Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

Author:

Park Jung Wook1ORCID,Lee John K.2,Sheu Katherine M.3ORCID,Wang Liang1,Balanis Nikolas G.3,Nguyen Kim4,Smith Bryan A.1,Cheng Chen5,Tsai Brandon L.1,Cheng Donghui1,Huang Jiaoti6ORCID,Kurdistani Siavash K.5789ORCID,Graeber Thomas G.378910ORCID,Witte Owen N.13789

Affiliation:

1. Department of Microbiology, Immunology, and Molecular Genetics, University of California–Los Angeles, Los Angeles, CA 90095, USA.

2. Division of Hematology and Oncology, Department of Medicine, University of California–Los Angeles, Los Angeles, CA 90095, USA.

3. Department of Molecular and Medical Pharmacology, University of California–Los Angeles, Los Angeles, CA 90095, USA.

4. Department of Ecology and Evolutionary Biology, University of California–Los Angeles, Los Angeles, CA 90095, USA.

5. Department of Biological Chemistry, University of California–Los Angeles, Los Angeles, CA 90095, USA.

6. Department of Pathology, School of Medicine, Duke University, Durham, NC 27710, USA.

7. Molecular Biology Institute, University of California–Los Angeles, Los Angeles, CA 90095, USA.

8. Jonsson Comprehensive Cancer Center, University of California–Los Angeles, Los Angeles, CA 90095, USA.

9. Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California–Los Angeles, Los Angeles, CA 90095, USA.

10. Crump Institute for Molecular Imaging, University of California–Los Angeles, Los Angeles, CA 90095, USA.

Abstract

Some (re)programming notes on cancer Epithelial cancers develop resistance to targeted therapies in a number of different ways. Several cancer types do so by undergoing phenotypic conversion to a highly aggressive cancer called small cell neuroendocrine carcinoma (SCNC). Whether distinct cancer types accomplish this “reprogramming” through the same mechanism has been unclear. Park et al. show that the same set of oncogenic factors transforms both normal lung and normal prostate epithelial cells into SCNCs that resemble clinical samples (see the Perspective by Kareta and Sage). This convergence of molecular pathways could potentially simplify the development of new therapies for SCNC, which is currently untreatable. Science , this issue p. 91 ; see also p. 30

Funder

National Institutes of Health

American Cancer Society

National Cancer Institute

W.M. Keck Foundation

Hal Gaba Fund for Prostate Cancer Research

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Cited by 207 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3