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Related Experiment Video

Updated: Jul 14, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

P38γ Promotes Tumorigenesis Through Activating Immune Evasion.

Naveenkumar Chandrashekar¹, Xiao-Mei Qi¹, Guan Chen^1,2

¹Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

|July 13, 2026

Summary

Stress-activated protein kinase p38γ (MAPK12) promotes tumorigenesis by reprogramming immune evasion in breast, pancreatic, and colon cancers. Targeting p38γ may offer a novel cancer therapy approach.

Keywords:

PD-L1 breast cancer colon cancer immune survival p38γMAPK pancreatic cancer

Related Experiment Videos

Last Updated: Jul 14, 2026

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Primary Sjogren's Syndrome Associated with Lung Adenocarcinoma: Probing the Potential Common Pathogenic Mechanisms and Experimental Verification

Published on: September 20, 2024

Area of Science:

Oncology
Molecular Biology
Immunology

Background:

Stress-activated protein kinase p38γ (MAPK12) is implicated in tumorigenesis, but its mechanisms are unclear.
p38γ plays a role in immune evasion across multiple cancer types.

Purpose of the Study:

To review and present evidence on the role of p38γ in promoting tumorigenesis through immune evasion in breast, pancreatic, and colon cancers.
To elucidate the mechanisms by which p38γ integrates oncogenic and inflammatory signals.

Main Methods:

Review of published and unpublished studies.
Analysis of murine models for breast, pancreatic (KPC and KTC), and colon cancer.
Investigation of signaling pathways including Wnt, CXCL5, CXCL13, and PD-L1 expression.

Main Results:

p38γ acts as an oncogene in triple-negative breast cancer (TNBC) and promotes breast tumorigenesis.
p38γ is essential for KRAS-oncogene-induced pancreatic cancer, supporting cell metabolism and fibrosis.
p38γ integrates colon cancer risk factors, amplifying oncogenic signaling via Wnt pathway and immune evasion (PD-L1).

Conclusions:

p38γ MAPK is a key integrator of oncogenic and inflammatory signals in multiple cancers.
p38γ promotes tumorigenesis by activating proliferative signaling and immune evasion.
Targeting p38γ represents a potential innovative strategy for cancer therapy.