Evidence mapPaperPMID 42317213Full record

ReviewHuman mutation2026

From Germline Susceptibility to Therapeutic Vulnerability: DNA Damage Response Gene Mutations Driving Multiple Myeloma Evolution and Precision Therapy.

Qian Shen, Ying Wang, Liuhuan Cai, Juan Qian

Abstract readReview
In one paragraph

Review in Human mutation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

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

4 authors.

Qian ShenDepartment of Hematology and Lymphoma, Tumor Hospital Affiliated to Nantong University, Nantong, China, ntzlyy.cn.ORCID https://orcid.org/0009-0002-0663-3784
Ying WangDepartment of Hematology and Lymphoma, Tumor Hospital Affiliated to Nantong University, Nantong, China, ntzlyy.cn.ORCID https://orcid.org/0009-0008-7369-7781
Liuhuan CaiDepartment of Hematology and Lymphoma, Tumor Hospital Affiliated to Nantong University, Nantong, China, ntzlyy.cn.ORCID https://orcid.org/0009-0001-4451-368X
Juan QianDepartment of Hematology and Lymphoma, Tumor Hospital Affiliated to Nantong University, Nantong, China, ntzlyy.cn.ORCID https://orcid.org/0009-0005-7198-1859

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is characterized by genomic instability and therapeutic resistance. Emerging evidence indicates that germline DNA damage response (DDR) mutations, including BRCA1/2, ATM, and CHEK2 variants, contribute to MM susceptibility, clonal evolution, and treatment response. Inherited DDR defects promote chromosomal instability, reshape the immune microenvironment, and facilitate therapy-driven disease progression. Recent advances in multiomics profiling, single-cell sequencing, and liquid biopsy have improved the functional interpretation and clinical monitoring of DDR alterations. Moreover, DDR-associated vulnerabilities provide opportunities for precision therapies, including PARP inhibitor-based synthetic lethality strategies. This review summarizes the mechanistic and clinical significance of germline DDR alterations in MM and highlights their translational potential in precision oncology.

Indexed as

DNA DamageGenetic Predisposition to DiseaseGerm-Line MutationMultiple MyelomaPrecision MedicineAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCheckpoint Kinase 2DNA RepairGenomic InstabilityHumansAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCheckpoint Kinase 2DNA damage responsegene mutationgenomic instabilitygermline mutationmultiple myelomaprecision medicine

Identifiers

PMID42317213
PMCPMC13273519

What Socratic holds

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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 Socratic graph.