Evidence map›Paper›PMID 32432717›Full record

ArticleBioscience reports2020

Combinatorial approach of in silico and in vitro evaluation of MLH1 variant associated with Lynch syndrome like metastatic colorectal cancer.

Komal Saleem, Tahir Zaib, Wei Ji, Chunhui Zhang, Qian Qin, Yusi Wang, Lidan Xu, Hanfei Yu, Siqi Zhu, Kexian Dong and 5 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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, top 94% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 1 institution in 1 country.

Komal SaleemLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Tahir ZaibLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Wei JiLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Chunhui ZhangDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin 150040, China.
Qian QinLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Yusi WangLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Lidan XuLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Hanfei YuLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Siqi ZhuLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Kexian DongLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Shuhan SiLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Xueyuan JiaLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Jie WuLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Songbin FuLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Wenjing SunLaboratory of Medical Genetics, Harbin Medical University, Harbin 150081, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most developing cancer worldwide and Lynch syndrome (LS) accounts for 3-4% of CRC. Genetic alteration in any of DNA mismatch repair (MMR) gene is the major cause of LS that disrupt the normal upstream and downstream MMR events. Germline mutation of MLH1 in heterozygous state have an increased risk for CRC. Defective MMR pathway mostly results in microsatellite instability (MSI) that occurs in high percentage of CRC associated tumors. Here, we reported a patient with LS like metastatic CRC (mCRC) associated with other related cancers. Whole exome sequencing (WES) of the proband was performed to identify potential causative gene. Genetic screening validated by Sanger sequencing identified a heterozygous missense mutation in exon 12 of MLH1 (c.1151T>A, p.V384D). The clinical significance of identified variant was elucidated on the basis of clinicopathological data, computational predictions and various in vitro functional analysis. In silico predictions classified the variant to be deleterious and evolutionary conserved. In vitro functional studies revealed a significant decrease in protein expression because of stability defect leading to loss of MMR activity. Mutant residue found in MutL transducer domain of MLH1 that localized in the nucleus but translocation was not found to be significantly disturbed. In conclusion, our study give insight into reliability of combinatorial prediction approach of in silico and in vitro expression analysis. Hence, we highlighted the pathogenic correlation of MLH1 variant with LS associated CRC as well as help in earlier diagnosis and surveillance for improved management and genetic counselling.

Indexed as

Colorectal cancerIn silico toolsIn vitro analysisLynch syndromeMLH1WES

Identifiers

PMID32432717
PMCPMC7269917
OpenAlexW3026200085

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LicenceCC BY
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Registered trials

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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.