Evidence map›Paper›PMID 32940721›Full record

ReviewCellular and molecular life sciences : CMLS2021

The tumor-promoting effects of the adaptive immune system: a cause of hyperprogressive disease in cancer?

Fabrizio Marcucci, Cristiano Rumio

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
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  4. Article
  5. Non-coding ribonucleic acid-mediatedFrontiers in genetics · 2022
    Article
  6. Review
  7. 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

2 authors.

Fabrizio MarcucciDepartment of Pharmacological and Biomolecular Sciences, University of Milan, via Trentacoste 2, Milan, Italy. fabmarcu@gmail.com.ORCID http://orcid.org/0000-0002-2977-294X
Cristiano RumioDepartment of Pharmacological and Biomolecular Sciences, University of Milan, via Trentacoste 2, Milan, Italy.ORCID http://orcid.org/0000-0002-2593-7620

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adaptive antitumor immune responses, either cellular or humoral, aim at eliminating tumor cells expressing the cognate antigens. There are some instances, however, where these same immune responses have tumor-promoting effects. These effects can lead to the expansion of antigen-negative tumor cells, tumor cell proliferation and tumor growth, metastatic dissemination, resistance to antitumor therapy and apoptotic stimuli, acquisition of tumor-initiating potential and activation of various forms of survival mechanisms. We describe the basic mechanisms that underlie tumor-promoting adaptive immune responses and try to identify the variables that induce the switching of a tumor-inhibitory, cellular or humoral immune response, into a tumor-promoting one. We suggest that tumor-promoting adaptive immune responses may be at the origin of at least a fraction of hyperprogressive diseases (HPD) that are observed in cancer patients during therapy with immune checkpoint inhibitors (ICI) and, less frequently, with single-agent chemotherapy. We also propose the use of non-invasive biomarkers allowing to predict which patients may undergo HPD during ICI and other forms of antitumor therapy. Eventually, we suggest possibilities of therapeutic intervention allowing to inhibit tumor-promoting adaptive immune responses.

Indexed as

Adaptive ImmunityAntibodiesB7-H1 AntigenB-LymphocytesCytokinesHumansImmune Checkpoint InhibitorsNeoplasmsProgrammed Cell Death 1 ReceptorT-LymphocytesAntibodiesB7-H1 AntigenCytokinesImmune Checkpoint InhibitorsProgrammed Cell Death 1 ReceptorAntibodiesB cellsHyperprogressive diseaseImmune responseT cellsTumor promoting

Identifiers

PMID32940721
PMCPMC11072297

What OpenQuestion holds

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Registered trials

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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.