Evidence map›Paper›PMID 42295372›Full record

ArticleCancer immunology, immunotherapy : CII2026

BAP1 loss impairs IFN-γ signaling and enhances NK cell-mediated cytotoxicity in myeloid leukemia.

Chiara Badami, Erna Islamagic, Linnea Blomén, Frida Svensson, Theebiga Kathirkamanathan, Kristoffer Hellstrand, Elin Bernson, Fredrik B Thorén

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Chiara BadamiTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Erna IslamagicTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Linnea BloménTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Frida SvenssonTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Theebiga KathirkamanathanTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Kristoffer HellstrandTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Elin BernsonTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden.
Fredrik B ThorénTIMM Laboratory at Sahlgrenska Center for Cancer Research, University of Gothenburg, Box 450, 405 30, Gothenburg, Sweden. fredrik.thoren@gu.se.

Funding

Swedish Cancer Society 22 2388Swedish Cancer Society 24 3472Swedish Research Council 2020-02783Swedish state via the ALF agreement ALFGBG-963642
6 · The paper itself

Abstract

Natural killer (NK) cells recognize and eliminate malignant cells through multiple receptor-ligand interactions. To uncover genetic determinants of the susceptibility of myeloid leukemia cells to NK cell cytotoxicity, we analyzed several genome-wide CRISPR screens. Among recurrent hits, the BRCA1-associated protein 1 (BAP1) gene emerged as a key factor protecting K562 leukemic cells from NK cell-mediated killing. Using BAP1 knockout (KO) models, we found that loss of BAP1 alone did not alter NK cell sensitivity. However, upon interferon-γ (IFN-γ) stimulation, BAP1 KO K562 cells exhibited reduced HLA class I induction, triggered enhanced NK cell degranulation, and showed increased sensitivity to NK cell-mediated cytotoxicity compared with wild-type cells. Further experiments revealed that BAP1-deficient cells displayed reduced expression of the IFN-γ receptor 1 (IFN-γ-R1). BAP1 knockdown across multiple myeloid leukemia cell lines selectively decreased HLA-E and IFN-γ-R1 expression in ASXL1-mutant backgrounds. These findings suggest that BAP1 may contribute to the regulation of IFN-γ responsiveness and immune evasion in myeloid leukemia.

Indexed as

Cytotoxicity, ImmunologicInterferon-gammaKiller Cells, NaturalLeukemia, MyeloidTumor Suppressor ProteinsUbiquitin ThiolesteraseCell Line, TumorHumansInterferon gamma ReceptorK562 CellsReceptors, InterferonSignal TransductionBAP1 protein, humanInterferon-gammaInterferon gamma ReceptorReceptors, InterferonTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1CRISPR/Cas9HLA-IIFN-γNK cells

Identifiers

PMID42295372
PMCPMC13269568

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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.