scholarly journals KIAA1114, a full-length protein encoded by the trophinin gene, is a novel surface marker for isolating tumor-initiating cells of multiple hepatocellular carcinoma subtypes

Oncotarget ◽  
2014 ◽  
Vol 5 (5) ◽  
pp. 1226-1240 ◽  
Author(s):  
Sae Won Kim ◽  
Hyun Gul Yang ◽  
Moon Cheol Kang ◽  
Seungwon Lee ◽  
Hong Namkoong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Surface Marker ◽  
Full Length ◽  
Tumor Initiating Cells ◽  
Multiple Hepatocellular Carcinoma

Aberrant β-catenin activity in hepatoid adenocarcinoma of the stomach

2020 ◽  
Vol 20 ◽  
Author(s):  
Nan Wang ◽  
Rui Kong ◽  
Wei Han ◽  
Jie Lu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Pearson Correlation ◽  
Clinicopathological Characteristics ◽  
Cancer Tissue ◽  
Hepatoid Adenocarcinoma ◽  
Tumor Initiating Cells ◽  
Significant Difference ◽  
Diagnostic Confusion ◽  
Hematoxylin And Eosin ◽  
Cancer Tissues

Background: Hepatoid adenocarcinoma of the stomach (HAS) has been recognized as a rare primary gastric tumor characterized by hepatocellular carcinoma-like histology. HAS often causes diagnostic confusion with conventional gastric adenocarcinoma (CGA) due to the difficulty to detect hepatoid differentiation solely based on findings from hematoxylin and eosin (H&E) staining. Hence, HAS should be distinguished from solid-type CGA based on their different biological behaviors. β-catenin is highly expressed in hepatocellular carcinoma (HCC), which is involved in the maintenance of tumor initiating cells, drug resistance, tumor progression, and metastasis. Methods and Results: Given the dearth of HAS cases, systematic examination of the expression of β-catenin in HAS remains under-explored. In this study, 14 cases were subjected to immunostaining with with AFP, β-catenin, glypican3, hepar-1 and CerbB-2. In parallel, the clinicopathological characteristics of these patients were collected. We detected statistically significant difference in the expression of β-catenin (P = 0.000), glypican3 (P = 0.019), and hepar-1 (P = 0.007) between HAS cancer tissues and the adjacent non-cancerous tissues. Furthermore, a significant correlation was observed between the expression of β-catenin in HAS cancer tissue and adjacent tissue (Pearson correlation coefficient: 0.686, P = 0.007). Moreover, in cancer tissues, a significant correlation was observed between the expression of β-catenin and survival time (Spearman correlationcoefficient= - 0.482, P = 0.003). However, we found the expression of β-catenin did not correlate with the degree of tumor differentiation and tumor size, age, gender, serum AFP levels, microinvasion, and metastasis (P > 0.05). Conclusion: Our findings establish β-catenin as a useful marker that can distinguish HAS from CGA and may improve the early diagnosis to guide the appropriate and timely treatment of HAS patients.

Identification of tumor-initiating cells in a canine hepatocellular carcinoma cell line

2014 ◽  
Vol 96 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Masaki Michishita ◽  
Shiori Ezaki ◽  
Kikumi Ogihara ◽  
Yuko Naya ◽  
Daigo Azakami ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Tumor Initiating Cells ◽  
Hepatocellular Carcinoma Cell Line ◽  
Hepatocellular Carcinoma Cell

scholarly journals Genetic and epigenetic characteristics of human multiple hepatocellular carcinoma

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Kazuya Taniguchi ◽  
Terumasa Yamada ◽  
Yo Sasaki ◽  
Kikuya Kato
Keyword(s):  
Hepatocellular Carcinoma ◽  
Multiple Hepatocellular Carcinoma

scholarly journals Analysis of Diagnostic Imagings and Histologic Features of Multiple Hepatocellular Carcinoma.

1996 ◽  
Vol 29 (7) ◽  
pp. 1623-1628
Author(s):  
Nobuhisa Ando ◽  
Akio Harada ◽  
Motoshi Yasui ◽  
Toshiaki Nonami ◽  
Akimasa Nakao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Multiple Hepatocellular Carcinoma

scholarly journals CD58, a novel surface marker, promotes self-renewal of tumor-initiating cells in colorectal cancer

Oncogene ◽  
2014 ◽  
Vol 34 (12) ◽  
pp. 1520-1531 ◽  
Author(s):  
S Xu ◽  
Z Wen ◽  
Q Jiang ◽  
L Zhu ◽  
S Feng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Surface Marker ◽  
Tumor Initiating Cells ◽  
Self Renewal

Abstract 3535: Identification of multiple hepatocellular carcinoma using genomic approach

2019 ◽  
Author(s):  
Yutaka Midorikawa ◽  
Shogo Yamamoto ◽  
Kenji Tatsuno ◽  
Hiroki Ueda ◽  
Tadatoshi Takayama ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Genomic Approach ◽  
Multiple Hepatocellular Carcinoma

scholarly journals EpCAM and the biology of hepatic stem/progenitor cells

2015 ◽  
Vol 308 (4) ◽  
pp. G233-G250 ◽  
Author(s):  
Laurent Dollé ◽  
Neil D. Theise ◽  
Eva Schmelzer ◽  
Luke Boulter ◽  
Olivier Gires ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adult Stem Cells ◽  
Fetal Liver ◽  
State Regulation ◽  
Full Length ◽  
Migration And Invasion ◽  
Tumor Initiating Cells ◽  
Transmembrane Glycoprotein ◽  
Molecular Events ◽  
Associated Functions

Epithelial cell adhesion molecule (EpCAM) is a transmembrane glycoprotein, which is frequently and highly expressed on carcinomas, tumor-initiating cells, selected tissue progenitors, and embryonic and adult stem cells. During liver development, EpCAM demonstrates a dynamic expression, since it can be detected in fetal liver, including cells of the parenchyma, whereas mature hepatocytes are devoid of EpCAM. Liver regeneration is associated with a population of EpCAM-positive cells within ductular reactions, which gradually lose the expression of EpCAM along with maturation into hepatocytes. EpCAM can be switched on and off through a wide panel of strategies to fine-tune EpCAM-dependent functional and differentiative traits. EpCAM-associated functions relate to cell–cell adhesion, proliferation, maintenance of a pluripotent state, regulation of differentiation, migration, and invasion. These functions can be conferred by the full-length protein and/or EpCAM-derived fragments, which are generated upon regulated intramembrane proteolysis. Control by EpCAM therefore not only depends on the presence of full-length EpCAM at cellular membranes but also on varying rates of the formation of EpCAM-derived fragments that have their own regulatory properties and on changes in the association of EpCAM with interaction partners. Thus spatiotemporal localization of EpCAM in immature liver progenitors, transit-amplifying cells, and mature liver cells will decisively impact the regulation of EpCAM functions and might be one of the triggers that contributes to the adaptive processes in stem/progenitor cell lineages. This review will summarize EpCAM-related molecular events and how they relate to hepatobiliary differentiation and regeneration.

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