Evidence map›Paper›PMID 37338595›Full record

ArticleMolecular genetics and genomics : MGG2023

Expression variations of DNA damage response genes ATM and ATR in blood cancer patients.

Aamir Parvez, Ishrat Mahjabeen, Azhar Mehmood, Asad Ullah Khan, Asif Nisar, Mahmood Akhtar Kayani

Abstract read
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In one paragraph

Article in Molecular genetics and genomics : MGG, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 75% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Article
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

6 authors at 1 institution in 1 country.

Aamir ParvezCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan.
Ishrat MahjabeenCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan.
Azhar MehmoodCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan.
Asad Ullah KhanCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan.
Asif NisarCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan.
Mahmood Akhtar KayaniCancer Genetics and Epigenetics Laboratory, Department of Biosciences, COMSATS University Islamabad, Park Road Tarlai Kalan, Islamabad, Pakistan. mkayani@comsats.edu.pk.ORCID http://orcid.org/0000-0001-9886-180X
COMSATS University Islamabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematological malignancies (HM) constitute a variety of cancers originating in blood, bone marrow (BM), and lymphatic systems. During the last two decades, the incidence of HM has dramatically increased worldwide. The etiology of HM is still debatable. Genetic instability is a major risk factor for HM. DDR network is a complex signal transduction cellular machinery that detects DNA damage and activates cellular repair factors, thus maintaining genomic integrity. DDR network detects a variety of DNA damage and triggers the activation of cell cycle control, DNA repair, senescence, and apoptosis. Among the DNA repairing pathways, the DNA damage response (DDR) pathway includes DNA damage signaling apparatus such as ATM and ATR genes. ATM tends to detect double-strand breaks (DSBs) while ATR detects single-strand DNA (ssDNA). The study was conducted to observe the expression deregulations of DNA damage response (DDR) pathway genes (ATM, ATR) at mRNA level in 200 blood cancer patients and 200 controls. The real-time PCR was used to analyze the expression of the target genes. The expression results showed statistically significant downregulation of ATM (p < 0.0001) and ATR (p < 0.0001) genes in blood cancer patients vs. controls. Moreover, a significant downregulation of ATM (p < 0.0001) and ATR (p < 0.0001) was obtained in chemotherapy-treated patients vs. healthy controls. The results suggest that dysregulation in ATM and ATR genes may be associated with increased blood cancer risk.

Indexed as

Hematologic NeoplasmsNeoplasmsAtaxia Telangiectasia Mutated ProteinsDNADNA DamageDNA RepairHumansAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanDNAATMATRBlood cancerDDR pathway genesqPCR

Identifiers

PMID37338595
OpenAlexW4381308514

What OpenQuestion holds

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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.