Researchers at the University of Texas have identified a link between bacteria that produce lactic acid inside tumors and a reduced response to radiation therapy in cervical cancer. The findings, reported in Cancer Cell, shed light on how the tumor microenvironment may influence treatment outcomes and point toward new strategies to improve radiosensitivity.
Cervical cancer, most commonly caused by human papillomavirus infection, often responds to standard treatments. Yet a subset of patients experiences tumor persistence or progression despite chemoradiotherapy. In this study, scientists examined the bacterial communities residing within cervical cancer tumors from 101 patients who underwent chemoradiotherapy between September 2015 and March 2022, aiming to understand how microbial factors might shape treatment response.
The team identified a specific bacterium, Lactobacillus descenders, associated with poorer responses to radiation and shorter survival. The critical mechanism appears to involve the bacterium’s production of L-lactate, a compound derived from lactic acid. Cancer cells can adapt by using lactate as an energy source to mitigate radiation-induced damage, rather than relying solely on glucose. This metabolic shift may help tumor cells survive after radiation therapy.
Previous research has linked tumor lactate production to more aggressive disease and worse prognoses across multiple cancer types. Building on these observations, the authors are pursuing approaches to disrupt these bacteria directly within tumors. By modulating the intratumoral microbial ecosystem, they hope to enhance the effectiveness of radiotherapy and potentially improve survival for patients with cervical cancer.
In parallel, the study touches on broader implications for cancer treatment, where bacterial metabolites in the tumor environment could either hinder or boost response to various therapies. Ongoing work seeks to identify safe interventions that selectively target lactate-producing bacteria or interrupt the metabolic pathways that support tumor resilience after radiation. The ultimate goal is to translate these insights into clinical strategies that complement existing cervical cancer therapies.
As researchers continue to map the interactions between tumor microbes and cancer cell metabolism, findings like these emphasize the importance of considering the tumor microbiome in treatment planning. The evolving field may yield diagnostic markers to predict radiosensitivity and open avenues for combination therapies that improve patient outcomes across diverse cancer types.
Notably, this line of inquiry aligns with a broader effort to personalize cancer care by integrating microbial, metabolic, and genomic data into decision making. If validated in larger studies, strategies targeting intratumoral bacteria could become part of a multi-pronged approach to overcoming radioresistance and extending survival for individuals facing cervical cancer.