Evidence map›Paper›PMID 32215870›Full record

ArticleCancer treatment and research2020

The Paradox of Cancer Immune Exclusion: Immune Oncology Next Frontier.

Sara I Pai, Alessandra Cesano, Francesco M Marincola

Open access · greenAbstract read
In one paragraph

Article in Cancer treatment and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
29.9field-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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Atezolizumab for Advanced Alveolar Soft Part Sarcoma.The New England journal of medicine · 2023
    Trial
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  16. Targeting T regulatory (TCancer drug resistance (Alhambra, Calif.) · 2024
    Review
  17. Article
  18. 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

3 authors at 3 institutions in 1 country.

Sara I PaiMassachusetts General Hospital, Harvard University, Boston, MA, USA. sara.pai@mgh.harvard.edu.
Alessandra CesanoESSA Pharmaceuticals, Inc., South San Francisco, CA, USA.
Francesco M MarincolaRefuge Biotechnologies, Inc., Menlo Park, CA, USA. franco.marincola@refugebiotech.com.
Essa Pharma (United States) · USHarvard University · USRefuge Biotechnologies (United States) · US

Funding

Strategies to Overcome Immune Resistance in Head and Neck CancersP01CA240239 · NCI · YALE UNIVERSITY · PI PAI, SARA ISABEL · 2019 to 2023
$8.4M
NCI NIH HHS P01 CA240239
6 · The paper itself

Abstract

Checkpoint inhibitor therapy (CIT) has revolutionized cancer treatment but it has also reached a standstill when an absent dialog between cancer and immune cells makes it irrelevant. This occurs with high prevalence in the context of "immune silent" and, even perhaps, "immune-excluded" tumors. The latter are characterized by T cells restricted to the periphery of cancer nests. Since in either case T cells do not come in direct contact with most cancer cells, CIT rests immaterial. Adoptive cell therapy (ACT), may also be affected by limited access to antigen-bearing cancer cells. While lack of immunogenicity intuitively explains the immune silent phenotype, immune exclusion is perplexing. The presence of T cells at the periphery suggests that chemo-attraction recruits them and an immunogenic stimulus promotes their persistence. However, what stops the T cells from infiltrating the tumors' nests and reaching the germinal center (GC)? Possibly, a concentric gradient of increased chemo-repulsion or decreased chemo-attraction demarcates an abrupt "do not trespass" warning. Various hypotheses suggest physical or functional barriers but no definitive consensus exists over the weight that each plays in human cancers. On one hand, it could be hypothesized that the intrinsic biology of cancer cells may degenerate from a "cancer stem cell" (CSC)-like phenotype in the GC toward a progressively more immunogenic phenotype prone to immunogenic cell death (ICD) at the periphery. On the other hand, the intrinsic biology of the cancer cells may not change but it is the disorderly architecture of the tumor microenvironment (TME) that alters in a centripetal direction cancer cell metabolism, both directly and indirectly, the function of surrounding stromal cells. In this chapter, we examine whether the paradoxical exclusion of T cells from tumors may serve as a model to understand the requirements for tumor immune infiltration and, correspondingly, we put forth strategies to restore the dialog between immune cells and cancer to enhance the effectiveness of immune oncology (IO) approaches.

Indexed as

HumansImmunogenic Cell DeathImmunotherapy, AdoptiveNeoplasmsT-LymphocytesTumor MicroenvironmentCancer immunotherapyCombination therapyImmune exclusionTumor microenvironment

Identifiers

PMID32215870
PMCPMC7423459
OpenAlexW3013454916

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.