NYU pancreatic cancer research has mapped 443,451 individual cells from 62 tumors, revealing genetically distinct cancer cell populations within the same tissue. Published in Nature Genetics on October 13, 2026, the study links MYC-related genetic changes to shifts in tumor cell states and examines how those differences relate to immune activity.
Key Takeaways
- NYU Langone Health researchers analyzed 443,451 individual cells from 62 pancreatic tumors collected from 56 patients
- The study identified genetically distinct cancer cell populations coexisting within individual tumors
- MYC gene changes were associated with shifts toward more aggressive molecular characteristics and reduced immune-response activity
- Researchers used spatial transcriptomics to examine 11 tumors and compared samples collected before and after chemotherapy from six patients
- The findings provide evidence about tumor biology but do not establish a new treatment or improved patient outcomes
NYU Langone Health researchers have identified genetic differences among cancer cells within individual pancreatic tumors, offering new evidence about how the disease changes at the cellular level.
The study, conducted through NYU Langone Health and its Perlmutter Cancer Center, found that genetically distinct groups of cells can coexist within a single tumor. Some displayed molecular characteristics associated with more aggressive disease, while others showed different patterns of gene activity.
Researchers also identified changes involving the MYC gene that were associated with shifts between cancer cell states. These findings may help explain aspects of pancreatic tumor development and immune activity, although their clinical significance requires additional investigation.
The analysis focused on pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer. The disease is known for its complex tumor biology and limited responses to certain treatments.
NYU Pancreatic Cancer Research Identifies Distinct Tumor Cell Groups
The research examined how cancer cells within the same pancreatic tumor can differ genetically and biologically. Rather than treating each tumor as a uniform collection of cells, investigators studied individual cell populations to identify patterns associated with disease progression.
Researchers analyzed 443,451 cells from 62 tumors collected from 56 patients with pancreatic ductal adenocarcinoma. They used single-cell RNA sequencing, a method that measures gene activity in individual cells instead of averaging signals across an entire tissue sample.
This approach allowed the team to distinguish genetically related groups of malignant cells, known as clones. These groups shared certain characteristics but differed in molecular activity, suggesting that multiple biological states can exist within the same tumor.
Unlike methods that analyze large groups of cells together, single-cell immune profiling methods can help researchers distinguish cellular populations based on differences in gene activity. Such techniques provide additional detail about cells that might otherwise appear similar in combined measurements.
According to NYU Langone Health, the analysis found multiple clones within individual tumors, including populations associated with classical and basal cancer cell states. These two states have previously been used to describe differences in pancreatic cancer biology.
The findings suggest that a single tumor classification may overlook smaller cell populations with distinct characteristics. Genetic differences between these populations could contribute to variations in tumor behavior, although the study doesn’t establish that every tumor follows the same pattern.
The researchers also examined tumor samples collected before and after chemotherapy from six patients. These paired samples provided an opportunity to compare cellular characteristics at different treatment stages.
However, the limited number of paired samples means the findings cannot establish how frequently particular genetic changes occur during chemotherapy. The comparisons contribute to understanding tumor diversity without demonstrating a consistent treatment-response pattern across patients.
The team also used spatial transcriptomics to analyze 11 tumors, covering 53,236 spatial measurement spots. This technique preserves information about where gene activity occurs within tissue, helping researchers examine relationships between cancer cells and their surroundings.
Combining the two approaches allowed investigators to compare genetic characteristics with spatial organization. The results showed that different cell populations could carry distinct molecular signals while occupying different areas of the tumor environment.
MYC Gene Changes Were Linked to More Aggressive Cancer Cell States
One of the study’s central findings involved MYC, a gene associated with cell growth and other biological processes.
Previous pancreatic cancer research has commonly described two major cell states, classical and basal. Classical cells generally display molecular features associated with less aggressive disease, while basal cells are linked to more aggressive tumor characteristics.
The new analysis suggested that these states may change within genetically related cancer cell populations. Researchers identified patterns indicating that some cells could shift from classical characteristics toward basal features as tumors evolve.
A specific finding involved increased copies of DNA in a region of chromosome 8 containing MYC. The researchers found that this genetic alteration was associated with classical-to-basal transitions more frequently than expected by chance.
By examining relationships among genetically distinct clones, the team identified patterns connecting MYC-related changes with differences in cell behavior. These findings suggest that variations in MYC activity may contribute to how certain pancreatic cancer cells acquire more aggressive molecular characteristics.
The researchers conducted additional experiments using mouse models and primary human cancer cell models. When MYC activity was reduced in selected basal-like cells, the cells showed a return of gene-expression patterns associated with the classical state.
