Evidence map›Paper›PMID 40665025›Full record

ArticleDiscover oncology2025

In silico analysis of the oncogenic role of myoferlin (MYOF) and suggestion of folate as a potential therapeutic for brain cancer in the Caucasian population.

Saanvi Muthuchetty

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

1 author.

Saanvi MuthuchettyAcademy for Allied Health and Biomedical Sciences, Woodbridge, NJ, USA. saanvimuthuchetty@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyoferlin (MYOF), a key gene in endocytosis, is known to be crucial for metastasis in cancer. While the involvement of MYOF as a biomarker is documented in cancer, a comprehensive study on its knockdown for targeted therapy via folate is a novel approach.

methodsIn the current study, the expression, pathways, mutations, and interacting genes of MYOF were analyzed via bioinformatics analysis, which included computational drug discovery and spatial transcriptomics coupled with generative artificial intelligence experiments that were performed to elucidate the role of folate in MYOF knockdown.

resultsThe findings identified MYOF as a predominantly expressed gene biomarker in brain cancer genesis and its progression. Literature-reported mutations of MYOF were linked to pathways associated with depression, reinforcing the connection between brain cancer, tyrosine mutations, and depression in Caucasian patients. Additionally, computational drug discovery and spatial transcriptomics involving generative artificial intelligence experiments demonstrated folate as a potential therapeutic in MYOF knockdown.

conclusionsThese results suggest that dysregulation and mutation of MYOF position it as an oncogenic factor, and it serves as a potential therapeutic target for folate therapy for brain cancer associated with Caucasians.

Identifiers

PMID40665025
PMCPMC12263491

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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.