Pancreatic cancer rewrites its DNA to evade treatment, study finds

Overview

Updated 1 hour ago

Pancreatic cancer kills about 85 percent of patients within five years of diagnosis. A new study tracing 443,451 individual cancer cells from 62 tumors shows part of the reason: the cancer continually reshapes its genetic makeup, spawning cell populations that resist treatment and spread.

Researchers at NYU Langone Health and UC San Diego found that blocking a gene called MYC pushed aggressive cancer cells back to a milder state and made them visible to immune cells. Clinical trials of drugs that inhibit MYC or a second gene, TIGIT, are already underway.

Why it matters

If MYC or TIGIT inhibitors work in trials, doctors gain a new weapon against a cancer that kills 85 percent of patients within five years.

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Key Indicators

443,451

Individual cells analyzed

Single-cell transcriptomics from 62 pancreatic tumors, the largest such study of its kind.

Tumors sampled

From 56 patients with pancreatic ductal adenocarcinoma; six gave samples before and after chemotherapy.

85%

Five-year mortality

Share of pancreatic ductal adenocarcinoma patients who die within five years of diagnosis.

2–11

Clones per tumor

Distinct cancer cell populations found in individual tumors, with differing behavior.

Voices

Curated perspectives — historical figures and your fellow readers.

Ever wondered what historical figures would say about today's headlines?

People Involved

Aristotelis Tsirigos

Senior study investigator, Perlmutter Cancer Center, NYU Langone Health

Quoted on clinical trials of MYC and TIGIT inhibitors already underway

Organizations Involved

NYU Langone Health / Perlmutter Cancer Center

Academic medical center and cancer center

Lead institution on the study

Led the single-cell analysis of 443,451 pancreatic cancer cells from 62 tumors at its Perlmutter Cancer Center.

UC San Diego Moores Cancer Center

National Cancer Institute-designated cancer center

Co-led the study with NYU

Co-led the study, analyzing how cancer cell clones evolve to resist treatment and spread.

Timeline

2 events Latest: Today

October 2026
Findings announced publicly
Today Announcement

NYU and UC San Diego announce that blocking MYC reverted aggressive pancreatic cancer cells and that MYC and TIGIT inhibitors are in clinical trials.
Today
Study published in Nature Genetics
Publication

NYU Langone and UC San Diego researchers publish a single-cell analysis of 443,451 pancreatic cancer cells from 62 tumors.
October 13th, 2026

Scenarios

MYC inhibitors show benefit in pancreatic cancer trials

Possible Resolves by End of 2028

Discussed by: Researchers at NYU Langone and UC San Diego; companies running MYC inhibitor trials

Clinical trials targeting MYC are already underway for pancreatic ductal adenocarcinoma. If blocking MYC reverts aggressive cells in humans as it did in lab experiments, treatment could push cancer toward a less dangerous state and expose it to immune attack. Early results would need to show a survival benefit to change practice.

TIGIT emerges as an immunotherapy target for pancreatic cancer

Possible Resolves by End of 2028

Discussed by: Immunotherapy researchers; developers of TIGIT inhibitors

The study found elevated TIGIT gene activity in cancer cells that evade immune detection, while PD1 activity dropped. That combination may explain why PD-1 immunotherapies fail against pancreatic cancer. TIGIT inhibitors, already in clinical trials, could offer an alternative or complementary approach if the mechanism holds in patients.

Findings deepen understanding but produce no new treatment

Possible Resolves by End of 2030

Discussed by: Observers who note that many lab discoveries fail to translate into approved drugs

Most promising lab findings do not survive clinical translation. If MYC or TIGIT inhibitors prove toxic, ineffective, or too narrow in humans, the study's value would be limited to a sharper understanding of how pancreatic tumors evolve and resist treatment.

Historical Context

2 moments from history that rhyme with this story — and how they unfolded.

1987 to 1998

HER2 and Herceptin (1987–1998)

In 1987, Dennis Slamon and colleagues found that about a quarter of breast cancer tumors carry extra copies of the HER2 gene, which drives aggressive growth. Within a decade, the antibody drug trastuzumab, sold as Herceptin, was targeting that gene in patients.

Then

Herceptin reached the U.S. market in 1998 and improved survival for HER2-positive breast cancer patients.

Now

It established the model of finding a genetic driver and building a therapy around it, changing how cancer drugs are developed.

Why this matters now

Like HER2, MYC is a genetic driver in a subset of cancers. The new study suggests blocking MYC could similarly reshape treatment for pancreatic cancer.

2011 to 2018

Checkpoint inhibitors and the 2018 Nobel (2011–2018)

James Allison and Tasuku Honjo won the 2018 Nobel Prize in Physiology or Medicine for discovering that blocking CTLA-4 and PD-1 proteins unleashes the immune system against tumors. Their work led to drugs like ipilimumab and pembrolizumab that transformed treatment of melanoma and lung cancer.

Then

Checkpoint inhibitors became standard treatments and extended survival for patients with several cancers.

Now

They exposed how tumors suppress immune responses, but pancreatic cancer has largely resisted these drugs.

Why this matters now

The new study's finding that PD1 activity drops while TIGIT rises in pancreatic clones may explain that resistance and point to an alternative target.