Evidence map›Paper›PMID 27638202›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Leveraging premalignant biology for immune-based cancer prevention.

Avrum Spira, Mary L Disis, John T Schiller, Eduardo Vilar, Timothy R Rebbeck, Rafael Bejar, Trey Ideker, Janine Arts, Matthew B Yurgelun, Jill P Mesirov and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. LncRNA IFITM4P promotes immune escape by up-regulating PD-L1 via dual mechanism in oral carcinogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  10. Review
  11. Article
  12. Preservation of antigen-specific responses in cryopreserved CD4Journal of translational autoimmunity · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Immune evasion in HPVProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. Review
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

14 authors.

Avrum SpiraDepartment of Medicine, Boston University School of Medicine, Boston, MA 02118;
Mary L DisisDepartment of Medicine, University of Washington, Seattle, WA 98195;
John T SchillerCenter for Cancer Research, National Cancer Institute, Bethesda, MD 20892;
Eduardo VilarDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, TX 77030;
Timothy R RebbeckDana-Farber Cancer Institute, Harvard T. H. Chan School of Public Health, Boston, MA 02215;
Rafael BejarDepartment of Medicine, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093;
Trey IdekerDepartment of Medicine, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093;
Janine ArtsJanssen Oncology Research & Development, Pharmaceutical Companies of Johnson & Johnson, 2300 Beerse, Belgium;
Matthew B YurgelunDepartment of Medical Oncology, Division of Population Sciences, Dana-Farber Cancer Institute, Boston, MA 02215;
Jill P MesirovDepartment of Medicine, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093;
Anjana RaoDivision of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037;
Judy GarberDepartment of Medical Oncology, Division of Population Sciences, Dana-Farber Cancer Institute, Boston, MA 02215;
Elizabeth M JaffeeDepartment of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Scott M LippmanDepartment of Medicine, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093; slippman@ucsd.edu.

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Understanding Papillomavirus Virion Proteins and VaccinesZIABC009052 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHILLER, JOHN T. · 2009 to 2025
$38.4M
SIGNAL TRANSDUCTION AND GENE INDUCTION IN T LYMPHOCYTESR01AI040127 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI HOGAN, PATRICK, RAO, ANJANA · 1996 to 2025
$13.3M
A Systems Approach to Mapping the DNA Damage ResponseR01ES014811 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI IDEKER, TREY · 2005 to 2021
$8.6M
Targeting the Immunosuppressive Tumor Microenvironment of Pancreatic Cancer with a Neoadjuvant Platform Clinical TrialR01CA197296 · NCI · JOHNS HOPKINS UNIVERSITY · PI William Reece Burns, Eric Christenson · 2015 to 2026
$5.7M
NCI NIH HHS P30 CA023100NCI NIH HHS R01 CA197296NIAID NIH HHS R01 AI040127NIEHS NIH HHS R01 ES014811
6 · The paper itself

Abstract

Prevention is an essential component of cancer eradication. Next-generation sequencing of cancer genomes and epigenomes has defined large numbers of driver mutations and molecular subgroups, leading to therapeutic advances. By comparison, there is a relative paucity of such knowledge in premalignant neoplasia, which inherently limits the potential to develop precision prevention strategies. Studies on the interplay between germ-line and somatic events have elucidated genetic processes underlying premalignant progression and preventive targets. Emerging data hint at the immune system's ability to intercept premalignancy and prevent cancer. Genetically engineered mouse models have identified mechanisms by which genetic drivers and other somatic alterations recruit inflammatory cells and induce changes in normal cells to create and interact with the premalignant tumor microenvironment to promote oncogenesis and immune evasion. These studies are currently limited to only a few lesion types and patients. In this Perspective, we advocate a large-scale collaborative effort to systematically map the biology of premalignancy and the surrounding cellular response. By bringing together scientists from diverse disciplines (e.g., biochemistry, omics, and computational biology; microbiology, immunology, and medical genetics; engineering, imaging, and synthetic chemistry; and implementation science), we can drive a concerted effort focused on cancer vaccines to reprogram the immune response to prevent, detect, and reject premalignancy. Lynch syndrome, clonal hematopoiesis, and cervical intraepithelial neoplasia which also serve as models for inherited syndromes, blood, and viral premalignancies, are ideal scenarios in which to launch this initiative.

Indexed as

Germ CellsHumansImmune SystemModels, BiologicalNeoplasm ProteinsNeoplasmsPrecancerous ConditionsTumor MicroenvironmentNeoplasm Proteinsbiologycancer preventionimmune oncologypremalignancyvaccines

Identifiers

PMID27638202
PMCPMC5047191

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.