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Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis (II)

ABSTRACT: Analysis of early changes in the R-H model of carcinogenesis in order to investigate the relationship between oval cell proliferation and preneoplastic foci

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE70321 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA288311

REPOSITORIES: GEO

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Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis (I)

Project description:Analysis of early changes in the R-H model of carcinogenesis in order to investigate the relationship between oval cell proliferation and preneoplastic foci 2 controls, 6 Oval cells, 5 Preneoplastic foci

2016-07-03 | E-GEOD-70320 | biostudies-arrayexpress

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis (II)

2016-07-03 | E-GEOD-70321 | biostudies-arrayexpress

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis (I)

Project description:Analysis of early changes in the R-H model of carcinogenesis in order to investigate the relationship between oval cell proliferation and preneoplastic foci

2016-01-01 | GSE70320 | GEO

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis.

Project description:UnlabelledAlthough the expression of the stem/progenitor cell marker cytokeratin-19 (CK-19) has been associated with the worst clinical prognosis among all HCC subclasses, it is yet unknown whether its presence in HCC is the result of clonal expansion of hepatic progenitor cells (HPCs) or of de-differentiation of mature hepatocytes towards a progenitor-like cell phenotype. We addressed this question by using two rat models of hepatocarcinogenesis: the Resistant-Hepatocyte (R-H) and the Choline-methionine deficient (CMD) models. Our data indicate that the expression of CK-19 is not the result of a clonal expansion of HPCs (oval cells in rodents), but rather of a further step of preneoplastic hepatocytes towards a less differentiated phenotype and a more aggressive behavior. Indeed, although HCCs were positive for CK-19, very early preneoplastic foci (EPFs) were completely negative for this marker. While a few weeks later the vast majority of preneoplastic nodules remained CK-19 negative, a minority became positive, suggesting that CK-19 expression is the result of de-differentiation of a subset of EPFs, rather than a marker of stem/progenitor cells. Moreover, the gene expression profile of CK-19-negative EPFs clustered together with CK-19-positive nodules, but was clearly distinct from CK-19 negative nodules and oval cells.Conclusionsi) CK-19-positive cells are not involved in the early clonal expansion observed in rat hepatocarcinogenesis; ii) CK-19 expression arises in preneoplastic hepatocyte lesions undergoing malignant transformation; iii) CK-19 positivity in HCCs does not necessarily reflect the cell of origin of the tumor, but rather the plasticity of preneoplastic cells during the tumorigenic process.

| S-EPMC4770734 | biostudies-literature

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-01-01 | GSE70322 | GEO

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-03 | E-GEOD-70322 | biostudies-arrayexpress

Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis

Project description:Cytokeratin-19 positivity is acquired along cancer progression and does not predict cell origin in rat hepatocarcinogenesis

| PRJNA288310 | ENA

Genome-wide analysis of different response of hepatocytes and oval cells to hepatitis B virus expression during HBV-related hepatocarcinogenesis

Project description:Analysis of genetic changes of hepatocytes and oval cells induced by HBV. The hypothesis tested in the present study was that hepatic progenitor cells (oval cells) are the founder cells of hepatocellular carcinoma (HCC). Results provide important information of the different responses of hepatocytes and oval cells to HBV expression during HBV-related hepatocarcinogenesis, such as up- or down-regulated oncogenes,tumor suppressor genes and signaling pathways.Results also provide new insights into the biology of human HCC.

2012-07-12 | GSE39289 | GEO

Genome-wide analysis of different response of hepatocytes and oval cells to hepatitis B virus expression during HBV-related hepatocarcinogenesis

2012-07-11 | E-GEOD-39289 | biostudies-arrayexpress

PIK3CA-dependent hepatocarcinogenesis. A microarray comparing PIK3CA E545K and H1047R injected mice compared to age matched controls.

Project description:Gene expression microarray analyses of PIK3CA H1047R and E545K induced preneoplastic lesions and tumors compared to age matched controls. Plasmids expressing oncogenic forms of PIK3CA (H1047R or E545K mutants) were delivered to the mouse liver by tail vein hydrodynamic injection combined with Sleeping Beauty–mediated somatic integration (SBT-HTVI). Resulting preneoplastic and neoplastic lesions were subjected to gene expression microarray analysis. The putative PIK3CA target gene Galectin1 (Gal1) was further characterized by in vitro studies. Transfection of either PIK3CA E545K or H1047R mutants via SBT-HTVI was sufficient to induce hepatocellular carcinomas in mice. A stepwise hepatocarcinogenesis from singular pericentral lipid-rich preneoplastic hepatocytes to clusters, expansive preneoplastic lesions, and HCCs was observed. In PIK3CA H1047R injected mice, HCCs were detected in the 12 months injection group, while PIK3CA E545K injections resulted in tumor occurrence as early as 3 months after SB-HTVI. Histologically, a predominant lipid-rich phenotype characterized all tumorigenesis stages, as confirmed by Sudan III staining and electron microscopy. Immunohistochemically, preneoplastic lesions and tumors displayed high levels of the lipid master regulators Fatty acid synthase and Stearoyl-CoA desaturase-1. Gal1 was commonly overexpressed in PIK3CA-driven preneoplastic and neoplastic liver lesions by gene expression microarray analysis compared with age-matched controls.

2021-05-06 | GSE173963 | GEO

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