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Australian-led Methods Toward Relevant Sub-types of Pancreatic Cancer

Two interesting studies with different methods and results have been published this year by international teams as led by Australian researchers with the aim of trying to establish key sub-types of pancreatic cancer (ductal adenocarcinoma of the pancreas) to aid in improved understanding, management and treatment of patients with pancreatic cancer.

The more extensive study included 149 collaborators from Australia, Britain, Europe and the U.S. under the aegis of the Australian Pancreatic Cancer Genome Initiative, who analyzed the genome of 456 separate tumors diagnosed as adenocarcinoma of the pancreas, finding common genetic mutations in 32 genes that were eventually devolved, per the authors’ analyses, into FOUR pancreatic cancer subtypes. This study was published in the March 3rd 2016 issue of the journal Nature.  The four subtypes identified include 1). Squamous, related to mutations in TP53 and KDM6A which appeared to carry a poor pancreatic cancer prognosis, 2). Pancreatic Progenitor Tumors, related to genes found in the early development of pancreatic cancer (FOXA2/3, PDX1, and MNX1), Immunogenic Tumors, related to pancreatic cancer immune suppression, and ADEX Tumors, related to KRAS gene mutation activity in pancreatic cancer. The authors suggest that these sub-types of pancreatic cancer carry different natural histories and vulnerabilities that may allow for more precise and efficacious treatment congruence, as more is learned.

Thirteen international authors (including five from the above discussed study) encompassing Scottish and German researchers, again as led by Australians published an intriguing article in the August 2016 issue of Molecular & Cellular Proteomics (The American Society for Biochemistry and Molecular Biology) that postulates THREE subtypes of pancreatic cancer as identified by using a different method. The authors used mass spectrometry to explicate tyrosine phosphorylation patterns in pancreatic cancer cell lines (ductal adenocarcinoma). They found three distinct patterns that appeared related to characteristics of signaling networks. The authors acknowledge this as a novel taxonomy for pancreatic cancer, but indicate that these results provide insight about how increased understanding of the biology of pancreatic ductal adenocarcinoma may offer distinctions for more tailored treatment and care of pancreatic cancer.

These are two highly interesting research studies that do credit to our colleagues from down under. Further practical extension of this work would seem in order. The age of precision medicine for pancreatic cancer is dawning.

 

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Dale O’Brien, MD