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Sampling several regions of metastatic pancreatic cancers showed that squamous-looking areas are the tissue form of the basal-like gene signature, usually a subclone inside an otherwise classical tumour, and that such cancers carry chromatin-gene mutations and uneven MYC gain.
Evolutionary analysis and expression profiling were integrated in multiregion-sampled metastatic pancreatic cancers. Squamous features were the histological correlate of the RNA-seq-defined basal-like subtype. In patients with coexisting basal-squamous and classical-glandular morphology, phylogenetics showed squamous morphology as a subclonal population within an otherwise classical tumour. Cancers with squamous features were more likely to have clonal mutations in chromatin modifiers, intercellular heterogeneity for MYC amplification and entosis.
It joins the pathology (adenosquamous), the transcriptome (basal-like) and the genome (KDM6A, MYC) into one account of the chemotherapy-resistant subtype, and shows a single biopsy can miss it.
Shares KDM6A, MYC, MYC, Pancreatic ductal adenocarcinoma.
Shares Clonal evolution & minimal residual disease, Memorial Sloan Kettering Cancer Center, Metastatic pancreatic ductal adenocarcinoma, Pancreatic ductal adenocarcinoma.
Shares Clonal evolution & minimal residual disease, Memorial Sloan Kettering Cancer Center, Pancreatic ductal adenocarcinoma.
Shares MYC, MYC, Pancreatic ductal adenocarcinoma.
Shares MYC, MYC, Memorial Sloan Kettering Cancer Center.
Shares Clonal evolution & minimal residual disease, Metastatic pancreatic ductal adenocarcinoma, Pancreatic ductal adenocarcinoma.
Shares MYC, MYC, Memorial Sloan Kettering Cancer Center.
Shares Memorial Sloan Kettering Cancer Center, Metastatic pancreatic ductal adenocarcinoma, Pancreatic ductal adenocarcinoma.