Evidence map›Paper›PMID 23093782›Full record

ArticleThe Journal of clinical investigation2012

Nanog signaling in cancer promotes stem-like phenotype and immune evasion.

Kyung Hee Noh, Bo Wook Kim, Kwon-Ho Song, Hanbyoul Cho, Young-Ho Lee, Jin Hee Kim, Joon-Yong Chung, Jae-Hoon Kim, Stephen M Hewitt, Seung-Yong Seong and 3 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
8.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

120 citing papers in PubMed, 193 citations in OpenAlex.

  1. Trial
  2. Proteomic profiling of CD133 + and CD326 + (EpCAM) subpopulations in A549 cells: insights into pluripotency and tumor heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  12. Novel CAR-T cells targeting TRKB for the treatment of solid cancer.Apoptosis : an international journal on programmed cell death · 2024
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60 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 2 countries.

Kyung Hee NohDivision of Infection and Immunology, Graduate School of Medicine, Korea University, Seoul, Republic of Korea.
Bo Wook Kim
Kwon-Ho Song
Hanbyoul Cho
Young-Ho Lee
Jin Hee Kim
Joon-Yong Chung
Jae-Hoon Kim
Stephen M Hewitt
Seung-Yong Seong
Chih-Ping Mao
T-C Wu
Tae Woo Kim
National Institutes of Health · USJohns Hopkins University · USYonsei University · KRKorea University · KRSeoul National University · KR

Funding

Treatment of HIV- and HIV+ Patients with HPV16+ CIN2/3 Using pNGLV4a-hCRTE6E7L2 DNA vaccine administered intramuscularly via electroporationP50CA098252 · NCI · JOHNS HOPKINS UNIVERSITY · PI WARNER KING HUH, TZYY-CHOOU WU · 2003 to 2026
$53.5M
CELLULAR &MOLECULAR MECH OF INFLAMMATORY REACTIONST32AI007247 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Joel L Pomerantz · 1985 to 2026
$10.2M
Tissue Array Research ProgramZICBC010923 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HEWITT, STEPHEN · 2009 to 2014
$4.7M
ENHANCING HPV-16 E6-SPECIFIC ANTITUMOR IMMUNITYR01CA114425 · NCI · JOHNS HOPKINS UNIVERSITY · PI WU, TZYY-CHOOU · 2005 to 2016
$3.0M
Nanog as a gateway to the immune-suppressive state in cancerF30CA177221 · NCI · JOHNS HOPKINS UNIVERSITY · PI MAO, CHIH-PING · 2013 to 2013
$47k
NCI NIH HHS F30 CA177221NCI NIH HHS P50 CA098252NCI NIH HHS R01 CA114425NIAID NIH HHS T32 AI007247
6 · The paper itself

Abstract

Adaptation of tumor cells to the host is a major cause of cancer progression, failure of therapy, and ultimately death. Immune selection drives this adaptation in human cancer by enriching tumor cells with a cancer stem cell-like (CSC-like) phenotype that makes them resistant to CTL-mediated apoptosis; however, the mechanisms that mediate CSC maintenance and proliferation are largely unknown. Here, we report that CTL-mediated immune selection drives the evolution of tumor cells toward a CSC-like phenotype and that the CSC-like phenotype arises through the Akt signaling pathway via transcriptional induction of Tcl1a by Nanog. Furthermore, we found that hyperactivation of the Nanog/Tcl1a/Akt signaling axis was conserved across multiple types of human cancer. Inhibition of Nanog in a murine model of colon cancer rendered tumor cells susceptible to immune-mediated clearance and led to successful, long-term control of the disease. Our findings establish a firm link among immune selection, disease progression, and the development of a stem-like tumor phenotype in human cancer and implicate the Nanog/Tcl1a/Akt pathway as a central molecular target in this process.

Indexed as

Tumor EscapeAnimalsApoptosisCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationColonic NeoplasmsFemaleHomeodomain ProteinsMiceMice, Inbred NODMice, SCIDNanog Homeobox ProteinNeoplasm TransplantationNeoplastic Stem CellsProto-Oncogene ProteinsHomeodomain ProteinsNanog Homeobox ProteinNANOG protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTCL1A protein, human

Identifiers

PMID23093782
PMCPMC3484451
OpenAlexW1998799674

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.