Bottom Line: Bacterial load was significantly higher in
pancreatic tumor samples from patients with pancreatic ductal adenocarcinoma compared with pancreatic tissue from normal individuals, and in studies using mice, eliminating certain «bad» bacteria slowed the growth of pancreatic cancer, reversed immune suppression, and upregulated the immune checkpoint protein PD1.
The team is now working to create a repository of
pancreatic tumor samples, coordinating with the National Cancer Institute.
Not exact matches
To better understand the formation of metastases in
pancreatic cancer, Christine Iacobuzio - Donahue, M.D., Ph.D., professor of pathology at Memorial Sloan Kettering Cancer Center, collected
tumor samples from eight patients with the most common form of
pancreatic cancer (
pancreatic ductal adenocarcinoma) immediately after their deaths.
A multicenter team of researchers reports that a full genomic analysis of
tumor samples from a small number of people who died of
pancreatic cancer suggests that chemical changes to DNA that do not affect the DNA sequence itself yet control how it operates confer survival advantages on subsets of
pancreatic cancer cells.
In this study,
samples were taken from patients»
tumors during surgery and transplanted into mice to grow new
pancreatic cancer
tumors.
Guided by a camera and the ultrasound probe, Waxman carefully positioned the endoscope over the
tumor and passed a fine needle into the
pancreatic lesion to
sample tissue cells for biopsy.
The researchers looked exclusively at small segments of DNA called promoters in
samples of
tumors taken from 308
pancreatic cancer patients.
In the first set of experiments, the Johns Hopkins scientists sequenced nearly all protein - encoding genes in 10 of the 68
samples of
pancreatic neuroendocrine
tumors and compared these sequences with normal DNA from each patient to identify
tumor - specific changes or mutations.