Evidence map›Paper›PMID 39320417›Full record

ArticleBiochemical genetics2025

Analysis of the Main Checkpoints of the JNK-MAPK Pathway in HTLV-1-Associated Leukemia/Lymphoma via Boolean Network Simulation.

Shayan Mardi, Arash Letafati, Amin Hosseini, Reza Faraji, Parastoo Hosseini, Sayed-Hamidreza Mozhgani

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Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

What it found

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Shayan Mardi *Student Research Committee, Arak University of Medical Sciences, Arak, Iran.
Arash Letafati *Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Amin HosseiniDepartment of Computer Engineering, Faculty of Engineering, Raja University, Qazvin, Iran.
Reza FarajiDepartment of Animal Sciences, College of Agriculture & Natural Resources, University of Tehran, Karaj, Iran.
Parastoo HosseiniDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Sayed-Hamidreza MozhganiNoncommunicable Disease Research Center, Alborz University of Medical Sciences, Karaj, Iran. hamidrezamozhgani@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The c-Jun N-terminal kinase (JNK) pathway is a signal transduction pathway that plays a critical role in cell growth and survival. Its dysregulation is related to various cancers, including adult T-cell leukemia/lymphoma (ATLL), an aggressive peripheral T-cell malignancy caused by human T-cell lymphotropic virus type 1 (HTLV-1) infection. There is currently no vaccine or definitive treatment for ATLL. This research aimed to identify the JNK-MAPK pathway checkpoints to identify possible therapeutic targets using Boolean network analysis. First, the genes involved in the JNK pathway and their interactions were identified and mapped. Next, a Boolean network analysis was performed using the R programming language, which suggested protein kinase B (AKT) and MAP kinase phosphatase (MKP) for further evaluation. Finally, to confirm the effect of these two genes, a clinical study was conducted among ATLL patients and healthy individuals. The quantitative real time polymerase chain reaction (qRT‒PCR) results revealed a statistically significant decrease in the expression of AKT and MKP in ATLL patients compared to normal controls. This highlights the potential role of these two genes as potential therapeutic targets in ATLL.

Indexed as

HTLV-I InfectionsHuman T-lymphotropic virus 1JNK Mitogen-Activated Protein KinasesLeukemia-Lymphoma, Adult T-CellMAP Kinase Signaling SystemGene Regulatory NetworksHumansMitogen-Activated Protein Kinase PhosphatasesProto-Oncogene Proteins c-aktJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase PhosphatasesProto-Oncogene Proteins c-aktATLLBoolean networkHTLV-1JNK pathwayReal-time PCR

Identifiers

PMID39320417

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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.