Evidence map›Paper›PMID 22337995›Full record

ArticleCancer research2012

Cancer vaccination drives Nanog-dependent evolution of tumor cells toward an immune-resistant and stem-like phenotype.

Kyung Hee Noh, Young-Ho Lee, Ju-Hong Jeon, Tae Heung Kang, Chih-Ping Mao, T-C Wu, Tae Woo Kim

Abstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
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  4. Biomarkers and targeted therapy for cancer stem cells.Trends in pharmacological sciences · 2024
    Review
  5. Article
  6. Article
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  9. Article
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  12. Article
  13. Immune evasion by cancer stem cells.Regenerative therapy · 2021
    Review
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  15. Article
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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

7 authors at 4 institutions in 3 countries.

Kyung Hee NohDivison of Infection and Immunology, Graduate School of Medicine, Korea University, Seoul, South Korea.
Young-Ho Lee
Ju-Hong Jeon
Tae Heung Kang
Chih-Ping Mao
T-C Wu
Tae Woo Kim
Johns Hopkins University · USKorea University · KRNational University College · PRSeoul 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
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

Due to the exquisite specificity and potency of the immune system, vaccination is in theory the most precise and powerful approach for controlling cancer. However, current data from clinical trials indicate that vaccination rarely yields significant benefits for cancer patients in terms of tumor progression and long-term survival. The poor clinical outcomes of vaccination are primarily caused by mechanisms of immune tolerance, especially within the tumor microenvironment. Here, we report that vaccination drives the evolution of tumor cells toward an immune-resistant and stem-like phenotype that promotes tumor growth and nullifies the CTL response. The emergence of this phenotype required the transcription factor Nanog, which is induced as a consequence of immune selection. Nanog expression enhanced the stem-like features of tumor cells and protected them from killing by tumor-reactive CTLs. Delivery of siNanog into tumor-bearing mice rendered the tumor vulnerable to immune surveillance and strongly suppressed its growth. Together, our findings show tumor adaptation to vaccination through gain of an immune-resistant, stem-like phenotype and identify Nanog as a central molecular target in this process. Future vaccination technology should consider Nanog an important target to enhance the immunotherapeutic response.

Indexed as

Immune ToleranceVaccinationAnimalsCancer VaccinesFemaleHomeodomain ProteinsHumansMiceMice, Inbred C57BLNanog Homeobox ProteinNeoplasms, ExperimentalNeoplastic Stem CellsPhenotypeT-Lymphocytes, CytotoxicCancer VaccinesHomeodomain ProteinsNanog Homeobox ProteinNANOG protein, humanNanog protein, mouse

Identifiers

PMID22337995
PMCPMC3319841
OpenAlexW2130234264

What OpenQuestion holds

Textmetadata
LicenceTDM
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.