<p>Renal cell carcinoma (RCC) and prostate cancer (PCa) are among the most prevalent and therapeutically challenging malignancies of the genitourinary system, particularly in advanced or metastatic stages. For advanced/metastatic RCC, targeted agents such as tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs) have improved progression-free and overall survival. For metastatic castration-sensitive PCa, androgen deprivation therapy (ADT) combined androgen receptor pathway inhibitors (ARPIs) with or without chemotherapy remains the standard of care. Despite these advances, therapeutic resistance, tumor recurrence, and treatment-related toxicities continue to limit long-term outcomes. Therefore, innovative immunotherapeutic strategies that can strengthen antitumor immunity, reduce relapse, and improve survival are urgently required. Cytokine-induced killer (CIK) cell therapy has emerged as a promising adoptive immunotherapy capable of enhancing antitumor immunity and improving outcomes. CIK cells are a heterogeneous population of immune effectors sharing features of T cells (CD3⁺CD56⁻), NK-like T cells (CD3⁺CD56⁺), and NK cells (CD3⁻CD56⁺). Their cytotoxic activity occurs in a major histocompatibility complex (MHC)-unrestricted manner through natural killer group 2 member D (NKG2D) receptor-ligand interactions, enabling the elimination of a wide spectrum of tumor types. In addition to their simple preparation, strong proliferative capacity, and low cost, CIK therapy offers several advantages, including reduced relapse rates, improved quality of life, prolonged survival, and favorable safety and tolerability. The versatility of CIK cells also allows integration with existing immunotherapies and targeted treatments. This review highlights recent advances in CIK cell therapy for RCC and PCa, emphasizing their biological mechanisms, preclinical and clinical evidence, and future perspectives for clinical translation and combination immunotherapy.</p>

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Therapeutic potential of cytokine-induced killer cell therapy for renal cell carcinoma and prostate cancer

  • I-Ta Lee,
  • Yung-Li Wang,
  • Jian-Hua Hong,
  • Chao-Yuan Huang,
  • Thi Thuy Tien Vo,
  • Wei-Ju Lee,
  • Chih-Hung Chiang

摘要

Renal cell carcinoma (RCC) and prostate cancer (PCa) are among the most prevalent and therapeutically challenging malignancies of the genitourinary system, particularly in advanced or metastatic stages. For advanced/metastatic RCC, targeted agents such as tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs) have improved progression-free and overall survival. For metastatic castration-sensitive PCa, androgen deprivation therapy (ADT) combined androgen receptor pathway inhibitors (ARPIs) with or without chemotherapy remains the standard of care. Despite these advances, therapeutic resistance, tumor recurrence, and treatment-related toxicities continue to limit long-term outcomes. Therefore, innovative immunotherapeutic strategies that can strengthen antitumor immunity, reduce relapse, and improve survival are urgently required. Cytokine-induced killer (CIK) cell therapy has emerged as a promising adoptive immunotherapy capable of enhancing antitumor immunity and improving outcomes. CIK cells are a heterogeneous population of immune effectors sharing features of T cells (CD3⁺CD56⁻), NK-like T cells (CD3⁺CD56⁺), and NK cells (CD3⁻CD56⁺). Their cytotoxic activity occurs in a major histocompatibility complex (MHC)-unrestricted manner through natural killer group 2 member D (NKG2D) receptor-ligand interactions, enabling the elimination of a wide spectrum of tumor types. In addition to their simple preparation, strong proliferative capacity, and low cost, CIK therapy offers several advantages, including reduced relapse rates, improved quality of life, prolonged survival, and favorable safety and tolerability. The versatility of CIK cells also allows integration with existing immunotherapies and targeted treatments. This review highlights recent advances in CIK cell therapy for RCC and PCa, emphasizing their biological mechanisms, preclinical and clinical evidence, and future perspectives for clinical translation and combination immunotherapy.