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Purpose of the review <p>The aim of this study was to provide a scoping review of the clinically approved tyrosine kinase inhibitors (TKIs) in cancer treatment and focus on the potential effect of these antineoplastic medicines on the metabolic effects of diabetes mellitus (DM), emphasizing how some of these medicines can work as anti-diabetic agents during cancer treatment.</p> Recent findings <p>TKIs are potential cancer therapeutic targets that have made significant strides in revolutionizing the field of cancer treatment. Notwithstanding their enormous promise, the development of TKIs continues to exhibit multiple endocrine effects, particularly on glycemic control. Given that β-cells are essential for maintaining glucose homeostasis and that the pathophysiology of DM involves a loss of β-cell function and survival, β-cell protection effect may be a significant response for the antidiabetic effects of TKIs. Treatment with TKIs in cancer patients with diagnosis of DM have significant potential to clinically affect glycemic control and produce anti-diabetic effects by maintaining functional β-cell mass, boosting insulin secretion and insulin sensitivity. These functions of TKIs are produced on several targets, including cellular Abelson non‑receptor tyrosine kinase (c‑Abl) inhibition, decreased Platelet-Derived Growth Factor Receptor (PDGFR) signaling, suppression of Vascular Endothelial Growth Factor Receptor (VEGFR), inhibition of Epidermal Growth Factor Receptor (EGFR), and obstruction of c-Kit signalling. These metabolic effects on blood glucose level were detected by many clinical reports in patients with type 1 DM (T1DM) and type 2 DM (T2DM) through multiple clinical effects, including, lower blood glucose level and HbA1c, increasing C-peptide levels which were associated with reducing the dose or stopping the treatment with antidiabetic medications. Most of these hypoglycemic effects were observed during the clinical use of imatinib, dasatinib, erlotinib, and sunitinib in cancer patients with diagnosis of DM.</p> Summary <p>TKIs are considered important approaches for the treatment of many cancer types. The use of these antineoplastic agents in patients with DM and a diagnosis of cancer shows that these agents have the ability to lower blood glucose, which can be associated with tapering down or discontinuing the use of anti-diabetic treatment.</p>

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Potential impact of tyrosine kinase inhibitors on glycemic control and diabetes mellitus progression: a clinical appraisal

  • 期刊论文

  • 发表日期：

    2025年12月11日

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  • Anmar Al-Taie,
  • Alyaa Abdulsalam Dayekh Al-Rashid,
  • Nesrine Nawel Rahim

摘要

Purpose of the review

The aim of this study was to provide a scoping review of the clinically approved tyrosine kinase inhibitors (TKIs) in cancer treatment and focus on the potential effect of these antineoplastic medicines on the metabolic effects of diabetes mellitus (DM), emphasizing how some of these medicines can work as anti-diabetic agents during cancer treatment.

Recent findings

TKIs are potential cancer therapeutic targets that have made significant strides in revolutionizing the field of cancer treatment. Notwithstanding their enormous promise, the development of TKIs continues to exhibit multiple endocrine effects, particularly on glycemic control. Given that β-cells are essential for maintaining glucose homeostasis and that the pathophysiology of DM involves a loss of β-cell function and survival, β-cell protection effect may be a significant response for the antidiabetic effects of TKIs. Treatment with TKIs in cancer patients with diagnosis of DM have significant potential to clinically affect glycemic control and produce anti-diabetic effects by maintaining functional β-cell mass, boosting insulin secretion and insulin sensitivity. These functions of TKIs are produced on several targets, including cellular Abelson non‑receptor tyrosine kinase (c‑Abl) inhibition, decreased Platelet-Derived Growth Factor Receptor (PDGFR) signaling, suppression of Vascular Endothelial Growth Factor Receptor (VEGFR), inhibition of Epidermal Growth Factor Receptor (EGFR), and obstruction of c-Kit signalling. These metabolic effects on blood glucose level were detected by many clinical reports in patients with type 1 DM (T1DM) and type 2 DM (T2DM) through multiple clinical effects, including, lower blood glucose level and HbA1c, increasing C-peptide levels which were associated with reducing the dose or stopping the treatment with antidiabetic medications. Most of these hypoglycemic effects were observed during the clinical use of imatinib, dasatinib, erlotinib, and sunitinib in cancer patients with diagnosis of DM.

Summary

TKIs are considered important approaches for the treatment of many cancer types. The use of these antineoplastic agents in patients with DM and a diagnosis of cancer shows that these agents have the ability to lower blood glucose, which can be associated with tapering down or discontinuing the use of anti-diabetic treatment.