Histopathological evidence of neoplastic progression of von Meyenburg complex to intrahepatic cholangiocarcinoma

Amarpreet Bhalla, Steven A. Mann, Shaoxiong Chen, Oscar Cummings, Jingmei Lin

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Von Meyenburg complex (VMC) is generally thought to be benign, although its preneoplastic potential for intrahepatic cholangiocarcinoma (iCC) has been a subject of contention. We retrospectively reviewed 86 hepatectomy specimens with a diagnosis of iCC. Morphologically, an association between iCC and VMC was appreciated in 35% of cases that illustrated a gradual neoplastic progression from benign VMC to dysplasia and then to iCC. Among them, 24 cases had VMC lined by epithelial cells with low-grade biliary dysplasia and 13 with high-grade biliary dysplasia. VMC-associated iCCs were smaller in size and well to moderately differentiated, with features of anastomosing glandular architecture, ductal carcinoma in situ–like growth pattern, peritumoral lymphocytic infiltrate, central fibrous scar, and complete pushing border. They often presented as T1 tumors. In contrast, non–VMC-associated iCCs were moderately to poorly differentiated with solid, cribriform or papillary growth patterns. They likely exhibited necrosis, perineural invasion, positive surgical margin, lymphovascular invasion, and high T stage. Additionally, Ki67 and p53 immunostains support the continuing neoplastic evolution from benign VMC to dysplasia and then to iCC. VMC could become neoplastic, serving as an in situ carcinoma lesion to transform to iCC. The underlying molecular alteration and clinical implication of this neoplastic transformation deserves further investigation.

Original languageEnglish (US)
Pages (from-to)217-224
Number of pages8
JournalHuman Pathology
Volume67
DOIs
StatePublished - Sep 1 2017

Fingerprint

Cholangiocarcinoma
Ductal Carcinoma
Carcinoma in Situ
Hepatectomy
Growth
Cicatrix
Necrosis
Epithelial Cells
Neoplasms

Keywords

  • Carcinogenesis
  • Intrahepatic cholangiocarcinoma
  • Ki67
  • Liver
  • p53
  • Von Meyenburg complex

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Histopathological evidence of neoplastic progression of von Meyenburg complex to intrahepatic cholangiocarcinoma. / Bhalla, Amarpreet; Mann, Steven A.; Chen, Shaoxiong; Cummings, Oscar; Lin, Jingmei.

In: Human Pathology, Vol. 67, 01.09.2017, p. 217-224.

Research output: Contribution to journalArticle

@article{4c6a21250d6c49feba478545b5768e74,
title = "Histopathological evidence of neoplastic progression of von Meyenburg complex to intrahepatic cholangiocarcinoma",
abstract = "Von Meyenburg complex (VMC) is generally thought to be benign, although its preneoplastic potential for intrahepatic cholangiocarcinoma (iCC) has been a subject of contention. We retrospectively reviewed 86 hepatectomy specimens with a diagnosis of iCC. Morphologically, an association between iCC and VMC was appreciated in 35{\%} of cases that illustrated a gradual neoplastic progression from benign VMC to dysplasia and then to iCC. Among them, 24 cases had VMC lined by epithelial cells with low-grade biliary dysplasia and 13 with high-grade biliary dysplasia. VMC-associated iCCs were smaller in size and well to moderately differentiated, with features of anastomosing glandular architecture, ductal carcinoma in situ–like growth pattern, peritumoral lymphocytic infiltrate, central fibrous scar, and complete pushing border. They often presented as T1 tumors. In contrast, non–VMC-associated iCCs were moderately to poorly differentiated with solid, cribriform or papillary growth patterns. They likely exhibited necrosis, perineural invasion, positive surgical margin, lymphovascular invasion, and high T stage. Additionally, Ki67 and p53 immunostains support the continuing neoplastic evolution from benign VMC to dysplasia and then to iCC. VMC could become neoplastic, serving as an in situ carcinoma lesion to transform to iCC. The underlying molecular alteration and clinical implication of this neoplastic transformation deserves further investigation.",
keywords = "Carcinogenesis, Intrahepatic cholangiocarcinoma, Ki67, Liver, p53, Von Meyenburg complex",
author = "Amarpreet Bhalla and Mann, {Steven A.} and Shaoxiong Chen and Oscar Cummings and Jingmei Lin",
year = "2017",
month = "9",
day = "1",
doi = "10.1016/j.humpath.2017.08.004",
language = "English (US)",
volume = "67",
pages = "217--224",
journal = "Human Pathology",
issn = "0046-8177",
publisher = "W.B. Saunders Ltd",

