Health · Medical Research · 6 hrs ago
Study maps how pancreatic cancer cells change to resist treatment
Researchers from UC San Diego and New York University analyzed 443,451 cells from 62 pancreatic tumors in 59 people with pancreatic ductal adenocarcinoma.
They found that cells within one tumor can form different groups, or clones, with distinct genetic activity.
These clones evolve in different ways, and some changes may help cancer resist treatment or spread.
The findings help explain why this cancer is difficult to treat and why tumors can behave differently.
The study also found that increased activity of the MYC gene was linked to aggressive cancer cells, while blocking MYC shifted cells toward a less aggressive form in experiments.
Some clones had higher TIGIT activity and lower PD-1 activity, which may help explain why PD-1-targeting immunotherapies often have little effect.
The researchers say tumor diversity may offer clues for more precise treatments.
Researchers analyzed 443,451 individual cells from 62 tumors in 59 people with pancreatic ductal adenocarcinoma.
The study found that cancer cell groups within tumors can change genetically in different ways, including developing treatment resistance or the ability to spread.
The findings suggest these genetic changes can help cancer cells shift between less aggressive classical and more aggressive basal forms.
Researchers found that blocking MYC activity shifted cells toward the classical form and exposed them to more immune cells.
The study was led by researchers at UC San Diego Moores Cancer Center and New York University and was published in Nature Genetics.
- Who
- Researchers at UC San Diego Moores Cancer Center and New York University led the study.
- What
- The team analyzed individual cells from pancreatic tumors to study how cancer cells change genetically and evade treatment.
- When
- The study’s publication date is not stated in the article text.
- Where
- The research was led at UC San Diego Moores Cancer Center and New York University. The tumor samples came from people with pancreatic ductal adenocarcinoma; their locations are not stated.
- Why
- Researchers aimed to understand how genetic changes within tumors drive cancer cell evolution, treatment resistance and spread.
This story does not have two clearly opposing sides.
Studies of pancreatic cancer cells in bulk divided them into classical and basal subtypes but did not explain how cells shift between them.
Researchers analyzed 443,451 single cells from 62 tumors in 59 people with pancreatic ductal adenocarcinoma.
Blocking MYC activity shifted cells toward the classical form and exposed them to more immune cells.
- Cells analyzed
- 443,451
- Tumors analyzed
- 62
- People represented
- 59
- Cancer type
- Pancreatic ductal adenocarcinoma
- Journal
- Nature Genetics
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What people are saying
Our work shows that within a single tumor, different clones are evolving in parallel, taking on different identities and interacting with the immune and stromal landscape in distinct ways. That heterogeneity is why the disease is so hard to treat, because every tumor is unique.
Clonal heterogeneity is part of why pancreatic cancer is so difficult to treat, but it also presents us with opportunities to discover more precise and effective therapies.
Our study provides the most granular view to date of pancreatic ductal adenocarcinoma, revealing how ongoing genetic reshaping drives tumor evolution over the course of disease