Energy Drink Molecule Found to Fuel Deadly Blood Cancers

Scientists have uncovered how blood cancers hijack a surprising nutrient source from their surroundings to fuel their growth. New research published in Nature reveals that aggressive leukemias depend on taurine—a sulfur-containing amino acid commonly found in energy drinks—delivered from specialized bone cells in their environment. This previously unknown cancer-supporting mechanism could lead to novel treatment strategies for difficult-to-treat blood cancers.

The study, led by researchers at the University of Rochester, provides the first evidence that taurine produced by bone marrow cells acts as a critical lifeline for leukemia stem cells—the rare cancer cells that drive disease progression and resist conventional treatments. By blocking this taurine supply line, scientists were able to significantly impair leukemia growth in laboratory models.

But how does an amino acid better known as an energy drink ingredient become entangled in cancer development? And what might this mean for patients with treatment-resistant blood cancers?

Mapping Cancer’s Relationship with Its Environment

Blood cancers like acute myeloid leukemia (AML) grow within the bone marrow, where they interact with various support cells that make up their microenvironment. The research team used sophisticated single-cell analysis techniques to map how these support cells change over time as leukemia progresses.

“While previous studies have described the cellular composition of normal bone marrow niche, their dynamic alterations during leukemia progression remain undefined,” the researchers explain in their study.

Their analysis revealed significant remodeling of the bone marrow environment as leukemia develops, with notable increases in mesenchymal stromal cells (MSCs) and immature bone cells, alongside decreases in certain blood vessel cells. These changing cell populations produce different signals that can either promote or inhibit cancer growth.

Taurine Production Rises During Cancer Progression

Among the most significant findings was that bone marrow MSCs and developing bone cells increase their production of taurine as leukemia progresses. The researchers identified an enzyme called cysteine dioxygenase type 1 (CDO1), which is crucial for taurine synthesis, as being highly expressed in these bone cells.

The team examined matched patient bone marrow samples and discovered a striking pattern: CDO1 levels increased substantially when myelodysplastic syndrome (MDS) transformed into more aggressive AML, and again when AML relapsed after treatment.

These observations suggested that taurine might play a previously unrecognized role in blood cancer development. To test this hypothesis, the researchers conducted a series of experiments that revealed:

• Leukemia bone marrow contains 1.7 times more taurine than normal bone marrow
• Preventing bone cells from producing taurine extended survival in leukemia models by 13.5%
• Adding taurine accelerated disease progression in animal models, making death about three times more likely
• Blocking taurine uptake in leukemia cells dramatically impaired their ability to establish and maintain disease

Leukemia’s Dependency on Taurine Transport

The researchers identified a protein called TAUT (encoded by the SLC6A6 gene) that acts as the door through which taurine enters leukemia cells. This protein is highly expressed in aggressive leukemias compared to normal blood stem cells.

When the researchers genetically removed TAUT from leukemia cells, they observed remarkable results. Animals receiving these modified leukemia cells survived significantly longer—in some experiments, 40% of animals survived indefinitely. The leukemia cells without TAUT showed impaired growth, increased cell death, and signs of cellular differentiation rather than continued stem-like growth.

Most importantly, removing TAUT had minimal effects on normal blood stem cell function, suggesting a potential therapeutic window for targeting this process in patients.

Synergy with Existing Treatments

The research team found that SLC6A6 expression is particularly high in leukemias that are resistant to venetoclax, a medication increasingly used to treat AML. When they combined venetoclax with methods to block taurine uptake, they observed synergistic effects that dramatically reduced leukemia cell growth.

“While primary human AML cells that were treated with GES, TAG or venetoclax alone formed 1.3- to 8.3-fold fewer colonies as compared to the controls, combining the treatments substantially impaired colony formation by 2.4- to 150-fold. These data indicate that taurine inhibitors can synergize with venetoclax in blocking the growth of human AML cells,” the researchers report.

How Taurine Fuels Cancer Growth

Investigating the molecular mechanisms, the researchers discovered that taurine activates mTOR, a master regulator of cell metabolism, which then drives glycolysis—the process cells use to generate energy from glucose. Without taurine, leukemia cells showed dramatic reductions in glycolysis and energy production.

This finding was particularly interesting as cancer cells are known to have unusual metabolic requirements. The study reveals taurine as a previously unknown metabolic controller in leukemia stem cells.

Using metabolic tracers, they confirmed that taurine itself—not a derivative compound—is what’s necessary for leukemia cells to maintain their aggressive growth pattern.

Implications for Patients and Treatment

The discovery that taurine supports leukemia growth raises important questions for patient care. Taurine is present in many energy drinks and is sometimes provided as a supplement to mitigate the side effects of chemotherapy.

“As taurine is a common ingredient in energy drinks, and is often provided as a supplement to mitigate the side-effects of chemotherapy, our work suggests that it may be of interest to carefully consider the benefits of supplemental taurine in patients with leukemia,” the researchers caution.

While the study primarily used genetic approaches to block taurine uptake, the researchers also tested small-molecule inhibitors of TAUT in laboratory models. These compounds impaired leukemia cell growth with minimal effects on normal blood stem cells, suggesting that pharmacological targeting of this pathway could be feasible.

As researchers continue developing more potent inhibitors of taurine transport, this newly discovered dependency could provide a promising avenue for treating aggressive leukemias, potentially in combination with existing therapies like venetoclax. For patients with treatment-resistant blood cancers, these findings offer hope for novel therapeutic approaches that target not just the cancer cells themselves, but the crucial support they receive from their surrounding environment.