Paper · 34529489

The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation.

Martin TD and 8 others. Science, 2021. Cited by 128 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

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ConductScience Library. The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation. Papers, record 34529489. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/34529489

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title: The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation.; PubMed
Journal: Science; PubMed
Year: 2021; PubMed
Publication types: Journal Article, Research Support, Non-U.S. Gov't; PubMed
PubMed: https://pubmed.ncbi.nlm.nih.gov/34529489/; PubMed
DOI: https://doi.org/10.1126/science.abg5784; PubMed
PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC13397623/; PubMed
The journal: https://conductscience.org/library/journal-index/0404511; PubMed
Citations, by iCite: 128; iCite
Relative citation ratio, by iCite: 5.23; iCite
Revised in PubMed: 2026-08-13; PubMed

Authors9

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

Order	Author	Forename	ORCID iD
1	Martin TD	Timothy D	https://orcid.org/0000-0002-4870-3624
2	Patel RS	Rupesh S	https://orcid.org/0000-0001-5792-5969
3	Cook DR	Danielle R
4	Choi MY	Mei Yuk
5	Patil A	Ajinkya	https://orcid.org/0000-0003-1080-1146
6	Liang AC	Anthony C	https://orcid.org/0000-0002-8792-8260
7	Li MZ	Mamie Z	https://orcid.org/0000-0002-7188-1330
8	Haigis KM	Kevin M
9	Elledge SJ	Stephen J	https://orcid.org/0000-0001-7923-6283

Source PubMed

Topics20

NLM's MeSH indexing of the paper, its major topics first.

MeSH term	Major
Carcinogenesis	Major topic
Gene Silencing	Major topic
Genes, Tumor Suppressor	Major topic
Immune Evasion	Major topic
Neoplasms, Experimental	Major topic
Animals
CRISPR-Cas Systems
Cell Line, Tumor
Chemokine CCL2
Female
GTP-Binding Protein alpha Subunits, G12-G13
Humans
Mammary Neoplasms, Experimental
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, SCID
Neoplasm Transplantation
Selection, Genetic
Tumor Microenvironment

Source PubMed

Grants3

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

Grant, as the record writes it	Agency	Country	NIH project	Stated by	Source
27144	Cancer Research UK	United Kingdom		PubMed	PubMed
U01 CA199252	NCI NIH HHS	United States	U01CA199252	PubMed and NIH	NIH RePORTER
	Howard Hughes Medical Institute	United States		PubMed	PubMed

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections3

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

Kind	PMID	Title	In Papers	Source
Comment in	34,529,483	Opposing roles of the immune system in tumors.	https://conductscience.org/library/papers/34529483	PubMed
Comment in	34,611,351	Under pressure.	https://conductscience.org/library/papers/34611351	PubMed
Comment in	35,027,544	A new perspective on immune evasion: escaping immune surveillance by inactivating tumor suppressors.	https://conductscience.org/library/papers/35027544	PubMed

References72

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

Order	PMID	Title	Journal	Year	In Papers	Source
1	22,628,553	Recurrent hemizygous deletions in cancers may optimize proliferative potential.	Science	2012	https://conductscience.org/library/papers/22628553	PubMed
2	30,837,996	Genome-Wide CRISPR Screening Identifies JAK1 Deficiency as a Mechanism of T-Cell Resistance.	Front Immunol	2019	https://conductscience.org/library/papers/30837996	PubMed
3	31,160,587	Tumour-associated macrophages exhibit anti-tumoural properties in Sonic Hedgehog medulloblastoma.	Nat Commun	2019	https://conductscience.org/library/papers/31160587	PubMed
4	29,719,257	CSF1R+ Macrophages Sustain Pancreatic Tumor Growth through T Cell Suppression and Maintenance of Key Gene Programs that Define the Squamous Subtype.	Cell Rep	2018	https://conductscience.org/library/papers/29719257	PubMed
5	20,844,553	Harnessing transposons for cancer gene discovery.	Nat Rev Cancer	2010	https://conductscience.org/library/papers/20844553	PubMed
6	10,591,652	Mouse models of tumor development in neurofibromatosis type 1.	Science	1999	https://conductscience.org/library/papers/10591652	PubMed
7	31,068,700	Next-generation characterization of the Cancer Cell Line Encyclopedia.	Nature	2019	https://conductscience.org/library/papers/31068700	PubMed
8	28,196,594	Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment.	Cancer Cell	2017	https://conductscience.org/library/papers/28196594	PubMed
9	29,301,958	A major chromatin regulator determines resistance of tumor cells to T cell-mediated killing.	Science	2018	https://conductscience.org/library/papers/29301958	PubMed
10	31,253,869	Determinants of immunological evasion and immunocheckpoint inhibition response in non-small cell lung cancer: the genetic front.	Oncogene	2019	https://conductscience.org/library/papers/31253869	PubMed

