{"slug":"pancreatic-molecular","tag":"pancreatic-molecular","variants":["pancreatic-molecular"],"description":"No description yet","count":7,"kinds":{"term":7},"related":[],"records":[{"id":"gata6-classical-basal-marker","kind":"term","name":"GATA6 as the marker of classical versus basal-like pancreatic cancer","route":"/terms/gata6-classical-basal-marker/","tldr":"GATA6 is the transcription factor that separates the two pancreatic cancer subtypes that survive every re-analysis: classical tumours express it, basal-like (squamous) tumours have lost it. A GATA6 stain on a biopsy can therefore call the subtype that predicts how a tumour answers first-line chemotherapy, although no guideline yet acts on the result."},{"id":"kras-allelic-imbalance","kind":"term","name":"KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer","route":"/terms/kras-allelic-imbalance/","tldr":"Beyond which KRAS mutation a pancreatic tumour carries, how many copies of the mutant allele it has matters: tumours that lose the normal copy or gain extra mutant copies behave more aggressively and lean towards the basal-like subtype, which is one reason two tumours with the same KRAS mutation can look and behave differently."},{"id":"caf-subtypes-pancreatic","kind":"term","name":"Fibroblast subtypes in the pancreatic cancer stroma (myCAF, iCAF and apCAF)","route":"/terms/caf-subtypes-pancreatic/","tldr":"The fibroblasts that make up most of a pancreatic tumour are not one cell type. Those pressed against the cancer cells become contractile myofibroblasts (myCAF), those further away secrete inflammatory signals (iCAF), and a third group carries antigen-presenting molecules (apCAF). The states are plastic, which is why stripping the stroma out failed and reprogramming it is the current idea."},{"id":"compass-study-pancreatic","kind":"term","name":"COMPASS: real-time sequencing of advanced pancreatic cancer for treatment selection","route":"/terms/compass-study-pancreatic/","tldr":"COMPASS was the Canadian study that took a fresh biopsy from people about to start chemotherapy for advanced pancreatic cancer, sequenced the whole genome and RNA within the time of a treatment decision, and showed that the basal-like subtype predicts poor response to first-line chemotherapy."},{"id":"caps-consortium-pancreatic-screening","kind":"term","name":"CAPS: the Cancer of the Pancreas Screening consortium and its surveillance studies (CAPS1 to CAPS5)","route":"/terms/caps-consortium-pancreatic-screening/","tldr":"CAPS is the Johns Hopkins-led programme that has followed people at high inherited risk of pancreatic cancer with yearly endoscopic ultrasound and MRI since the late 1990s, and the consortium whose consensus statements set who should be watched and how. Its cohorts are the evidence that surveillance finds most cancers at stage I."},{"id":"detect-a-study","kind":"term","name":"DETECT-A: a blood test plus PET-CT to screen 10,006 women with no symptoms","route":"/terms/detect-a-study/","tldr":"DETECT-A was the first prospective study to give a multi-cancer blood test to people with no symptoms and act on the result: 10,006 women had the test, positives were confirmed by PET-CT, and 26 cancers were found by the blood test, with about 1% of women sent for imaging that found nothing and 0.22% having an invasive procedure that was not needed."},{"id":"ccga-study","kind":"term","name":"CCGA: the Circulating Cell-free Genome Atlas behind the Galleri methylation test","route":"/terms/ccga-study/","tldr":"CCGA is the case-control programme of about 15,000 people that trained and validated the Galleri blood test, which reads methylation patterns on cell-free DNA to say whether a cancer signal is present and where it comes from. Its third sub-study set the figures still quoted: very few false positives, but only about one in six stage I cancers detected."}]}