Evidence map›Paper›PMID 35701637›Full record

ReviewNature reviews. Drug discovery2022

Adaptive immune resistance at the tumour site: mechanisms and therapeutic opportunities.

Tae Kon Kim, Esten N Vandsemb, Roy S Herbst, Lieping Chen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 2 pooled it
34.5field-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

218 citing papers in PubMed, 2 syntheses or guidelines pooled it, 339 citations in OpenAlex.

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  14. Adaptive resistance in cancer immunotherapy.Cellular & molecular immunology · 2026
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158 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Tae Kon KimDivision of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Esten N VandsembDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Roy S HerbstDepartment of Medicine (Medical Oncology), Yale University School of Medicine, New Haven, CT, USA.
Lieping ChenDepartment of Medicine (Medical Oncology), Yale University School of Medicine, New Haven, CT, USA. lieping.chen@yale.edu.ORCID 0000-0002-6825-3069
Yale University · USNorwegian University of Science and Technology · NOYale Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumours employ various tactics to adapt and eventually resist immune attack. These mechanisms are collectively called adaptive immune resistance (AIR). The first defined and therapeutically validated AIR mechanism is the selective induction of programmed cell death 1 ligand 1 (PDL1) by interferon-γ in the tumour. Blockade of PDL1 binding to its receptor PD1 by antibodies (anti-PD therapy) has resulted in remission of a fraction of patients with advanced-stage cancer, especially in solid tumours. However, many clinical trials combining anti-PD therapy with other antitumour drugs conducted without a strong mechanistic rationale have failed to identify a synergistic or additive effect. In this Perspective article, we discuss why defining AIR mechanisms at the tumour site should be a key focus to direct future drug development as well as practical approaches to improve current cancer therapy.

Indexed as

B7-H1 AntigenNeoplasmsAntibodiesHumansAntibodiesB7-H1 Antigen

Identifiers

PMID35701637
OpenAlexW4282935115

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.