Evidence map›Paper›PMID 38074804›Full record

ArticleAmerican journal of translational research2023

Immune modulation and prognostic significance of MCM10 in pan-cancer: a comprehensive analysis.

Mostafa A Abdel-Maksoud, Komal Iqbal, Sanobar Gull, Sanjay Kirshan Kumar, Maryam Mastoor, Saeedah Musaed Almutairi, Taghreed N Almanaa, Akram A Alfuraydi, Ayman Mubarak, Mohamed H Kotob and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2023. 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
0.5field-weighted citation impact, top 27% 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. Article
  2. Review
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

12 authors at 1 institution in 1 country.

Mostafa A Abdel-MaksoudDepartment of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Komal IqbalBasic Health Unit Hindwan, Department of Primary Secondary Health Sahiwal, Sargodha 40210, Punjab, Pakistan.
Sanobar GullDepartment of Biochemistry, Government College University Faisalabad Faisalabad, Pakistan.
Sanjay Kirshan KumarBahria University Health Sciences Karachi, Pakistan.
Maryam MastoorDepartment of Biochemistry, Amna Inayat Medical College Lahore, Pakistan.
Saeedah Musaed AlmutairiDepartment of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Taghreed N AlmanaaDepartment of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Akram A AlfuraydiDepartment of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Ayman MubarakDepartment of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Mohamed H KotobDepartment of Pharmaceutical Sciences, Division of Pharmacology and Toxicology, University of Vienna Vienna, Austria.
Muhammad JamilPARC Arid Zone Research Center Dera Ismail Khan 29050, Pakistan.
Mohamed Y ZakyUPMC Hillman Cancer Center, Division of Hematology and Oncology, Department of Medicine, University of Pittsburgh Pittsburgh, PA 15213, USA.
Bahria University · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOncogenic processes in cancer are often characterized by dysregulation of critical genes. Our study focused on the minichromosome maintenance 10 replication initiation factor (MCM10) gene's expression and its potential diagnostic and prognostic implications in pan-cancer.

methodLeveraging large-scale genomic datasets, and experimental validation we embarked on a comprehensive analysis to shed light on the diagnostic and prognostic role of MCM10.

resultsOur findings underscore the wide-ranging up-regulation of MCM10 across 24 major cancer types, positioning it as a ubiquitous player in tumorigenesis. Significantly, MCM10 up-regulation was strongly associated with poorer overall survival in Kidney Renal Papillary Cell Carcinoma (KIRP), Liver Hepatocellular Carcinoma (LIHC), and Lung Adenocarcinoma (LUAD), emphasizing its potential as a valuable prognostic marker in these cancers. While genetic mutations often drive oncogenic processes, our mutational analysis revealed the relative stability of MCM10 in KIRP, LIHC, and LUAD. This suggests that epigenetic (hypomethylation) and non-mutational regulatory mechanisms predominantly govern MCM10 expression in these cancer types. Further analyses demonstrated positive correlations between MCM10 expression and immune cell infiltration, particularly CD8+ T cells and CD4+ T cells, offering insights into the gene's influence on the tumor immune microenvironment. Additionally, pathway enrichment analysis highlighted MCM10-associated genes' involvement in crucial signaling pathways, such as the cell cycle, DNA replication, and repair. Exploring the therapeutic potential, we examined important drugs capable of regulating MCM10 expression, opening doors to personalized treatment strategies.

conclusionOur study elucidates the multifaceted roles of MCM10 in KIRP, LIHC, and LUAD. Its pervasive up-regulation, prognostic significance, epigenetic regulation, and influence on the immune microenvironment provide valuable insights into these cancers. This research contributes to the growing body of evidence surrounding MCM10 and invites further investigation, validation, and potential translational efforts to harness its clinical relevance.

Indexed as

cancerdiagnosisMCM10prognosis

Identifiers

PMID38074804
PMCPMC10703649
OpenAlexW4389803291

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.