Evidence map›Paper›PMID 35326731›Full record

ReviewCancers2022

Addressing the Elephant in the Immunotherapy Room: Effector T-Cell Priming versus Depletion of Regulatory T-Cells by Anti-CTLA-4 Therapy.

Megan M Y Hong, Saman Maleki Vareki

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07083375 (A Phase II Clinical Trial of Iparomlimab and Tuvonralimab in Combination With Bevacizumab and Platinum-based Chemotherapy in Previously Untreated Patients With Extensive-stage Small Cell Lung Cancer.), which is not on this map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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.

NCT07083375 phase2not yet recruitingnot on this mapstarted 2025, after this paper: background citation

A Phase II Clinical Trial of Iparomlimab and Tuvonralimab in Combination With Bevacizumab and Platinum-based Chemotherapy in Previously Untreated Patients With Extensive-stage Small Cell Lung Cancer.

TypeinterventionalSponsorZhijie WangRan2025 to 2027Enrolled56ConditionsExtensive Small Cell Lung CancerArmsQL1706 , bevacizumab, etoposide , cisplatin or carboplatin
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Standard Versus Modified Ipilimumab, in Combination With Nivolumab, in Advanced Renal Cell Carcinoma: A Randomized Phase II Trial (PRISM).Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Trial
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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 at 1 institution in 1 country.

Megan M Y HongDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, ON N6A 3K7, Canada.ORCID 0000-0001-6179-122X
Saman Maleki VarekiDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, ON N6A 3K7, Canada.ORCID 0000-0002-9615-7779
Western University · CA

Funding

CIHR MOP#389137London Regional Cancer Program's Catalyst Grant Program, Keith Smitt Translational Research grant N/A
6 · The paper itself

Abstract

Cytotoxic T-lymphocyte Associated Protein 4 (CTLA-4) is an immune checkpoint molecule highly expressed on regulatory T-cells (Tregs) that can inhibit the activation of effector T-cells. Anti-CTLA-4 therapy can confer long-lasting clinical benefits in cancer patients as a single agent or in combination with other immunotherapy agents. However, patient response rates to anti-CTLA-4 are relatively low, and a high percentage of patients experience severe immune-related adverse events. Clinical use of anti-CTLA-4 has regained interest in recent years; however, the mechanism(s) of anti-CTLA-4 is not well understood. Although activating T-cells is regarded as the primary anti-tumor mechanism of anti-CTLA-4 therapies, mounting evidence in the literature suggests targeting intra-tumoral Tregs as the primary mechanism of action of these agents. Tregs in the tumor microenvironment can suppress the host anti-tumor immune responses through several cell contact-dependent and -independent mechanisms. Anti-CTLA-4 therapy can enhance the priming of T-cells by blockading CD80/86-CTLA-4 interactions or depleting Tregs through antibody-dependent cellular cytotoxicity and phagocytosis. This review will discuss proposed fundamental mechanisms of anti-CTLA-4 therapy, novel uses of anti-CTLA-4 in cancer treatment and approaches to improve the therapeutic efficacy of anti-CTLA-4.

Indexed as

ADCC/Panti-CTLA-4CD28 costimulationCTLA-4FOXP3immunotherapyipilimumabTregs

Identifiers

PMID35326731
PMCPMC8946681
OpenAlexW4220969080

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.