Review
Copyright ©The Author(s) 2019.
World J Gastroenterol. Aug 21, 2019; 25(31): 4343-4359
Published online Aug 21, 2019. doi: 10.3748/wjg.v25.i31.4343
Table 1 Main similarities and differences in terms of embryologic origin and molecular characteristics between biliary and pancreatic neoplastic lesions
Biliary tractPancreasRef.
Embryologic origin of the ductal systemEHBDs and large IHBD from ventral part of foregut; small IHBD from Mesenchymal cells surrounding the septum transversumVentral part of MPD from the ventral part of foregut. Dorsal part of MPD from the dorsal bud that obliterates completely; the ducts of the dorsal bud fuse with the ductal system of the ventral part[1-5]
Niches of Stem/progenitors’ cellsPBGs located in EHBDs and large IHBDs. Canals of HeringPDGs located in MPD and larger interlobular ducts > 300 μm[6-12]
Microscopic (intraepithelial) precursors of cancerBilIN-1 low grade, BilIN-2 intermediate grade, BilIN-3 high gradePanIN low grade, previously -1, -2 PanIN high grade, previously -3[21-26,29,37-39]
Macroscopic (intraductal) precursors of cancerIPNBIPMN[54-62]
Kras role in cancerMutated in 15%-30%Mutated in > 90%[44,123,124,127,129]
p53 role in cancerMutated in 35%-60%Mutated 40%-87%[49,125-129]
SHH role in cancerOverexpressed ~ 50%Overexpressed ~ 70%[159,160]
Mucin expression in biliopancreatic cancersMUC-1+ 45%-70% MUC-4+ 35%-50% (worse prognosis compared to MUC4 negative) MUC5AC+ 30%-60%MUC-1 + ~ 80% MUC-4+ 30%-80% (worse prognosis compared to MUC4 negative) MUC5AC+ 10%-70%[106-122]
S100P expressionupregulated in ~75%upregulated in ~ 90%[42,43,130,131]