Study explores insulin resistance link to cancer risk
As the Cancer Center and Research Institute continues to expand its research impact in cancer biology and translational medicine, investigators are advancing the center’s vision of understanding the complex biological links between metabolic diseases and cancer. Recent research from the laboratory of Dr. Jawed Siddiqui, a CCRI faculty member, has shed new light on the relationship between insulin resistance and cancer development. This work, published in the journal Molecular Aspects of Medicine, highlights the growing recognition of metabolic dysfunction as a critical contributor to cancer risk.
The study was conducted by Siddiqui and his research team, including postdoctoral fellow Dr. Mohammad Abdullah Khan and instructor Dr. Gunjan Sharma. Their work explores how insulin resistance may act as a key biological link between metabolic disorders and cancer progression. Researchers are increasingly recognizing a link between diabetes and cancer, but the exact reasons behind this connection are still not fully understood. One major factor appears to be insulin resistance, which sits at the crossroads of metabolism and cancer development. Other contributors — such as high blood sugar, abnormal cholesterol levels, chronic inflammation, hormone imbalances, and changes in the gut microbiome — may also help increase the risk of cancer in people with obesity or diabetes.
Scientists still need to clarify the specific biological pathways that turn long‑term metabolic stress into tumor growth. The picture becomes even more complicated when considering diabetes medications: some seem to lower cancer risk, while others may raise it, though no clear cause‑and‑effect relationship has been proven.
The gut microbiome is another emerging piece of the puzzle. People with diabetes often have fewer beneficial butyrate‑producing bacteria and more inflammatory microbes, such as E. coli and Proteobacteria, which can worsen insulin resistance and inflammation. Certain bacteria — such as Fusobacterium nucleatum — have also been linked to cancers of the colon, gallbladder, and pancreas. What remains unclear is whether these microbes directly cause cancer or simply influence metabolic and inflammatory pathways that increase risk.
To better understand how diabetes severity and duration affect cancer risk, researchers need large, high‑quality, population‑based studies that use biomarkers and advanced tools. This knowledge could support better prevention strategies, earlier cancer screening, and improved treatment for diabetic patients.
Another challenge is that many cancer clinical trials exclude people with diabetes — especially older adults or those with uncontrolled blood sugar and multiple health issues. This limits how well trial results apply to real‑world patients. One promising solution is simulation modeling, which uses clinical data and large datasets to create virtual patient populations. These models can help predict outcomes for groups often left out of traditional trials.
Ultimately, reducing cancer risk in people with diabetes will require community‑level strategies — such as promoting healthy weight, increasing physical activity, and improving early screening and education. At the same time, precision‑medicine approaches using metabolomics, genomics and microbiome profiling may help identify individuals at highest risk and guide more personalized treatments. Together, these efforts could significantly reduce deaths linked to diabetes and cancer.