Evidence map›Paper›PMID 34493821›Full record

ReviewBritish journal of cancer2022

Lymphoid-specific helicase in epigenetics, DNA repair and cancer.

Xiangyu Chen, Yamei Li, Karla Rubio, Bi Deng, Yuyi Li, Qinwei Tang, Chao Mao, Shuang Liu, Desheng Xiao, Guillermo Barreto and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

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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

11 authors at 3 institutions in 5 countries.

Xiangyu ChenDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.
Yamei LiDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.
Karla RubioUniversité de Lorraine, CNRS, Laboratoire IMoPA, UMR 7365, Nancy, France.ORCID http://orcid.org/0000-0002-8337-3106
Bi DengDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.
Yuyi LiDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.
Qinwei TangDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.
Chao MaoDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China.ORCID http://orcid.org/0000-0002-8685-8539
Shuang LiuDepartment of Oncology, Institute of Medical Sciences, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Desheng XiaoDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China. xdsh96@csu.edu.cn.
Guillermo BarretoUniversité de Lorraine, CNRS, Laboratoire IMoPA, UMR 7365, Nancy, France. Guillermo.barreto@univ-lorraine.fr.ORCID http://orcid.org/0000-0002-7777-4712
Yongguang TaoDepartment of Pathology, Xiangya Hospital, Central South University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan, China. taoyong@csu.edu.cn.ORCID http://orcid.org/0000-0003-2354-5321
Ministry of Education of the People's Republic of China · CNCentral South University · CNCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphoid-specific helicase (LSH) is a member of the SNF2 helicase family of chromatin-remodelling proteins. Dysfunctions or mutations in LSH causes an autosomal recessive disease known as immunodeficiency-centromeric instability-facial anomaly (ICF) syndrome. Interestingly, LSH participates in various aspects of epigenetic regulation, including nucleosome remodelling, DNA methylation, histone modifications and heterochromatin formation. Further, LSH plays a crucial role during DNA-damage repair, specifically during double-strand break (DSB) repair, since murine LSH was shown to be essential for non-homologous end joining (NHEJ) and homologous recombination (HR). Accordingly, overexpression of LSH drives tumorigenesis and malignancy. On the other hand, LSH homologs stabilise the genome. Thus, LSH might be implemented as a biomarker for various cancer types and potential target molecule to develop therapeutic strategies against them. In this review, we focus on the role of LSH in orchestrating chromatin rearrangements, such as DNA methylation and histone modifications, as well as in DNA-damage repair. Changes in chromatin structure may facilitate gene expression signatures that cause malignant transformation. We summarise recent findings of LSH in cancers and raise critical open questions for further studies.

Indexed as

Chromatin Assembly and DisassemblyDNA End-Joining RepairDNA RepairEpigenesis, GeneticHomologous RecombinationAnimalsDNA HelicasesHumansDNA HelicasesHELLS protein, human

Identifiers

PMID34493821
PMCPMC8770686
OpenAlexW3198593174

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.