Premium
Expression of deleted in malignant brain tumours 1 (DMBT1) relates to the proliferation and malignant transformation of hepatic progenitor cells in hepatitis B virus‐related liver diseases
Author(s) -
Deng Huan,
Gao YaBo,
Wang HuaFeng,
Jin XiaoLong,
Xiao JiaCheng
Publication year - 2012
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2011.04082.x
Subject(s) - progenitor cell , malignant transformation , hepatocellular carcinoma , pathology , cirrhosis , hepatitis b virus , biology , cancer research , hepatitis , hepatitis b , medicine , virus , stem cell , virology , genetics
Deng H, Gao Y‐B, Wang H‐F, Jin X‐L & Xiao J‐C
(2012) Histopathology 60, 249–260
Expression of deleted in malignant brain tumours 1 (DMBT1) relates to the proliferation and malignant transformation of hepatic progenitor cells in hepatitis B virus‐related liver diseases Aims: The molecular mechanisms underlying proliferation and malignant transformation of hepatic progenitor cells (HPCs) remain largely unknown. The purpose of this study was to evaluate the correlation between the expression of deleted in malignant brain tumours 1 (DMBT1) and the biological behaviour of HPCs in different hepatitis B virus (HBV)‐related human liver diseases. Methods and results: Expression of DMBT1 in HPCs was investigated by double immunofluorescence labelling in control‐group and HBV‐related liver diseases, including hepatitis, hepatocellular carcinoma (HCC), non‐tumoral liver tissue away from HCC, non‐tumoral cirrhotic tissue adjacent to HCC, and non‐HCC cirrhosis. DMBT1‐positive HPCs were isolated by laser capture microdissection and subjected to duplex polymerase chain reaction in order to detect homozygous deletion of DMBT1 . The number of DMBT1‐positive HPCs increased in direct proportion to inflammation severity. Loss of heterozygosity for DMBT1 was more frequent in HCC tumour area and non‐tumoral cirrhotic tissue adjacent to HCC, compared with other HBV‐related liver diseases ( P < 0.05). Conclusions: DMBT1 may play an important role in the proliferation of HPCs in HBV‐related liver diseases. Moreover, down‐expression of DMBT1 might enhance the risk of malignant transformation of HPCs.