Evidence map›Paper›PMID 34729299›Full record

ReviewActa pharmaceutica Sinica. B2021

Alterations of DNA damage response pathway: Biomarker and therapeutic strategy for cancer immunotherapy.

Minlin Jiang, Keyi Jia, Lei Wang, Wei Li, Bin Chen, Yu Liu, Hao Wang, Sha Zhao, Yayi He, Caicun Zhou

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed, 1 pooled it
20.0field-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

208 citing papers in PubMed, 1 synthesis or guideline pooled it, 311 citations in OpenAlex.

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148 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

10 authors at 1 institution in 1 country.

Minlin JiangDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Keyi JiaDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Lei WangDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Wei LiDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Bin ChenDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Yu LiuDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Hao WangDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Sha ZhaoDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Yayi HeDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Caicun ZhouDepartment of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability remains an enabling feature of cancer and promotes malignant transformation. Alterations of DNA damage response (DDR) pathways allow genomic instability, generate neoantigens, upregulate the expression of programmed death ligand 1 (PD-L1) and interact with signaling such as cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling. Here, we review the basic knowledge of DDR pathways, mechanisms of genomic instability induced by DDR alterations, impacts of DDR alterations on immune system, and the potential applications of DDR alterations as biomarkers and therapeutic targets in cancer immunotherapy.

Indexed as

ATM, ataxia-telangiectasia mutatedATR, ataxia telangiectasia and Rad3 relatedBAP1, BRCA1-associated protein 1BER, base excision repairBRAF, v-RAF murine sarcoma viral oncogene homologue BBRCA, breast cancer susceptibility genecGAS, cyclic GMP–AMP synthasecGAS–STINGCHEK, cell-cycle checkpoint kinaseCHK1, checkpoint kinase 1DAMP, damage-associated molecular patternsDDR, DNA damage responseDNA damage responseDNA repairDR, direct repairDSBs, double-strand breaksFDA, United State Food and Drug AdministrationGenomic instabilityGSK3β, glycogen synthase kinase 3βHMGB1, high mobility group box-1HRR, homologous recombination repairICI, immune checkpoint inhibitorIFNγ, interferon gammaIHC, immunohistochemistryImmunotherapyIRF1, interferon regulatory factor 1JAK, Janus kinaseMAD1, mitotic arrest deficient-like 1MGMT, O6-methylguanine methyltransferaseMLH1, MutL homolog 1MMR, mismatch repairMNT, MAX network transcriptional repressorMSH2/6, MutS protein homologue-2/6MSI, microsatellite instabilityMUTYH, MutY homologMyD88, myeloid differentiation factor 88NEK1, NIMA-related kinase 1NER, nucleotide excision repairNGS, next generation sequencingNHEJ, nonhomologous end-joiningNIMA, never-in-mitosis ANSCLC, non-small cell lung cancerORR, objective response rateOS, overall survivalPALB2, partner and localizer of BRCA2PARP, poly-ADP ribose polymerasePCR, polymerase chain reactionPD-1PD-1, programmed death 1PD-L1PD-L1, programmed death ligand 1PFS, progression-free survivalRAD51C, RAD51 homolog CRB1, retinoblastoma 1RPA, replication protein ARSR, replication stress responseSCNAs, somatic copy number alterationsssDNA, single-stranded DNASTAT, signal transducer and activator of transcriptionSTING, stimulator of interferon genesTBK1, TANK-binding kinase 1TILs, tumor-infiltrating lymphocytesTLR4, Toll-like receptor 4TMB, tumor mutational burdenTME, tumor microenvironmentTP53, tumor protein P53TRIF, Toll-interleukin 1 receptor domain-containing adaptor inducing INF-βTumor microenvironmentXRCC4, X-ray repair cross complementing protein 4

Identifiers

PMID34729299
PMCPMC8546664
OpenAlexW3119518737

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.