---
title: A High-Fat Diet Switched On a Pathway That Helps Colon Cancer Reach the Liver in Mice
description: A Science study in mice found dietary fat raised ceramides that switch on a repair program helping colorectal cancer seed the liver.
author: Dr Marina Nani (Editor-in-Chief)
date: 2026-09-24T23:54:20.560Z
updated: 2026-09-24T23:54:20.566Z
canonical: https://richhealthmagazine.com/article/high-fat-diet-colon-cancer-liver-spread-mice
image: https://cdn.nanimediahouse.com/pexels-friends-sharing-a-meal-of-hamburgers-and-fries-dipping-in-sa-14836694.jpg
categories: Longevity & Science
content_type: News
region: Global
publication: Rich Health Magazine
schema_type: Article
---

In mice with colorectal cancer, a high-fat diet raised levels of a fat molecule that pushes some cancer cells into a tissue-repair state, and those cells went on to seed tumors in the liver, researchers at Albert Einstein College of Medicine and MIT reported today in the journal Science. The liver is the organ colorectal cancer most often spreads to, and the spread of cancer beyond its first tumor causes most cancer deaths.

The results come mostly from mice, backed by a pattern in human tumor data, and the researchers say they do not yet translate into dietary advice for people who have already been diagnosed. The team did not test any change of diet in people. For people, the established guidance comes from the American Cancer Society, which counts excess body weight as a risk factor for [both developing and dying from colorectal cancer](https://www.cancer.org/cancer/types/colon-rectal-cancer/causes-risks-prevention/risk-factors.html), with a stronger link in men, and says getting to and staying at a healthy weight may help lower that risk.

[The study](https://montefioreeinstein.org/news/2026/09/24/study-reveals-how-dietary-fat-may-help-colorectal-cancer-spread) was led by Swagata Goswami, an assistant professor of molecular pharmacology at Albert Einstein College of Medicine and the Montefiore Einstein Comprehensive Cancer Center. It began during her postdoctoral training in the MIT lab of Omer Yilmaz, a biology professor and director of the MIT Stem Cell Initiative, who is a co-author.

The research looks at how colorectal cancer spreads, not at why more younger adults are developing it. US cases are rising 3% a year among people aged 20 to 49 and falling 2.5% a year among those 65 and older, [according to the American Cancer Society](https://www.cancer.org/research/acs-research-news/colorectal-cancer-drops-in-older-adults-and-rises-in-young-ones.html), which estimates 158,850 new diagnoses and 55,230 deaths in 2026. Half of people diagnosed before 50 are aged 45 to 49, the age range in which people at average risk are eligible for screening.

## Ceramides From a High-Fat Diet Switched On a Repair Program in Cancer Stem Cells

Ceramides are a type of fat found naturally in the body's cells. In several mouse models of colorectal cancer, a high-fat diet increased ceramide production. The extra ceramide turned on YAP (also known as YAP1), a protein that controls cell growth and tissue repair, and the number of cancer stem cells linked to spread went up.

"Cancer stem cells are a small group of cells within a tumor that can renew themselves, produce other cancer cells, and shift from one cellular state to another," Goswami said. "We found that some colorectal cancer stem cells activate a program normally used to repair the intestinal lining. In cancer cells, however, this regenerative program enhances their ability to form tumors elsewhere in the body."

When the researchers genetically blocked ceramide production, YAP activity dropped, fewer cells entered the repair state and the mice developed fewer liver metastases, while the primary tumors stayed the same size. Stopping cancer cells from breaking ceramides down had the opposite result, with more YAP activity and more spread. In a separate experiment, repair-state cells transplanted into mice produced no bigger primary tumors than other cancer cells but seeded substantially more liver tumors, and removing them from established tumors greatly reduced spread to the liver.

"These findings suggest that the ability to form metastases reflects a change in the state of some cancer stem cells rather than simply faster or more aggressive growth of the original tumor," Goswami said.

## Tumors From Heavier Patients Showed Stronger YAP1 Gene Activity

In human tumor data, [the MIT team found](https://news.mit.edu/2026/biologists-identify-cellular-pathway-allows-colorectal-cancer-metastasize-0924) that genes switched on by YAP1 were more active in patients with a higher BMI than in normal-weight patients, and that patients with higher levels of those genes had lower survival rates. Among patients whose cancer had spread to the liver, genes tied to the repair state were more active in tumors from people with obesity than in tumors from leaner patients, the Einstein release says.

"We don't think that the YAP1 program is specific to obesity. It's just that it becomes accentuated in obesity, and that may account for why obesity is known to drive the progression of colorectal cancer," Yilmaz said.

## The Team Plans Drugs Against Two Enzymes That Make Ceramides

"If we shut down the enzymes that make ceramides, tumor cells can't switch on this regenerative program, and they largely fail to seed metastases in the liver," Yilmaz said.

The researchers plan to develop drugs that block DEGS1 and DEGS2, two enzymes involved in making ceramides. Any such drug will have to be highly selective, they caution, because the same fats are essential in healthy tissue.

In the US, colon cancer is usually diagnosed at stage 2 or 3, before it has spread to distant organs, but up to a third of those patients later relapse with metastatic disease even after successful surgery, the MIT team says. Goswami said blocking ceramide production, inhibiting YAP and removing repair-state cells from primary tumors are all possible ways to prevent or limit that spread, and could be used alongside treatments that remove the original tumor.

## FAQ

**Q: What stage is colon cancer once it has spread to the liver?**
Colon cancer that has reached a distant organ such as the liver or lung is stage IV, according to the American Cancer Society. Stage IVA means spread to one distant organ or one distant set of lymph nodes and IVB to more than one, in both cases without reaching distant parts of the peritoneum, the lining of the abdominal cavity. Spread to the peritoneum is stage IVC.

**Q: How often are younger adults diagnosed before colorectal cancer spreads?**
Not often. The American Cancer Society says about 3 in 4 adults under 50 with colorectal cancer are diagnosed at an advanced stage, either regional or distant, and about 1 in 4 (27%) at the distant stage.

**Q: Which groups are seeing early-onset colorectal cancer rise fastest?**
Among adults diagnosed before age 50, the American Cancer Society reports incidence rising in every racial and ethnic group: 4% a year in the Hispanic population; 3% a year in the Asian American and Native Hawaiian and Pacific Islander, American Indian and Alaska Native, and White populations; and 2% a year in Black people.