Hepatic neoplasia: reflections and ruminations

Aterman, K.

doi:10.1007/bf00203732

Cited by 7 publications

(3 citation statements)

References 223 publications

(191 reference statements)

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“…Interestingly, some cells were rich in AFP granules in cytoplasm, increased in size, and existed with c-Myc-positive cells (Figure 3B), which was most likely hepatocytes in premalignant transformation [20, 21]. Furthermore, transcription factor octamer-binding transcription factor (Oct)-4 co-expressed with ALB in cytoplasm (Figure 3C).…”

Section: Resultsmentioning

confidence: 99%

Premalignant alteration assessment in liver-like tissue derived from embryonic stem cells by aristolochic acid I exposure

Jin

Zhu

et al. 2016

Oncotarget

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The in vitro predictive evaluation of chemical carcinogenicity based on hepatic premalignance has so far not been established. Here, we report a novel approach to investigate the premalignant events triggered by human carcinogen aristolochic acid I (AAI) in the liver-like tissue derived from mouse embryonic stem cells. By AAI exposure, the liver-like tissue exhibited the paracrine interleukin-6 phenotypic characteristics. Hepatocytes expressed STAT3/p-STAT3, c-Myc and Lin28B in parallel. Some of them displayed the dedifferentiation characteristics, such as full of α-fetoprotein granules, increase in size, and nucleocytoplasmic shuttle of Oct4. When these cells were injected into mice, the xenografts mostly displayed the uniform area of hepatic-like tissue with malignant nuclei. The hepatic malignant markers, α-fetoprotein, cytokeratin 7 and cytokeratin 19, were co-expressed in albumin-positive areas, respectively. In conclusion, we established an approach to predict the hepatic premalignance triggered by carcinogen AAI. This premalignant assay system might aid to evaluate the effects of potential carcinogens in liver, and probably to screen the protecting against hepatocarcinogenic efficacy of pharmaceuticals in vitro.

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Section: Resultsmentioning

confidence: 99%

Premalignant alteration assessment in liver-like tissue derived from embryonic stem cells by aristolochic acid I exposure

Jin

Zhu

et al. 2016

Oncotarget

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“…This idea was first articulated by Van Rensselaer Potter and colleagues in the early 1970s, who proposed that primary liver cancer would rather be due to blockage during the development of immature liver cells than de-differentiation of mature cells (49)(50)(51). However, this concept was challenged by the fact that in addition to HCC, fetal type liver enzymes are also present in preneoplastic nodules (52). Currently, the cells in nodules are no longer considered to develop cancer, but rather act as protectors to remove toxicity of carcinogens (43).…”

Section: Cellular Origins Of Hepatocellular Carcinomamentioning

confidence: 99%

Hepatocellular carcinoma stem cells origins and roles in hepatocarcinogenesis and disease progression

Cao¹

2012

Front Biosci

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Introduction 3. Stem cells and liver development and regeneration 3.1. Liver development 3.2. Liver regeneration 3.3. Effects of liver regenerating process on tumor growth 4. Liver stem cells and hepatocellular carcinoma 4.1. Cellular origins of hepatocellular carcinoma 4.2. Malignant transformation of liver stem/progenitor cells 4.2.1. Hepatocytes 4.2.2. Hepatic progenitor cells (oval cells) 4.2.3. Bone marrow stem cells 4.3. Precursor lesions in the evolution of hepatocellular carcinoma 5. Hepatocellular carcinoma stem cells 5.1. Cancer stem cells 5.2. Deregulation of cell cycle during hepatocarcinogenesis 5.3. Cell surface marker and tumorigenicity of hepatocellular carcinoma stem cells 5.4. Cancer stem cell signaling in hepatocellular carcinoma 5.4.1. Angiogenic signaling 5.4.2. Wnt/β-catenin pathway 5.4.3. Hedgehog signaling 6. Therapeutic implications 7. Acknowledgement 8.

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“…Subsequently, they increase in size and become moderately or poorly differentiated cancerous tissues producing AFP [73]. This suggests that HCC might arise due to dedifferentiation of mature hepatocytes that have retained their ability to divide [74]. In addition, it is now accepted that the arrested differentiation of tissue-based stem cells or their immediate progenitors, the concept of blocked ontogeny, is linked to hepatocarcinogenesis [75–77].…”

Section: Translating Liver Development To Disease Modelsmentioning

confidence: 99%

Liver Development, Regeneration, and Carcinogenesis

Kung

Currie

Forbes

et al. 2010

Journal of Biomedicine and Biotechnology

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The identification of putative liver stem cells has brought closer the previously separate fields of liver development, regeneration, and carcinogenesis. Significant overlaps in the regulation of these processes are now being described. For example, studies in embryonic liver development have already provided the basis for directed differentiation of human embryonic stem cells and induced pluripotent stem cells into hepatocyte-like cells. As a result, the understanding of the cell biology of proliferation and differentiation in the liver has been improved. This knowledge can be used to improve the function of hepatocyte-like cells for drug testing, bioartificial livers, and transplantation. In parallel, the mechanisms regulating cancer cell biology are now clearer, providing fertile soil for novel therapeutic approaches. Recognition of the relationships between development, regeneration, and carcinogenesis, and the increasing evidence for the role of stem cells in all of these areas, has sparked fresh enthusiasm in understanding the underlying molecular mechanisms and has led to new targeted therapies for liver cirrhosis and primary liver cancers.

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Hepatic neoplasia: reflections and ruminations

Cited by 7 publications

References 223 publications

Premalignant alteration assessment in liver-like tissue derived from embryonic stem cells by aristolochic acid I exposure

Premalignant alteration assessment in liver-like tissue derived from embryonic stem cells by aristolochic acid I exposure

Hepatocellular carcinoma stem cells origins and roles in hepatocarcinogenesis and disease progression

Liver Development, Regeneration, and Carcinogenesis

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