Evidence map›Paper›PMID 35508649›Full record

ArticleScientific reports2022

Multi-staged gene expression profiling reveals potential genes and the critical pathways in kidney cancer.

Hamed Ishaq Khouja, Ibraheem Mohammed Ashankyty, Leena Hussein Bajrai, P K Praveen Kumar, Mohammad Amjad Kamal, Ahmad Firoz, Mohammad Mobashir

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

15 citing papers in PubMed, 25 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

7 authors at 3 institutions in 4 countries.

Hamed Ishaq KhoujaDepartment of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia. hkhoja@kau.edu.sa.
Ibraheem Mohammed AshankytyDepartment of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Leena Hussein BajraiSpecial Infectious Agents Unit-BSL3, King Fahad Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
P K Praveen KumarDepartment of Biotechnology, Sri Venkateswara College of Engineering, Sriperumbudur, 602105, India.
Mohammad Amjad KamalWest China School of Nursing/Institutes for Systems Genetics, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Ahmad FirozDepartment of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Mohammad MobashirSciLifeLab, Department of Oncology and Pathology, Karolinska Institutet, Box 1031, 171 21, Stockholm, Sweden. m.mobashir@cdslifesciences.com.
King Abdulaziz University · SAKarolinska Institutet · SENational Heart Foundation of Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is among the highly complex disease and renal cell carcinoma is the sixth-leading cause of cancer death. In order to understand complex diseases such as cancer, diabetes and kidney diseases, high-throughput data are generated at large scale and it has helped in the research and diagnostic advancement. However, to unravel the meaningful information from such large datasets for comprehensive and minute understanding of cell phenotypes and disease pathophysiology remains a trivial challenge and also the molecular events leading to disease onset and progression are not well understood. With this goal, we have collected gene expression datasets from publicly available dataset which are for two different stages (I and II) for renal cell carcinoma and furthermore, the TCGA and cBioPortal database have been utilized for clinical relevance understanding. In this work, we have applied computational approach to unravel the differentially expressed genes, their networks for the enriched pathways. Based on our results, we conclude that among the most dominantly altered pathways for renal cell carcinoma, are PI3K-Akt, Foxo, endocytosis, MAPK, Tight junction, cytokine-cytokine receptor interaction pathways and the major source of alteration for these pathways are MAP3K13, CHAF1A, FDX1, ARHGAP26, ITGBL1, C10orf118, MTO1, LAMP2, STAMBP, DLC1, NSMAF, YY1, TPGS2, SCARB2, PRSS23, SYNJ1, CNPPD1, PPP2R5E. In terms of clinical significance, there are large number of differentially expressed genes which appears to be playing critical roles in survival.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsBiomarkers, TumorComputational BiologyCritical PathwaysFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksGTPase-Activating ProteinsHumansIntegrin beta1MalePhosphatidylinositol 3-KinasesProtein Phosphatase 2Tumor Suppressor ProteinsBiomarkers, TumorDLC1 protein, humanGTPase-Activating ProteinsIntegrin beta1ITGBL1 protein, humanPhosphatidylinositol 3-KinasesPPP2R5E protein, humanProtein Phosphatase 2Tumor Suppressor Proteins

Identifiers

PMID35508649
PMCPMC9065671
OpenAlexW4225403904

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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.