang & Minjia Tan , 2022.
"ARID1A loss induces polymorphonuclear myeloid-derived suppressor cell chemotaxis and promotes prostate cancer progression,"
Nature Communications, Nature, vol. 13(1), pages 1-20, December.
- Huiqiang Cai & Bin Zhang & Johanne Ahrenfeldt & Justin V. Joseph & Maria Riedel & Zongliang Gao & Sofie K. Thomsen & Ditte S. Christensen & Rasmus O. Bak & Henrik Hager & Mikkel H. Vendelbo & Xin Gao , 2024.
"CRISPR/Cas9 model of prostate cancer identifies Kmt2c deficiency as a metastatic driver by Odam/Cabs1 gene cluster expression,"
Nature Communications, Nature, vol. 15(1), pages 1-18, December.
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