A groundbreaking study from the Huntsman Cancer Institute at the University of Utah sheds new light on the intricate relationship between obesity and triple-negative breast cancer, revealing that lipids—the fatty acids often elevated in individuals with obesity—play a crucial role in fueling tumor growth. This investigation, funded by the National Cancer Institute, utilizes preclinical mouse models to demonstrate that it is the surplus of lipids, rather than other typical metabolic markers such as high glucose or insulin, that accelerates cancer progression. These findings challenge prior assumptions in cancer metabolism and open avenues for novel therapeutic strategies aimed at lipid reduction to hinder tumor development.
The research pivots around the concept that cancer cells are, in effect, lipid-addicted. As explained by Dr. Keren Hilgendorf, an assistant professor of biochemistry and Investigator at the Huntsman Cancer Institute, lipids have been underestimated in their role within the obesity-cancer nexus. The study reveals that triple-negative breast cancer cells exploit the abundance of fatty acids circulating in the bloodstream of obese individuals to sustain and propagate their growth. The implication is profound: controlling lipid levels could directly influence tumor aggressiveness.
Hyperlipidemia, characterized by elevated circulating lipids, emerges as a critical metabolic state underlying this phenomenon. Dr. Amandine Chaix, who specializes in nutrition and integrative physiology, explained that lipids are essential components of the cell’s surface membrane, constituting the building blocks necessary for cellular replication. Their presence in high concentrations essentially provides the raw materials needed for cancer cells to proliferate rapidly, reinforcing the concept that lipid abundance directly correlates with tumor acceleration.
The experimental strategy employed involved high-fat diet mouse models alongside genetically engineered mice exhibiting hyperlipidemia independent of other obesity markers like hyperglycemia or hyperinsulinemia. Strikingly, these models demonstrated that elevated lipid profiles alone sufficed to expedite tumor progression. Such a finding suggests that targeting lipid metabolism could be a viable independent therapeutic axis distinct from glucose or insulin signaling interventions.
Furthermore, when lipid levels were experimentally reduced even in the presence of high glucose and insulin, tumor growth significantly decelerated. This impactful observation suggests potential clinical applicability, where lipid-lowering agents, already widely used for cardiovascular indications, might be repurposed to aid breast cancer treatment. The translation of these results from murine models to humans will require extensive validation, but they lay a promising groundwork for future clinical trials.
The study also raises caution regarding dietary recommendations for breast cancer patients with obesity. Popular weight loss strategies, such as ketogenic diets high in fat and low in carbohydrates, may inadvertently exacerbate tumor growth by increasing lipid availability. Dr. Greg Ducker, biochemistry assistant professor and Huntsman investigator, emphasizes that individualized medical guidance is essential before adopting such diets. The complex metabolic landscape in cancer requires a more nuanced understanding than a one-size-fits-all approach.
Currently, obesity is recognized as a significant risk factor for breast cancer incidence and progression, but explicit guidelines on nutritional management remain scarce. These findings suggest that weight loss interventions for breast cancer patients should prioritize lipid management rather than merely caloric restriction or carbohydrate limitation. This paradigm shift could influence oncological dietetics profoundly, promoting lipid lowering as a cornerstone of adjunctive cancer therapy.
Beyond triple-negative breast cancer, the researchers hypothesize that lipid-driven tumor acceleration may extend to other cancer types prevalent among obese individuals, including ovarian and colorectal cancers. This broadens the potential impact of their work and warrants extensive exploration in diverse oncological contexts. Investigating how anti-lipid therapies interact with existing chemotherapy regimens could catalyze synergistic treatment modalities.
The research team is committed to dissecting the cellular mechanisms by which lipids are assimilated and utilized within cancer cells. Understanding these metabolic pathways at a molecular level may unlock additional therapeutic targets, potentially disrupting the lipid supply chain critical to tumor sustenance. Such insight will be paramount for designing interventions with precise metabolic specificity.
While the risks of high-fat diets in obesity-related breast cancer have been illuminated, the investigators note that ketogenic or similar diets might retain therapeutic value in other malignancies. This highlights the cancer-type specificity of metabolic vulnerabilities and underscores the necessity for detailed metabolic profiling in personalized oncology care.
Concluding, this seminal research highlights the pivotal role of lipids in obesity-accelerated triple-negative breast cancer growth and challenges the oncology community to rethink metabolic influences beyond glucose-centric paradigms. If validated clinically, lipid modulation could become a transformative adjunct to conventional breast cancer treatments, improving outcomes for patients burdened with obesity.
Their findings were recently published in the journal Cancer & Metabolism, authored by Renan Vieira and colleagues, underscoring the collaboration between metabolic science and cancer biology at the forefront of contemporary research. Supported by multiple grants from the National Cancer Institute and the Huntsman Cancer Foundation, this work exemplifies the interdisciplinary approach driving innovations in cancer therapeutics and prevention.
Subject of Research: The role of hyperlipidemia in driving tumor growth in obesity-associated triple-negative breast cancer
Article Title: Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth
News Publication Date: 28-Aug-2025
Web References:
DOI link to article
Cancer & Metabolism Journal
References:
Chaix, A., Hilgendorf, K., Ducker, G., et al. (2025). Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth. Cancer & Metabolism. DOI: 10.1186/s40170-025-00407-0.
Image Credits: University of Utah Health
Keywords: Breast cancer, Obesity, Lipid metabolism, Hyperlipidemia, Triple-negative breast cancer, Cancer metabolism, Ketogenic diet, Tumor growth, Metabolic therapy, Obesity-associated cancers, Lipid-lowering drugs, Animal models
Tags: cancer metabolism researchfatty acids and tumor growthhigh-fat diets and cancerHuntsman Cancer Institute Researchhyperlipidemia and cancerlipid metabolism in cancerNational Cancer Institute fundingobesity and cancer progressionobesity-related breast cancer riskpreclinical mouse models in cancer studytherapeutic strategies for lipid reductiontriple-negative breast cancer study
