Publication: Distribution of dysplasia and cancer in the gallbladder: an analysis from a high cancer-risk population
Program
KU-Authors
KU Authors
Co-Authors
Koshiol, Jill
Bellolio, Enrique
Vivallo, Carolina
Cook, Paz
Carlos Roa, Juan
McGee, Emma E.
Losada, Hector
Van Dyke, Alison L.
Van De Wyngard, Vanessa
Prado, Rodrigo
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Abstract
Gallbladder dysplasia can progress to cancer and may be associated with increased cancer risk at other biliary tract sites. Thus, its accurate identification is relevant both for etiologic understanding and for clinical purposes. Data on the frequency and distribution of gallbladder dysplasia are lacking owing to limited gallbladder sampling and inability to visualize dysplasia grossly. An expert pathology group used consensus criteria to review 140 totally sampled consecutive cholecystectomy specimens from Chilean women. Three cases (2%) revealed incidental invasive carcinoma, all T2, along with high-grade dysplasia (HGD). The surface areas covered by dysplasia or cancer in these cases were 9%, 37%, and 87%. Although the first longitudinal ("diagnostic") section of the whole gallbladder captured HGD or cancer in all 3 cases, the deepest focus of invasive carcinoma was not present in this section. Fourteen additional cases (10%) had low-grade dysplasia (LGD), which was typically very focal (covering <5% of the surface) and most often occurred in the fundus. LGD was not present in the diagnostic section of 5 cases (38%) and would have been missed without additional sampling. None of the cancers or dysplasias were grossly visible. Although HGD and carcinoma are likely to be identified in "diagnostic" sections, accurate staging requires total sampling. LGD is typically very focal and would often be missed in routine practice. To identify cancer precursors, additional sampling, particularly of the fundus, may be warranted. The predominance of LGD in the fundus also provides etiologic insight, supporting the contribution of gallstones and chronic inflammation.
Source
Publisher
Elsevier
Subject
Pathology
Citation
Has Part
Source
Human Pathology
Book Series Title
Edition
DOI
10.1016/j.humpath.2018.07.015