The study reveals how Gal-1 contributes to liver cancer's resistance to heat-based treatments by promoting energy production through sugar metabolism, helping cancer cells survive thermal stress and grow faster after treatment.

Disrupting Gal-1 functions could open new avenues for enhancing treatment responses across all stages of liver cancer.

This protein's role in enhancing sugar metabolism allows liver cancer cells to survive heat treatment and accelerate tumor growth.

Using genetically modified cell cultures and mouse models, researchers demonstrated that inhibiting Gal-1 reduces cancer cells' energy production and tumor size when combined with thermal ablation.

Patient samples and animal studies confirmed Gal-1's role in supporting cancer cell energy production under thermal stress.

Recurrence at the tumor margins is linked to the reduced heat effectiveness in these areas, with Gal-1 facilitating the survival of resistant cells.

Analysis of biopsy samples from 58 patients showed higher Gal-1 levels in tumors that recurred rapidly post-treatment, indicating a link between Gal-1 overproduction and quick recurrence.

Research from UCLA's Jonsson Comprehensive Cancer Center shows that targeting Galectin-1 (Gal-1) could improve the effectiveness of thermal ablation for early-stage, non-resectable liver cancer and reduce the risk of recurrence.

A combined approach using thermal ablation and the Gal-1 inhibitor OTX008 led to a two-fold reduction in tumor size and decreased energy production in cancer cells in mice.

Dr. Jason Chiang, the senior author of the study, explains that Gal-1 fuels liver cancer cells, allowing them to recover quickly and progress faster after thermal ablation.

Gal-1 boosts the energy production capabilities of hepatocellular carcinoma cells, enabling them to withstand thermal stress and proliferate more rapidly following ablation.

Up to 40% of liver cancer patients experience recurrence after ablation, especially at the tumor edges where heat is less effective; Gal-1 plays a critical role in the survival and regrowth of these peripheral cancer cells.

The Gal-1 inhibitor OTX008 significantly enhances the effects of thermal ablation in experimental models, suggesting it could be a promising new therapeutic strategy.