Cancer Biology and Therapy · Available online 28 Jul 2026 · In press · DOI 10.1080/15384047.2026.2708386
Sivakumar S. Moni, Fatma Ayish, Shaqraa Musawi, Ahmad Salawi, Mohamed Eltaib Elmobark, Aamena Jabeen, Mawada Abubaker Abdelgadir Mohammed, Maha Jubran Aqdi, Maram Yahya Aziabi, Raneem Hafiz Harbi, Al Anoud Mohammed Ghazwani, Sara Hassan Almalki, Raghad Abdullah Sharif, Hanin Mohammed Ezzi, Hind Mohammed Suwaydi, Taif E. Alajam, Safa Abdullah Awaji, Amwaj Yahya Marwai Nammazi, Amirah Mosa Maashi, Nesreen Ibrahim Faqiri, Atyaf Saleh Ahmed Dohal, Nahlah Salah Burayk
Insulin resistance (IR) is involved in the development, progression, and treatment resistance of cancer. Apart from contributing to obesity and type 2 diabetes, IR leads to hyperinsulinemia, disruption of insulin-like growth factor signaling, chronic inflammation, and metabolic remodeling, which fosters a pro-tumorigenic milieu. These changes stimulate the PI3K–Akt–mTOR, MAPK, JAK–STAT, and NF-κB pathways, which increase proliferation, survival, angiogenesis, immune escape, and metastasis. IR also modifies the tumor microenvironment (TME) and dampens anti-tumor immunity. IGF-1R, IL-6, IL-1β, TNF-α, PD-1, PD-L1, and CTLA-4 monoclonal antibodies could be beneficial by inhibiting inflammatory and oncogenic pathways and reinitiating immune surveillance. Tumor resistance and heterogeneity are significant obstacles. This is a structured narrative review of the molecular connections, antibody treatments, translational obstacles, and future refined approaches in oncology.
Abstract from DOAJ. Public domain (CC0 1.0).
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Moni, S., Ayish, F., Musawi, S., et al. (2026). Molecular interplay of insulin resistance and cancer: advances in monoclonal antibody therapeutics. Cancer Biology and Therapy. https://doi.org/10.1080/15384047.2026.2708386