Diabetes mellitus (DM) and cancer are major global health challenges that increasingly coexist due to shared risk factors including aging, obesity, sedentary behavior, and chronic low-grade inflammation. Beyond being a common comorbidity, DM—particularly type 2 diabetes—has emerged as an important modifier of cancer risk, progression, treatment tolerance, and survival. Epidemiological studies consistently associate DM with a higher incidence of several malignancies, including pancreatic, liver, colorectal, breast, and endometrial cancers, as well as increased cancer-specific and overall mortality. The biological link between dysglycemia and cancer is complex and multifactorial. Chronic hyperglycemia, hyperinsulinemia, and insulin resistance promote tumor development and progression through altered cellular metabolism (Warburg effect), activation of insulin and insulin-like growth factor pathways, systemic inflammation, oxidative stress, immune dysfunction, and changes in the tumor microenvironment and gut microbiota. This review summarizes current evidence on the interplay between dysglycemia and cancer and explores how integrating continuous glucose monitoring (CGM)-based strategies into multidisciplinary oncology care may improve both metabolic and oncologic outcomes. A comprehensive search of online databases, including PubMed, ISI Web of Science, and Scopus, was conducted to identify studies assessing the impact of glycemic disturbances and glycemic control on cancer outcomes. Poor glycemic control and increased glucose variability are associated with worse oncologic outcomes, higher rates of treatment-related complications, reduced adherence to therapy, and diminished efficacy of chemotherapy, targeted agents, and immune checkpoint inhibitors. Severe hypoglycemia has also emerged as an independent predictor of poor prognosis. Although HbA1c has long been the cornerstone of glycemic assessment, it incompletely captures the dynamic glucose fluctuations commonly observed during cancer therapy. CGM provides a more comprehensive and clinically meaningful assessment of glycemic control, with the potential to reduce hypoglycemia, improve glycemic stability, and enhance tolerance and adherence to anticancer treatments. Current evidence indicates that diabetes and dysglycemia are key modifiers of cancer risk, progression, treatment tolerance, and survival. Optimizing glycemic control may therefore contribute to improved cancer outcomes. CGM represents a promising tool for personalizing diabetes management in oncology settings.

Diabetes and cancer. Glucose control impact on survival and tumor outcomes / Ruggeri, R.M., Grossrubatscher, E.M., Arrivi, G., Ciocca, E., Filice, A., Golisano, B., Mazzilli, R., Prinzi, N., Colao, A., Faggiano, A.. - In: REVIEWS IN ENDOCRINE AND METABOLIC DISORDERS. - ISSN 1573-2606. - (2026). [10.1007/s11154-026-10040-x]

Diabetes and cancer. Glucose control impact on survival and tumor outcomes

Arrivi, Giulia;Ciocca, Eleonora;Filice, Alessia;Golisano, Bianca;Mazzilli, Rossella;Prinzi, Natalie;Faggiano, Antongiulio
2026

Abstract

Diabetes mellitus (DM) and cancer are major global health challenges that increasingly coexist due to shared risk factors including aging, obesity, sedentary behavior, and chronic low-grade inflammation. Beyond being a common comorbidity, DM—particularly type 2 diabetes—has emerged as an important modifier of cancer risk, progression, treatment tolerance, and survival. Epidemiological studies consistently associate DM with a higher incidence of several malignancies, including pancreatic, liver, colorectal, breast, and endometrial cancers, as well as increased cancer-specific and overall mortality. The biological link between dysglycemia and cancer is complex and multifactorial. Chronic hyperglycemia, hyperinsulinemia, and insulin resistance promote tumor development and progression through altered cellular metabolism (Warburg effect), activation of insulin and insulin-like growth factor pathways, systemic inflammation, oxidative stress, immune dysfunction, and changes in the tumor microenvironment and gut microbiota. This review summarizes current evidence on the interplay between dysglycemia and cancer and explores how integrating continuous glucose monitoring (CGM)-based strategies into multidisciplinary oncology care may improve both metabolic and oncologic outcomes. A comprehensive search of online databases, including PubMed, ISI Web of Science, and Scopus, was conducted to identify studies assessing the impact of glycemic disturbances and glycemic control on cancer outcomes. Poor glycemic control and increased glucose variability are associated with worse oncologic outcomes, higher rates of treatment-related complications, reduced adherence to therapy, and diminished efficacy of chemotherapy, targeted agents, and immune checkpoint inhibitors. Severe hypoglycemia has also emerged as an independent predictor of poor prognosis. Although HbA1c has long been the cornerstone of glycemic assessment, it incompletely captures the dynamic glucose fluctuations commonly observed during cancer therapy. CGM provides a more comprehensive and clinically meaningful assessment of glycemic control, with the potential to reduce hypoglycemia, improve glycemic stability, and enhance tolerance and adherence to anticancer treatments. Current evidence indicates that diabetes and dysglycemia are key modifiers of cancer risk, progression, treatment tolerance, and survival. Optimizing glycemic control may therefore contribute to improved cancer outcomes. CGM represents a promising tool for personalizing diabetes management in oncology settings.
2026
antidiabetic drugs; cancer; continuous glucose monitoring; diabetes; dysglycemia; hyperglycemia; prognosis; survival
01 Pubblicazione su rivista::01a Articolo in rivista
Diabetes and cancer. Glucose control impact on survival and tumor outcomes / Ruggeri, R.M., Grossrubatscher, E.M., Arrivi, G., Ciocca, E., Filice, A., Golisano, B., Mazzilli, R., Prinzi, N., Colao, A., Faggiano, A.. - In: REVIEWS IN ENDOCRINE AND METABOLIC DISORDERS. - ISSN 1573-2606. - (2026). [10.1007/s11154-026-10040-x]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1769420
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