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Area of Science:

  • Oncology
  • Immunology
  • Cancer Metabolism

Background:

  • Immune-checkpoint blockade (ICB) improves survival in advanced cancers, but response rates need enhancement.
  • The acidic tumor microenvironment (TME) suppresses anti-tumor immune responses.
  • Carbonic anhydrase IX (CAIX), a hypoxia-induced enzyme, regulates tumor pH.

Purpose of the Study:

  • To investigate the role of CAIX in melanoma and its potential as a therapeutic target.
  • To evaluate the efficacy of targeting CAIX in combination with ICB.

Main Methods:

  • Assessed CAIX expression in 449 melanoma patients.
  • Utilized the small molecule SLC-0111 to inhibit CAIX.
  • Evaluated the impact of SLC-0111 on tumor cell metabolism, extracellular acidification, and immune cell killing.
  • Investigated combination therapy with ICB in preclinical models.
  • Analyzed TCGA cohorts for CA9 expression and Th1 response correlation.

Main Results:

  • High CAIX expression correlated with worse overall survival in melanoma patients.
  • SLC-0111 reduced tumor cell glycolysis and extracellular acidification, enhancing immune cell killing.
  • Combination therapy of SLC-0111 and ICB sensitized tumors to ICB, boosting Th1 response, reducing tumor growth, and metastasis.
  • Increased CA9 expression was linked to a reduced Th1 response in metastatic melanoma and breast cancer.

Conclusions:

  • Targeting CAIX can reverse TME-driven immune suppression.
  • Combination of CAIX inhibition with ICB represents a promising strategy for hypoxic solid tumors.
  • This approach may enhance therapeutic responses and survival in patients with advanced cancers.