Evidence map›Paper›PMID 38074816›Full record

ArticleAmerican journal of translational research2023

PTPN3 in cancer: unveiling its immune-mediated impact on prognosis and dysregulated signaling pathways.

Mostafa A Abdel-Maksoud, Sajid Ullah, Amun Nadeem, Qurat Ul Ain Khan, Muhammad Khurram Zia, Saqib Ali, Adel M Zakri, Taghreed N Almanaa, Akram A Alfuraydi, Wahidah H Al-Qahtani and 1 more

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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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 5 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

11 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.
Sajid UllahBadr Al Samaa Hospital Muscat, Oman.
Amun NadeemDepartment of Pathology, Gujranwala Medical College Teaching Hospital Gujranwala, Pakistan.
Qurat Ul Ain KhanDepartment of Anatomy, Liaquat College of Medicine and Dentistry Karachi, Pakistan.
Muhammad Khurram ZiaDepartment of Surgery, Liaquat College of Medicine and Dentistry Karachi Pakistan.
Saqib AliDepartment of Computer Science, University of Agriculture Faisalabad, Pakistan.
Adel M ZakriDepartment of Plant Production, College of Food and Agricultural Sciences, King Saud University 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.
Wahidah H Al-QahtaniDepartment of Food Sciences & Nutrition, College of Food and Agricultural Sciences, King Saud University Riyadh 11451, Saudi Arabia.
Yasir HameedDepartment of Biotechnology, Institute of Biochemistry Biotechnology and Bioinformatics, The Islamia University of Bahawalpur Bahawalpur 63100, Punjab, Pakistan.
University of Agriculture Faisalabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesOncogenic processes in cancer are frequently marked by the dysregulation of critical genes, and PTPN3 (Protein Tyrosine Phosphatase, Non-Receptor Type 3) has emerged as a gene of interest due to its potential involvement in various cellular processes. This study delves into the diagnostic and prognostic implications of PTPN3 in a pan-cancer context.

methodsLeveraging comprehensive genomic datasets and experimental validation, we aimed to shed light on the role of PTPN3 in cancer.

resultsOur findings revealed the pervasive up-regulation of PTPN3 across 33 cancer types, making it a ubiquitous player in tumorigenesis. Of particular note, PTPN3 up-regulation exhibited a strong association with reduced overall survival in breast cancer (BRCA) and lung adenocarcinoma (LUAD). This underscores PTPN3's potential as a valuable prognostic marker in these cancers. While genetic mutations often drive oncogenic processes, our mutational analysis demonstrated the relative stability of PTPN3 in BRCA and LUAD. Promoter methylation analysis showed that hypomethylation plays a predominant role in PTPN3 dysregulation in BRCA and LUAD. Furthermore, our study unveiled positive correlations between PTPN3 expression and CD8+ T cell infiltration, offering insights into the gene's influence on the tumor immune microenvironment. Pathway enrichment analysis highlighted the involvement of PTPN3-associated genes in crucial signaling pathways. In addition, drug prediction analysis pinpointed potential drugs capable of modulating PTPN3 expression, opening avenues for personalized treatment strategies.

conclusionIn summary, our study elucidates the multifaceted roles of PTPN3 in BRCA and LUAD, underlining its significant up-regulation, prognostic relevance, epigenetic regulation, and its impact on the tumor immune microenvironment.

Indexed as

biomarkerBRCALUADPTPN3

Identifiers

PMID38074816
PMCPMC10703673
OpenAlexW4389800048

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.