1 to 10 of 72

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Cited by105

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 128 citations.

PMID	Title	Journal	Year	In Papers	Source
42,903,966	Interactions between microbiota and innate immunity in tumor microenvironment: Novel insights into cancer progression and immunotherapy.	Hlife	2025	https://conductscience.org/library/papers/42903966	PubMed
42,829,916	CD112 Lactylation Drives Dual Immune Evasion From CD8+ T Cells and NK Cells.	Adv Sci (Weinh)	2026	https://conductscience.org/library/papers/42829916	PubMed
42,703,176	An Insight into the Emerging Role of Extracellular Vesicle-derived Noncoding RNAs in Colorectal Cancer.	Microrna	2026	https://conductscience.org/library/papers/42703176	PubMed
42,685,085	Changes in the transcriptome and synthetic lethal dependencies following KRAS mutant expression reveal profound tissue specificity.	Proc Natl Acad Sci U S A	2026	https://conductscience.org/library/papers/42685085	PubMed
42,539,061	EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.	Res Sq	2026	https://conductscience.org/library/papers/42539061	PubMed
42,420,609	Breast cancer driver genes found by screening chromosome aberrations in vivo.	Nature	2026	https://conductscience.org/library/papers/42420609	PubMed
42,297,823	Tumor suppressor genotype influences the extent and mode of immunosurveillance in lung cancer.	Nat Commun	2026	https://conductscience.org/library/papers/42297823	PubMed
42,270,598	CFTR-driven immune microenvironment reprogramming synergizes with anti-PD-L1 antibody in hepatocellular carcinoma.	Cell Death Dis	2026	https://conductscience.org/library/papers/42270598	PubMed
42,225,068	Temporal control of sgRNA library activation unlocks large-scale in vivo CRISPR screens.	Cell Rep Methods	2026	https://conductscience.org/library/papers/42225068	PubMed
42,204,538	The mycobiome, virome and archaeome in gastrointestinal cancers: molecular pathogenesis and therapeutic intervention.	Mol Cancer	2026	https://conductscience.org/library/papers/42204538	PubMed

1 to 10 of 105

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Genes0

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

None in this release.

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed: 2026-11-06; PubMed
iCite: 2026-11-05; iCite
PMC's ID file: 2026-11-05; PMC's ID file
NIH RePORTER's grant and paper links: 2026-11-01; NIH RePORTER's grant and paper links
Trials: 2026-11-12
Gene search: 2026-11-11
Pipelines: 2026-09-18

Sources 11

ChEMBL, through Open TargetsCC BY-SA 3.0
ClinicalTrials.govNo license stated
HGNCCC0
iCiteCC BY 4.0
NCBI GenePublic domain (US government)
NIH RePORTER's grant and paper linksPublic domain
Open TargetsCC0 1.0
PMC's ID filePublic domain (US government)
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0

Each source's terms

ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
ClinicalTrials.govnone stated
HGNCCC0: https://www.genenames.org/about/license/
iCiteCC BY 4.0
NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
PubMedNLM's terms
PubTator 3Public domain
UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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