Evidence map›Paper›PMID 37774059›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2023

Potential Candidate Genes for Therapeutic Targeting in Chronic Myeloid Leukemia: A Pilot Study.

Khaldoon Alsamman, Ali M Alamri, Chittibabu Vatte, Amani Y Owaidah, Fatimah Alhassan, Roba Mubarki, Omar S El-Masry

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 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 65% 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

7 authors at 2 institutions in 1 country.

Khaldoon AlsammanDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahaman Bin Faisal University, Dammam, Saudi Arabia.
Ali M AlamriDepartment of Internal Medicine, King Fahd Hospital of the University, Imam Abdulrahaman Bin Faisal University, Alkhobar, Saudi Arabia.
Chittibabu VatteDepartment of Clinical Biochemistry, College of Medicine, Imam Abdulrahman bin Faisal University, Dammam, Saudi Arabia.ORCID 0000-0003-3026-5520
Amani Y OwaidahDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahaman Bin Faisal University, Dammam, Saudi Arabia.
Fatimah AlhassanDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahaman Bin Faisal University, Dammam, Saudi Arabia.
Roba MubarkiDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahaman Bin Faisal University, Dammam, Saudi Arabia.
Omar S El-MasryDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdulrahaman Bin Faisal University, Dammam, Saudi Arabia.ORCID 0000-0002-0226-2923
Imam Abdulrahman Bin Faisal University · SAKing Fahd Hospital of the University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic myeloid leukemia (CML) is a prevalent hematological malignancy known for the presence of the Philadelphia chromosome and activation of the BCR-Abl kinase activity. Although tyrosine kinase inhibitors are widely used as the standard treatment, resistance remains a concern among certain patients. This study aimed to investigate the gene expression profile of a group of CML patients in comparison to a control group in order to identify novel candidate genes associated with the disease.

methodsWhole transcriptome sequencing was performed, and gene expression levels were validated using quantitative real-time PCR. Additionally, single nucleotide and insertion/deletion variants were analyzed in the selected candidate genes among 10 CML patients and 4 healthy control subjects.

resultsAnalysis revealed a set of differentially expressed genes, whose up- or downregulation was further confirmed by qRT-PCR. Among the upregulated genes in the patient group were ribosomal protein like (RPL) members, specifically RPL9, RPL34, RPL36A, and RPL39, while downregulation was observed in CCDC170, LDB1, and SBF1 compared to the healthy subjects. Furthermore, gene variant studies identified novel genetic changes in these candidate genes, suggesting potential clinical significance in CML.

conclusionsThis study highlights RPL9, RPL34, RPL36A, RPL39, CCDC170, LDB1, and SBF1 as potential targets in CML. Additionally, it underscores the importance of investigating these genes and their variants in larger cohort studies to assess their clinical significance in CML patients.

Indexed as

Fusion Proteins, bcr-ablLeukemia, Myelogenous, Chronic, BCR-ABL PositiveChronic DiseaseDrug Resistance, NeoplasmHumansLIM-Homeodomain ProteinsPilot ProjectsProtein Kinase InhibitorsFusion Proteins, bcr-ablLIM-Homeodomain ProteinsProtein Kinase InhibitorsCCDC170CMLLDB1RPLSBF1

Identifiers

PMID37774059
PMCPMC10762750
OpenAlexW4387164472

What OpenQuestion holds

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LicenceCC BY-NC
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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.