What question did this study set out to answer?

To establish a conceptual framework detailing how oncogenic, metabolic, and inflammatory pressures rewire lysosomal programs to actively mediate tumor immune evasion.

August 16, 2026Immunology and Cell Biology

Lysosomal Rewiring Perpetuates Tumor Immune Evasion in Cancer

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Authors

NANawal Al‐Hoshani AUAsad Ullah MAMuhammad Muddassir Ali

Discussion

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Overview

Mechanistic review reveals how lysosomal rewiring drives tumor immune evasion across cancer models, highlighting therapeutic targets to restore anti-tumor immunity.

Key Points

To establish a conceptual framework detailing how oncogenic, metabolic, and inflammatory pressures rewire lysosomal programs to actively mediate tumor immune evasion.
Reviewed signaling networks integrating metabolic stress, hypoxia, oncogenic drivers, and inflammation with lysosomal functional adaptations.
Evaluated the druggability and translational readiness of molecular targets governing lysosomal remodeling and immune resistance.
Defined six distinct lysosomal rewiring states where TFEB/TFE3-dependent lysosomal biogenesis and autophagic flux promote the degradation of immune effectors like IL-1β and MHC complexes, impairing T-cell priming.
Demonstrated that oncogenic PI3K-AKT-mTOR and MYC signaling mobilize Arl8b-BORC-kinesin complexes to drive lysosomal exocytosis and surface MHC-I clearance.
Stratified therapeutic candidates into clinically actionable agents like mTOR inhibitors and chloroquine versus strictly preclinical targets such as TPC2, Arl8b-BORC, and currently undruggable TFEB/TFE3 factors.

Cite This Study

Al‐Hoshani et al. (2026) studied this question.

synapsesocial.com/papers/6a8179dcf2fb91fc834ad519 https://doi.org/10.1111/imcb.70157

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August 16, 2026Immunology and Cell Biology

Lysosomal Rewiring Perpetuates Tumor Immune Evasion in Cancer

View Full Paper

Ask AI

Bookmark

Authors

NANawal Al‐Hoshani AUAsad Ullah MAMuhammad Muddassir Ali

Discussion

Member takes

Overview

Mechanistic review reveals how lysosomal rewiring drives tumor immune evasion across cancer models, highlighting therapeutic targets to restore anti-tumor immunity.

Key Points

To establish a conceptual framework detailing how oncogenic, metabolic, and inflammatory pressures rewire lysosomal programs to actively mediate tumor immune evasion.
Reviewed signaling networks integrating metabolic stress, hypoxia, oncogenic drivers, and inflammation with lysosomal functional adaptations.
Evaluated the druggability and translational readiness of molecular targets governing lysosomal remodeling and immune resistance.
Defined six distinct lysosomal rewiring states where TFEB/TFE3-dependent lysosomal biogenesis and autophagic flux promote the degradation of immune effectors like IL-1β and MHC complexes, impairing T-cell priming.
Demonstrated that oncogenic PI3K-AKT-mTOR and MYC signaling mobilize Arl8b-BORC-kinesin complexes to drive lysosomal exocytosis and surface MHC-I clearance.
Stratified therapeutic candidates into clinically actionable agents like mTOR inhibitors and chloroquine versus strictly preclinical targets such as TPC2, Arl8b-BORC, and currently undruggable TFEB/TFE3 factors.

Cite This Study

Al‐Hoshani et al. (2026) studied this question.

synapsesocial.com/papers/6a8179dcf2fb91fc834ad519 https://doi.org/10.1111/imcb.70157

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