Table 2.
Classification based on molecular techniques | ||||||
---|---|---|---|---|---|---|
Collision et al42 | Waddell et al44 | Moffitt et al45 | Bailey et al43 | |||
Year | 2011 | 2015 | 2015 | 2016 | ||
Number of samples | 27+34 | 142 | 357 | 456 | ||
Sample type | Patient derived (27), cell lines (34) | Primary resected tumors | Primary, metastatic, cell lines, and normal tissue | Primary resected tumors | ||
Methods, techniques | Gene expressions microarray | WGS and CNV | Virtual microdissection, microarrays, and RNAseq | Integrated genomic analysis | ||
Subtypes identified | 1. Classical 2. Quasi-mesenchymal 3. Exocrine-like |
1. Stable 2. Locally rearranged 3. Scattered 4. Unstable |
Tumor: 1. Classical 2. Basal-like |
Stroma: 1. Normal 2. Activated |
1. Squamous 2. Pancreatic progenitor 3. Immunogenic 4. ADEX |
|
Comparison of these subtypes | ||||||
Collision et al42 | Waddell et al44 | Moffitt et al45 | Bailey et al43 | |||
Subtypes | Classical | Stable | Classical | Pancreatic progenitor | ||
Quasi-mesenchymal | Unstable | Basal-like | Squamous | |||
Exocrine-like | ADEX | |||||
Locally rearranged | ||||||
Scattered | ||||||
Immunogenic |
Notes: Overview of comprehensive pancreatic ductal adenocarcinoma studies.42–45 Detailed investigation of familial pancreatic carcinoma revealed that in families with documented BRCA1 or BRCA2 mutations, the mean age of pancreatic cancer diagnosis was significantly lower, suggesting that mutations of BRCA1 and BRCA2 are genetic factors for early onset of pancreatic cancer. Interestingly, in one of the pancreatic ductal adenocarcinoma subtypes defined by Waddell et al44 (unstable), loss of BRCA1 and/or BRCA2 was frequently observed. Overlap of pancreatic ductal adenocarcinoma subtypes based on whole-genome and whole-exome studies.42–45
Abbreviations: ADEX, aberrantly differentiated endocrine exocrine; CNV, copy number variations; WGS, whole genome sequencing.