}

TY - JOUR

T1 - Histopathological evidence of neoplastic progression of von Meyenburg complex to intrahepatic cholangiocarcinoma

AU - Bhalla, Amarpreet

AU - Mann, Steven A.

AU - Chen, Shaoxiong

AU - Cummings, Oscar

AU - Lin, Jingmei

PY - 2017/9/1

Y1 - 2017/9/1

N2 - Von Meyenburg complex (VMC) is generally thought to be benign, although its preneoplastic potential for intrahepatic cholangiocarcinoma (iCC) has been a subject of contention. We retrospectively reviewed 86 hepatectomy specimens with a diagnosis of iCC. Morphologically, an association between iCC and VMC was appreciated in 35% of cases that illustrated a gradual neoplastic progression from benign VMC to dysplasia and then to iCC. Among them, 24 cases had VMC lined by epithelial cells with low-grade biliary dysplasia and 13 with high-grade biliary dysplasia. VMC-associated iCCs were smaller in size and well to moderately differentiated, with features of anastomosing glandular architecture, ductal carcinoma in situ–like growth pattern, peritumoral lymphocytic infiltrate, central fibrous scar, and complete pushing border. They often presented as T1 tumors. In contrast, non–VMC-associated iCCs were moderately to poorly differentiated with solid, cribriform or papillary growth patterns. They likely exhibited necrosis, perineural invasion, positive surgical margin, lymphovascular invasion, and high T stage. Additionally, Ki67 and p53 immunostains support the continuing neoplastic evolution from benign VMC to dysplasia and then to iCC. VMC could become neoplastic, serving as an in situ carcinoma lesion to transform to iCC. The underlying molecular alteration and clinical implication of this neoplastic transformation deserves further investigation.

AB - Von Meyenburg complex (VMC) is generally thought to be benign, although its preneoplastic potential for intrahepatic cholangiocarcinoma (iCC) has been a subject of contention. We retrospectively reviewed 86 hepatectomy specimens with a diagnosis of iCC. Morphologically, an association between iCC and VMC was appreciated in 35% of cases that illustrated a gradual neoplastic progression from benign VMC to dysplasia and then to iCC. Among them, 24 cases had VMC lined by epithelial cells with low-grade biliary dysplasia and 13 with high-grade biliary dysplasia. VMC-associated iCCs were smaller in size and well to moderately differentiated, with features of anastomosing glandular architecture, ductal carcinoma in situ–like growth pattern, peritumoral lymphocytic infiltrate, central fibrous scar, and complete pushing border. They often presented as T1 tumors. In contrast, non–VMC-associated iCCs were moderately to poorly differentiated with solid, cribriform or papillary growth patterns. They likely exhibited necrosis, perineural invasion, positive surgical margin, lymphovascular invasion, and high T stage. Additionally, Ki67 and p53 immunostains support the continuing neoplastic evolution from benign VMC to dysplasia and then to iCC. VMC could become neoplastic, serving as an in situ carcinoma lesion to transform to iCC. The underlying molecular alteration and clinical implication of this neoplastic transformation deserves further investigation.

KW - Carcinogenesis

KW - Intrahepatic cholangiocarcinoma

KW - Ki67

KW - Liver

KW - p53

KW - Von Meyenburg complex

UR - http://www.scopus.com/inward/record.url?scp=85029543934&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85029543934&partnerID=8YFLogxK

U2 - 10.1016/j.humpath.2017.08.004

DO - 10.1016/j.humpath.2017.08.004

M3 - Article

VL - 67

SP - 217

EP - 224

JO - Human Pathology

JF - Human Pathology

SN - 0046-8177

ER -