The experiments also identified changes in immune-response pathways. This observation supported a possible relationship between MYC activity, cancer cell identity, and how tumor cells interact with surrounding immune cells.
Previous pancreatic cancer treatment research has also examined experimental approaches in laboratory models, where findings must be distinguished from demonstrated clinical benefits. The NYU experiments similarly investigated biological mechanisms rather than testing a treatment in patients.
Despoina Kalfakakou, PhD, a postdoctoral research fellow at NYU Grossman School of Medicine and the study’s lead investigator, addressed the potential significance of the findings in NYU Langone Health’s public announcement.
“These findings suggest that targeting the mechanisms underlying tumor evolution, including MYC, may help restrain the cancer’s rapid progression,” Kalfakakou said.
The statement identifies a possible direction for investigation rather than an established treatment strategy. The study did not test whether a MYC-targeting medicine improves survival or reduces tumor growth in patients.
Aristotelis Tsirigos, PhD, a professor in the Departments of Medicine and Pathology at NYU Grossman School of Medicine, served as a co-senior investigator.
The broader research team included collaborators from the University of California San Diego and Oregon Health & Science University. Their work examined how genetic variation, changing cell states, and interactions with surrounding tissue contribute to pancreatic tumor biology.
Immune Activity and Tumor Location Reveal Additional Differences
The researchers also investigated how genetically distinct pancreatic cancer cells interact with the surrounding tumor environment.
Pancreatic tumors contain immune cells, connective tissue, and other cellular components that influence their biological characteristics. The research identified differences in molecular communication between cancer cell populations and neighboring cells.
These differences included changes in genes associated with immune regulation. According to NYU Langone Health, some cancer cell clones displayed increased TIGIT-related activity, while PD1 gene activity was reduced in the same populations.
TIGIT and PD1 are associated with pathways that regulate immune responses. Differences in their activity may help researchers investigate why certain pancreatic tumors show limited responses to immune-based treatments.
However, the study did not establish that these specific molecular patterns directly determine an individual patient’s response to immunotherapy.
Some immunotherapies work by interfering with signals that limit immune-cell activity. The molecular findings may provide additional context for studying these pathways in pancreatic cancer, although they do not establish new criteria for selecting patients for treatment.
The spatial analysis provided another perspective on tumor behavior. Researchers identified dispersed cancer cell populations with molecular features associated with cell movement and reduced immune-response activity.
Some of these populations also showed characteristics associated with metastatic potential and involvement of lymph node regions. The findings were based on molecular and spatial observations rather than direct predictions of disease spread in individual patients.
By combining cell-level genetic data with information about tissue location, the team examined how different tumor populations may interact with their surroundings. The study suggests that genetic differences among clones are associated with changes in both tumor cell behavior and the local immune environment.
The research primarily examined tumor samples and experimental models rather than testing treatments in patients. It did not report a randomized treatment comparison, a new drug approval, or evidence that modifying MYC activity improves patient survival.
The study received funding support from National Institutes of Health grants and the Sky Foundation. Its findings appeared in the peer-reviewed journal Nature Genetics under the title “Clonal heterogeneity in human pancreatic ductal adenocarcinoma and its impact on tumor progression.”
The NYU pancreatic cancer research provides detailed evidence of differences among genetically related cancer cell populations, including changes involving MYC and immune-response activity. The study did not determine whether these molecular patterns can reliably predict treatment outcomes in individual patients.
Frequently Asked Questions
What did the NYU pancreatic cancer research discover?
The NYU pancreatic cancer research identified genetically distinct cancer cell populations within individual pancreatic tumors. The study linked changes involving the MYC gene to shifts in tumor cell states and associated differences in immune-response activity.
How many pancreatic cancer cells were analyzed?
Researchers analyzed 443,451 individual cells from 62 pancreatic tumors collected from 56 patients. The study also included spatial analysis of 11 tumors and paired samples collected before and after chemotherapy from six patients.
What role does the MYC gene play in the findings?
The researchers found that DNA changes involving MYC were associated with shifts toward basal-like cancer cell characteristics. Experiments in research models suggested that reducing MYC activity could alter these molecular patterns, although patient treatment benefits weren’t established.
Does the study establish a new pancreatic cancer treatment?
The study does not establish a new treatment or demonstrate improved clinical outcomes. Its findings concern genetic variation, cancer cell behavior, and immune-related molecular activity, with treatment implications remaining under investigation.
Disclaimer: This article is for informational purposes only and is based on publicly available scientific research. The findings discussed do not establish a new pancreatic cancer treatment or demonstrate improved patient outcomes. The information should not be considered medical advice or a substitute for professional diagnosis, treatment, or consultation with a qualified healthcare provider.
