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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
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Targeting OxLDL-mediated CD36 + CAF reprogramming potentiates PD-1 immunotherapy in osteosarcoma.

Anyu Zeng1, Hongmin Chen1, Tianqi Luo1

  • 1Department of Musculoskeletal Oncology, State Key Laboratory of Oncology in South China,Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P.R. China.

Molecular Cancer
|December 18, 2025
PubMed
Summary

Cancer-associated fibroblasts (CAFs) in osteosarcoma create an immunosuppressive tumor microenvironment (TME) by secreting ANGPTL4, which exhausts CD8+ T cells. Targeting this via Vitamin E (VitE) enhances immunotherapy response.

Keywords:
Cancer-associated fibroblastsImmune checkpoint blockadeImmunotherapy resistanceLipid metabolism reprogrammingOsteosarcoma

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Area of Science:

  • Oncology
  • Immunology
  • Cancer Metabolism

Background:

  • Osteosarcoma exhibits poor response to PD-1 blockade due to an immunosuppressive tumor microenvironment (TME).
  • The precise role of cancer-associated fibroblasts (CAFs) in osteosarcoma immunosuppression remains unclear.

Purpose of the Study:

  • Investigate the mechanisms by which CAFs contribute to immune suppression in osteosarcoma.
  • Determine the impact of CAF-derived factors on CD8+ T cell function and immunotherapy response.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of osteosarcoma tissues from patients receiving neoadjuvant chemotherapy and anti-PD-1 therapy.
  • Analysis of cellular composition, gene expression, and signaling pathways within the TME.
  • Functional assays, binding validation, and in vivo mouse models to assess CAF-mediated effects on T cells.

Main Results:

  • Identified CD36+ CAFs with activated PPARG-FABP4 axis, facilitating oxidized low-density lipoprotein (OxLDL) uptake.
  • Discovered OxLDL-driven ANGPTL4 secretion by CAFs, which activates JAK2-STAT3 in CD8+ T cells, causing exhaustion.
  • Demonstrated that Vitamin E (VitE) scavenges OxLDL, improves TME, boosts CD8+ T cell infiltration, and synergizes with PD-1 blockade in vivo.

Conclusions:

  • CD36+ CAFs promote osteosarcoma immune evasion through the OxLDL-PPARG-ANGPTL4 metabolic pathway, leading to CD8+ T cell exhaustion and immunotherapy resistance.
  • Targeting this CAF-driven metabolic reprogramming with VitE can overcome immune suppression and enhance anti-PD-1 therapy efficacy.
  • These findings support the development of metabolism-based combination strategies for osteosarcoma treatment.