---
title: "New Treatment Turns Cancer Genes Into “Eat Me” Signs For Immune System"
description: "Scientists at UCSF say they've developed a new treatment that causes cancer cells to rat on themselves, allowing the immune system to easily kill them."
date: "2022-09-16"
modified: "2022-09-16"
authors:
  - name: "Frank Landymore"
    job_title: "Contributing Writer"
    link: "https://futurism.com/authors/flandymore"
url: "https://futurism.com/neoscope/treatment-cancer-immunotherapy"
categories:
  - "Cancer"
  - "Genetics"
  - "Health & Medicine"
  - "Medical"
  - "Treatments"
tags:
  - "cancer"
  - "cancer treatments"
  - "immunotherapy"
  - "tumors"
---

# New Treatment Turns Cancer Genes Into “Eat Me” Signs For Immune System

![Scientists at UCSF say they've developed a new treatment that causes cancer cells to rat on themselves, allowing the immune system to easily kill them.](<https://futurism.com/wp-content/uploads/2022/09/treatment-cancer-genes-eat-me-signs.jpg>)
*\<em\>Image: Getty Images\</em\>*

If our immune system could easily detect cancer cells, it could supercharge [new treatments for the disease](<https://futurism.com/neoscope/treatment-immunotherapy-cancer-remission>). What if a drug could cause cancer cells to reveal themselves to the immune system, which could then target and kill them?

That's essentially the approach that a burgeoning form of cancer treatment — yet to be tested in humans — is adopting, as described in a new study [published](<https://www.cell.com/cancer-cell/fulltext/S1535-6108(22)00318-X>) in the peer-reviewed publication *Cancer Cell* on Monday.

In a nutshell, the treatment works by drawing a protein of the cancer causing KRAS gene, which is believed to be responsible for a full quarter of all tumors, to the cancer cell’s surface. From there, the treatment turns the now-surfaced protein into a giant "eat me" signal to the body’s immune system, in the words of the study's [press release](<https://www.ucsf.edu/news/2022/09/423661/drug-turns-cancer-gene-eat-me-flag-immune-system>).

"The immune system already has the potential to recognize mutated KRAS, but it usually can’t find it very well," said study co-author Kevin Shokat, a UCSF chemist, in the release. "When we put this marker on the protein, it becomes much easier for the immune system."

It sounds like a simple and logical premise, but it’s one that doctors have struggled to put into practice.

The problem is that it’s very hard for drugs to bind to a mutated, cancer-causing KRAS protein’s surface — and that’s assuming you can even reach the protein, because most of them reside inside the cell, where it avoids detection from the body’s immune system.

Thanks, in part, to Shokat’s research into KRAS over the years, scientists have been able to develop drugs, such as sotorasib (aka [Lumakras](<https://www.reuters.com/business/healthcare-pharmaceuticals/amgen-says-lumakras-cuts-risk-lung-cancer-progression-by-34-2022-09-11/>)), that help block KRAS’s tumor-growing effects. But to really weed out and kill KRAS cells, the researchers turned to another drug: ARS1620.

In the *Cancer Cell* study, the researchers found that ARS1620 not only bound to KRAS proteins and blocked their tumorous effects, but also drew them to the cell’s surface. Better yet, when bound together, the drug-KRAS complex they formed alerted the body’s immune system to come get rid of the cell they're located on.

"This mutated protein is usually flying under the radar because it’s so similar to the healthy protein," said Charles Craik, one of the study's authors and a professor of pharmaceutical chemistry at UCSF, in the same release. "But when you attach this drug to it, it gets spotted right away."

From there, the researchers say they were able to develop a new form of immunotherapy that incites the immune system to recognize and target cancerous KRAS that are bound to ARS1620. The study even found that the treatment works on KRAS cells that were already resistant to the drug.

It’s a promising development, but a lot more work needs to be done before the treatment graduates to human testing. Still, Craik remains optimistic.

"This is a platform technology," said Craik. "We’d like to go after other targets that might also move molecules to the cell surface and make them amenable to immunotherapy."

**More on cancer:** [*Young People Are Getting Way More Cancer Than Old People Did*](<https://futurism.com/neoscope/young-people-cancer-health-medical>)

## Author
At Futurism, my work has often centered on bringing a sense of clarity and insight to complex topics ranging from the regulation of emerging technologies to the esoteric ideologies of Silicon Valley executives, while striving not to lose the poetic sense of awe inspired by often-obscure fields like astrophysics and quantum computing. I broke the story of CNET using AI to produce articles that turned out to be riddled with factual errors and plagiarism — a dam-breaking inflection point, as I've reported, that's inspired copycats and endless discourse while beguiling stakeholders ranging from tech giants to purveyors of spam around the web. My work at Futurism has been cited by publications including CBS News, the Los Angeles Times, Vice, Gizmodo, Engadget, the Verge, and Vanity Fair. I grew up in locales ranging from India to China, and now live in the exotic suburbs of Virginia. In my free time, I'm an avid reader of weird sci-fi literature, an aficionado of East Asian cinema, and, regrettably, a relapsed gamer. Allegedly, I’m working on a debut novel, currently untitled.

### Author social links  
[Bluesky](<https://bsky.app/profile/f-w-l.bsky.social>)