Scientists at The University of Texas MD Anderson Cancer Center have developed an antibody-toxin conjugate (ATC) that doesn’t just kill tumors—it forces the immune system to do it instead. Published in Nature Cancer, their approach could offer longer-lasting protection against recurrence.

Antibody-drug conjugates (ADCs) have been oncology’s golden child for years. The idea is beautifully simple: attach a toxic drug to an antibody that targets cancer cells, deliver the payload with precision, and kill the tumor while sparing healthy tissue. But in practice? Not so simple. ADCs don’t always finish the job, and resistant cancer cells often return stronger than before.

This new ATC, however, flips the script. Instead of relying on direct destruction, it hijacks the immune system—essentially tricking it into seeing tumors as a real threat. If it works, this could mean more durable treatments, fewer side effects, and fewer chances for cancer to slip away and return later.

Why ADCs Aren’t the Perfect Cancer Killers

Let’s start with the basics. ADCs have a modular design—one part binds to a tumor-specific protein, the other part delivers a toxic payload. They’ve been an exciting development, but they share a fundamental problem with conventional chemotherapy: they rely on direct tumor cell destruction.

And tumors don’t like to go down easily.

"ADCs destroy tumor cells, but often incompletely, leading to resistance and recurrence," explains Dr. Wen Jiang, associate professor of Radiation Oncology at MD Anderson and senior author of the study.

His team decided to take a different approach. Instead of fighting cancer cells directly, they engineered a way to expose them, forcing the immune system to launch an attack.

How the ATC Exposes Tumors to the Immune System

Most solid tumors have a trick up their sleeve: they express CD47, a protein that acts as a "don’t eat me" signal to immune cells, allowing cancer to hide in plain sight.

MD Anderson’s new ATC exploits this weakness in two ways:

1. Targeting CD47. The ATC binds to CD47, tagging the cancer cell for destruction.
2. Delivering a bacterial toxin instead of chemotherapy. This toxin doesn’t kill the cell outright—instead, it hacks the immune cell’s internal processes, causing it to leak intact tumor fragments.

These escaped tumor fragments act as cellular “wanted posters”, training the immune system to recognize and attack the cancer on its own. It’s a clever biological trick—borrowed straight from bacteria.

"Bacteria have evolved mechanisms to escape from immune cells while keeping the host alive," says Jiang. "We’re using that same strategy to shuttle tumor material into immune cells and teach the body to better recognize cancer."

The Immune System Learns—and Remembers

Preclinical models of breast cancer and melanoma showed promising results. Not only did immune cells eliminate tumors across the body, but T cells generated through the process remained active for over two months. That’s a strong indicator of immune memory, which could reduce the risk of recurrence.

Dr. Benjamin Schrank, a radiation oncology resident and first author of the study, sees this as a new frontier in cancer treatment:

"We want to train the immune system so it keeps fighting cancer even after the treatment is done."

It’s a radically different strategy: Instead of endlessly designing new drugs to kill tumors, why not just get the immune system to do it?

Pairing With Radiation for a One-Two Punch

This method could also work alongside traditional treatments, particularly radiation therapy. Many tumors react to radiation by upregulating CD47, a last-ditch survival move that actually makes them even more vulnerable to the ATC.

"This immune-stimulating ATC concept extends beyond CD47," says Dr. Betty Kim, professor of Neurosurgery and co-lead of the study. "We’re already working on ATCs that target other tumor-specific receptors."

Their goal? A platform technology that can be adapted to a wide range of cancers.

What’s Next?

The research team hopes to begin clinical testing within the next three to five years. Of course, that’s assuming it survives the brutal transition from lab studies to human trials. Many promising therapies have failed at that hurdle before.

But if this holds up, it could represent a seismic shift in how we treat cancer—not just killing tumors but forcing the immune system to do what it should have been doing all along.