Sugar and cancer tumour growth: What science shows

Scientists have long known that cancer cells are hungry for glucose, a simple sugar our bodies use for energy. 

So let's keep that in mind: Cancer has a sweet tooth, a scientific fact established about 100 years ago, and known as the "Warburg effect".

But now, new research shows that another sugar — fructose, commonly found in table sugar and high-fructose corn syrup — can also fuel cancer, though not in a direct way.

Fructose is a monosaccharide, also known as a simple sugar.

A study published in Nature and funded by the National Institutes of Health (NIH) reveals that fructose consumption accelerates tumour growth by triggering a form of "indirect cooperation", or "oursourcing", between the liver and cancer cells.

This hidden process is known as also "metabolic cross-talk".

Researchers at Washington University in St. Louis discovered that:

To better understand the process, the researchers used mouse and zebrafish models implanted with human cancers — including skin, breast, and cervical tumours — and fed them high-fructose corn syrups.

The result: their tumours grew significantly faster. 

When liver cells were blocked from processing fructose using an experimental drug, tumour growth slowed down.

Interestingly, the mice did not gain weight or show changes in blood sugar levels — two health markers often associated with fructose intake. This finding was critical, said Dr. Gary Patti, the study’s senior author.

“High-fructose corn syrup is linked to obesity, and obesity is linked to cancer. But in our studies, cancer growth occurred without weight gain or metabolic syndrome. That suggests a different mechanism is at play,” Patti explained.

To dig deeper, the team examined how cancer cells respond to fructose in the lab.

What they found was surprising: the cancer cells weren’t using fructose at all.

The reason? These cells lacked the enzyme KHK (ketohexokinase) — the key molecular tool needed to break down fructose. Without KHK, the cells couldn't process the sugar.

So how were tumours still benefiting from it?

The researchers suspected another player was involved: the liver.

To test this theory, scientists created a co-culture — combining human cancer cells and mouse liver cells in the same lab dish — and fed them fructose.

The results were striking.

While the cancer cells still couldn’t metabolise fructose directly, their growth increased dramatically. The liver cells, rich in KHK, had converted the fructose into a variety of fats known as lipids, which the cancer cells then eagerly absorbed.

One particular type of lipid stood out: LPCs (lysophospholipids).

These molecules are essential building blocks for cell membranes, which surround and protect every cell.

Cancer cells, which divide much more frequently than normal cells, require large amounts of LPCs to build new membranes and sustain their aggressive growth.

By indirectly using fructose — via liver metabolism — cancer cells were essentially outsourcing the hard work to nearby healthy tissue and reaping the benefits.

Metabolic cross-talk is the way different organs and cell types coordinate through shared nutrients, hormones, and signals to regulate metabolism. It’s how your body keeps everything in balance during activities like eating, exercising, or fasting.

In the context of this study:

This concept has been observed before — for example, some pancreatic tumours rely on nearby cells to deliver key nutrients.

The relationship between cancer and sugar has been highlighted by Dr Thomas Seyfried, a professor in the Biology Department at Boston College and a known expert in genetics and biochemistry.

He stated that cancer cells are fermenting, which means they need sugar as fuel. “Cut off their two fermentable fuels - glucose and glutamine - and the cancer cells will die,” said Seyfried. 

No. The study doesn’t say that eating fructose causes cancer. What it does show is that excess fructose can help existing tumours grow — especially when consumed through ultra-processed foods. Importantly, not all fructose is the same. 

According to Dr. Kristine Willis of the National Cancer Institute:

“The sugars in whole fruits and vegetables are metabolised differently than the fructose in junk food. Apples are still healthy—junk food still isn’t.”

Advances in “metabolomics” — the science of tracking nutrients inside the body — helped researchers trace fructose from diet to liver to tumour.

Using mouse models and lab-grown cells, they:

That is the hope.

The fact that blocking KHK in the liver slows down tumour growth opens the door for targeted therapies.

PF-06835919, originally tested for fatty liver disease, may become a candidate for cancer treatment — particularly in patients with high-fructose diets or tumours that rely on this metabolic cross talk.

This study is a breakthrough in understanding how diet and organ interactions can influence cancer.

It highlights: