Hepatocellular carcinoma with progenitor cell features distinguishable by the hepatic stem/progenitor cell marker NCAM

2011 ◽  
Vol 309 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Atsunori Tsuchiya ◽  
Hiroteru Kamimura ◽  
Yasushi Tamura ◽  
Masaaki Takamura ◽  
Satoshi Yamagiwa ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Progenitor Cell ◽  
Cell Marker

scholarly journals EpCAM- and/or NCAM-Expressing Hepatocellular Carcinoma in Which Behavior of Hepatic Progenitor Cell Marker-Positive Cells Are Followed

2019 ◽  
Vol 13 (1) ◽  
pp. 118-124 ◽  
Author(s):  
Atsunori Tsuchiya ◽  
Takeshi Suda ◽  
Chiyumi Oda ◽  
Atsushi Kimura ◽  
Kazunori Hosaka ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Cells ◽  
Vascular Invasion ◽  
Progenitor Cell ◽  
Cell Marker ◽  
Hepatic Progenitor Cell ◽  
Invasion And Metastasis ◽  
Metastatic Lesions ◽  
Important Target ◽  
Hepatocellular Carcinomas

Hepatic progenitor cell (HPC) marker-positive hepatocellular carcinomas (HCCs) have recently been extensively analyzed, and their prognosis has been reported as poor compared to HPC marker-negative HCCs. However, previous studies have analyzed the existence of HPC marker-positive cancer cells only in primary lesions, as well as the recurrence rate and prognosis of such tumors. Here, we are the first to report the behavior of HPC marker-positive cancer cells during vascular invasion and metastasis of an HCC. We concurrently analyzed EpCAM- and/or NCAM-expressing cancer cells in the primary, vascular invasion, and metastatic lesions of an HCC. An HCC which includes EpCAM- and/or NCAM-expressing cancer cells has not been previously reported. EpCAM- and/or NCAM-positive cancer cells invaded the vessels and formed heterogeneous populations of these HPC marker-positive cancer cells with HPC marker-negative cancer cells. The frequency of HPC marker-positive cancer colonies and cells in vessels was higher than that in the primary HCC. In the metastatic lesions, EpCAM-positive cancer cells were more frequently detected than NCAM-positive cancer cells, indicating that EpCAM may be more important than NCAM for cancer cell settlement in the metastatic lesions. Furthermore, bigger metastatic tumors tended to include HPC marker-positive cancer cells, suggesting that HPC marker-positive cancer cells have a growth advantage in the metastatic lesions. These results showed that HPC marker-positive cancer cells would be important for vascular invasion and metastasis and suggested that HPC marker-positive cancer cells are an important target in HCC treatment.

P0327 : Analysis of hepatic progenitor cell marker positive hepatocellular carcinoma and their prognostic significance

2015 ◽  
Vol 62 ◽  
pp. S431-S432
Author(s):  
A. Tsuchiya ◽  
Y. Kojima ◽  
S. Seino ◽  
Y. Watanabe ◽  
M. Nomoto ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Progenitor Cell ◽  
Prognostic Significance ◽  
Cell Marker ◽  
Hepatic Progenitor Cell

MRI features of hepatocellular carcinoma expressing progenitor cell markers

2011 ◽  
pp. n/a-n/a
Author(s):  
Hyeon Tae Jeong ◽  
Myeong-Jin Kim ◽  
Yeo-Eun Kim ◽  
Young Nyun Park ◽  
Gi Hong Choi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Progenitor Cell ◽  
Cell Markers ◽  
Mri Features

Cancer stem cell marker expression in hepatocellular carcinoma and liver metastases is not sufficient as single prognostic parameter

2009 ◽  
Vol 275 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Alexei V. Salnikov ◽  
Grace Kusumawidjaja ◽  
Vanessa Rausch ◽  
Helge Bruns ◽  
Wolfgang Gross ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Liver Metastases ◽  
Stem Cell Marker ◽  
Cancer Stem Cell Marker ◽  
Cell Marker ◽  
Prognostic Parameter ◽  
Marker Expression

scholarly journals SOX9 is a novel cancer stem cell marker surrogated by osteopontin in human hepatocellular carcinoma

