Evidence map›Paper›PMID 33167967›Full record

ArticleBMC medical genomics2020

In silico pathway analysis based on chromosomal instability in breast cancer patients.

Akeen Kour, Vasudha Sambyal, Kamlesh Guleria, Neeti Rajan Singh, Manjit Singh Uppal, Mridu Manjari, Meena Sudan

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
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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

7 authors at 2 institutions in 1 country.

Akeen KourHuman Cytogenetics Laboratory, Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, India.
Vasudha SambyalHuman Cytogenetics Laboratory, Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, India. vasudhasambyal@yahoo.co.in.ORCID 0000-0002-6648-1906
Kamlesh GuleriaHuman Cytogenetics Laboratory, Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, India.
Neeti Rajan SinghDepartment of Surgery, Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Amritsar, Punjab, India.
Manjit Singh UppalDepartment of Surgery, Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Amritsar, Punjab, India.
Mridu ManjariDepartment of Pathology, Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Amritsar, Punjab, India.
Meena SudanDepartment of Radiotherapy, Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Amritsar, Punjab, India.
Institute of Medical Sciences · INGuru Nanak Dev University · IN

Funding

Council of Scientific and Industrial Research, India 09/254(0258)/2016-EMR-IUniversity Grants Commission 41-824/2012/(SR)
6 · The paper itself

Abstract

backgroundComplex genomic changes that arise in tumors are a consequence of chromosomal instability. In tumor cells genomic aberrations disrupt core signaling pathways involving various genes, thus delineating of signaling pathways can help understand the pathogenesis of cancer. The bioinformatics tools can further help in identifying networks of interactions between the genes to get a greater biological context of all genes affected by chromosomal instability.

methodsKaryotypic analyses was done in 150 clinically confirmed breast cancer patients and 150 age and gender matched healthy controls after 72 h Peripheral lymphocyte culturing and GTG-banding. Reactome database from Cytoscape software version 3.7.1 was used to perform in-silico analysis (functional interaction and gene enrichment).

resultsFrequency of chromosomal aberrations (structural and numerical) was found to be significantly higher in patients as compared to controls. The genes harbored by chromosomal regions showing increased aberration frequency in patients were further analyzed in-silico. Pathway analysis on a set of genes that were not linked together revealed that genes HDAC3, NCOA1, NLRC4, COL1A1, RARA, WWTR1, and BRCA1 were enriched in the RNA Polymerase II Transcription pathway which is involved in recruitment, initiation, elongation and dissociation during transcription.

conclusionThe current study employs the information inferred from chromosomal instability analysis in a non-target tissue for determining the genes and the pathways associated with breast cancer. These results can be further extrapolated by performing either mutation analysis in the genes/pathways deduced or expression analysis which can pinpoint the relevant functional impact of chromosomal instability.

Indexed as

Chromosomal InstabilityGene Regulatory NetworksAbnormal KaryotypeAdultAgedAneuploidyBreast NeoplasmsBreast Neoplasms, MaleCarcinoma, Ductal, BreastChromosome AberrationsComputer SimulationFemaleHumansKaryotypingMaleMiddle AgedRNA Polymerase IIBreast cancerChromosomal instabilityPathway analysis

Identifiers

PMID33167967
PMCPMC7653868
OpenAlexW3103689070

What OpenQuestion holds

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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.