Kras, Pten, NF-κB, and inflammation: Dangerous liaisons

Paul J. Chiao; Jianhua Ling

doi:10.1158/2159-8290.CD-11-0115

Kras, Pten, NF-κB, and inflammation: Dangerous liaisons

Paul J. Chiao, Jianhua Ling

Molecular & Cellular Oncology

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

Ying and colleagues identify a novel function of Pten as a haploinsufficient tumor suppressor in human pancreatic cancer development. Genomic, genetic, and biochemical data reveal that Pten loss and Kras mutation cooperate to accelerate pancreatic cancer development by altering PI3K regulation to enhance NF-κB activation and upregulate downstream cytokine genes; this provides a protumorigenic and metastatic microenvironment.

Original language	English (US)
Pages (from-to)	103-105
Number of pages	3
Journal	Cancer discovery
Volume	1
Issue number	2
DOIs	https://doi.org/10.1158/2159-8290.CD-11-0115
State	Published - Jul 18 2011

ASJC Scopus subject areas

Oncology

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10.1158/2159-8290.CD-11-0115

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title = "Kras, Pten, NF-κB, and inflammation: Dangerous liaisons",

abstract = "Ying and colleagues identify a novel function of Pten as a haploinsufficient tumor suppressor in human pancreatic cancer development. Genomic, genetic, and biochemical data reveal that Pten loss and Kras mutation cooperate to accelerate pancreatic cancer development by altering PI3K regulation to enhance NF-κB activation and upregulate downstream cytokine genes; this provides a protumorigenic and metastatic microenvironment.",

author = "Chiao, {Paul J.} and Jianhua Ling",

year = "2011",

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AU - Chiao, Paul J.

AU - Ling, Jianhua

PY - 2011/7/18

Y1 - 2011/7/18

N2 - Ying and colleagues identify a novel function of Pten as a haploinsufficient tumor suppressor in human pancreatic cancer development. Genomic, genetic, and biochemical data reveal that Pten loss and Kras mutation cooperate to accelerate pancreatic cancer development by altering PI3K regulation to enhance NF-κB activation and upregulate downstream cytokine genes; this provides a protumorigenic and metastatic microenvironment.

AB - Ying and colleagues identify a novel function of Pten as a haploinsufficient tumor suppressor in human pancreatic cancer development. Genomic, genetic, and biochemical data reveal that Pten loss and Kras mutation cooperate to accelerate pancreatic cancer development by altering PI3K regulation to enhance NF-κB activation and upregulate downstream cytokine genes; this provides a protumorigenic and metastatic microenvironment.

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SP - 103

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ER -

Kras, Pten, NF-κB, and inflammation: Dangerous liaisons

Abstract

ASJC Scopus subject areas

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