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Takayuki Kawai ◽  
Kentaro Yasuchika ◽  
Takamichi Ishii ◽  
Yuya Miyauchi ◽  
Hidenobu Kojima ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Human Hepatocellular Carcinoma ◽  
Stem Cell Marker ◽  
Cancer Stem Cell Marker ◽  
Cell Marker

scholarly journals Activation of Hepatic Stem Cell Marker EpCAM by Wnt–β-Catenin Signaling in Hepatocellular Carcinoma

2007 ◽  
Vol 67 (22) ◽  
pp. 10831-10839 ◽  
Author(s):  
Taro Yamashita ◽  
Anuradha Budhu ◽  
Marshonna Forgues ◽  
Xin Wei Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cell ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Hepatic Stem Cell

Increased Activity of Aldehyde Dehydrogenase, a Stem/Progenitor Cell Marker, in Chronic Lymphocytic Leukemia,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3867-3867
Author(s):  
Raymond P. Wu ◽  
Christina C.N. Wu ◽  
Tomoko Hayashi ◽  
Laura Z. Rassenti ◽  
Thomas J. Kipps ◽  
...  
Keyword(s):  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Board Of Directors ◽  
Research Funding ◽  
Progenitor Cell ◽  
Lymphocytic Leukemia ◽  
Cell Marker ◽  
Aldh Activity ◽  
Advisory Committees ◽  
Aldefluor Assay

Abstract Abstract 3867 Introduction: Despite their mature appearance, the B cells from chronic lymphocytic leukemia (CLL) possess immature characteristics both functionally and biochemically. CLL B cells display known biochemical markers characteristic of cells early in the blood lineage, including ROR1, Wnt16, and LEF1. In addition, CLL B cells have higher levels of Reactive Oxygen Species (ROS) and of the oxidant-induced transcription factor Nrf2 [NFE2L2], compared to normal peripheral blood mononuclear cells (PBMC). Intracellular ROS status has been suggested to be a marker of cancer stem/progenitor cells possibly due to their high expression of oncogenes. Downstream targets of Nrf2 include the Aldehyde dehydrogenase [ALDH] enzymes, which are believed to play a crucial role in stem cell biology because they protect the cells against oxidative stress caused by accumulation of aldehydes. Here, we use ALDH activity to visualize populations of CLL B cells that may have stem/progenitor properties. Materials and Methods: Isolated PBMC from normal donors and CLL patients with aggressive and indolent disease were stained for ALDH activity with an Aldefluor assay kit (StemCell Technologies). The ALDH inhibitor, diethylaminobenzaldehyde (DEAB), was used to confirm that the fluorescent activity was due to ALDH activity. At the end of the Aldefluor assay, the cells were stained for cell surface markers, CD19, CD5, CD38 and CD34. 50,000 total events were collected for FACS analysis. Normalized Mean Fluorescence Intensity (MFI) values were calculated by dividing each MFI value to average MFI value of normal CD19+ cells for each experiment. Data analyses were performed by FlowJo software and Prizm. P-values were calculated by One-Way ANOVA analysis with Post-Bonferroni's multiple comparison test. Results: We examine the level of ALDH expression and activity in CD19+ cells of healthy donors (n = 9), CLL samples that expressed unmutated IgVH and that were ZAP-70 positive (defined as “aggressive”, n = 14) or samples that expressed mutated IgVH and were ZAP-70 negative (defined as “indolent”, n=12). CLL B cells from patients with aggressive disease had significantly higher ALDH activities compared to normal B cells (p < 0.001) and indolent CLL B cells (p < 0.05) (Figure1). Indolent CLL B cells also have higher level of ALDH activities compared to normal B cells (p < 0.01) (Figure1). Treatment with the ALDH inhibitor, DEAB, suppressed the increased fluorescence observed in CLL B cells. In addition, ALDH high CLL B cells are CD34 negative. These data show that CLL B cells express a marker known to be associated with stem/progenitor cells, but these populations are different from CD34 positive hematopoietic stem cells. In addition, our data show that a stem/progenitor cell marker is associated with the pathogenesis of CLL. Disclosures: Kipps: Igenica: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Research Funding; Abbot Industries: Research Funding; Pharmacyclics: Membership on an entity's Board of Directors or advisory committees; Genentech: Research Funding; GSK: Research Funding; Gilead Sciences: Consultancy, Research Funding; Amgen: Research Funding.

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