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Xin Chen - One of the best experts on this subject based on the ideXlab platform.

  • bmi1 functions as an oncogene independent of ink4a arf repression in Hepatic Carcinogenesis
    Molecular Cancer Research, 2009
    Co-Authors: Susie A. Lee, Prashant V Bommi, Goberdhan P. Dimri, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

  • Bmi1 Functions as an Oncogene Independent of Ink4A/Arf Repression in Hepatic Carcinogenesis
    Molecular Cancer Research, 2009
    Co-Authors: Chuanrui Xu, Prashant V Bommi, Goberdhan P. Dimri, Coral Ho, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in HCC development has not been well studied. In this manuscript, we report that Bmi1 is over-expressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. T o investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, co-expression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study demonstrates that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

  • Bmi1 Functions as an Oncogene Independent of Ink4A/Arf Repression in Hepatic Carcinogenesis
    Molecular cancer research : MCR, 2009
    Co-Authors: Susie A. Lee, Prashant V Bommi, Goberdhan P. Dimri, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

Robert A. F. M. Chamuleau - One of the best experts on this subject based on the ideXlab platform.

  • Correlation of repressed transcription of α-tocopherol transfer protein with serum α-tocopherol during hepatoCarcinogenesis
    International Journal of Cancer, 1997
    Co-Authors: C.g. Wu, Frans J. Hoek, Maarten Groenink, Sander J H Van Deventer, Pieter H Reitsma, Robert A. F. M. Chamuleau
    Abstract:

    : Using a subtraction-enhanced display technique, we identified a rodent alpha-tocopherol transfer protein (alpha-TTP) cDNA which exhibited markedly lower messenger RNA (mRNA) amounts in rat hepatocellular carcinoma (HCC) than in healthy controls. Several lines of evidence have substantiated that abnormal alpha-TTP results in isolated vitamin E deficiency. In this study, we investigated the Hepatic mRNA amounts of alpha-TTP during rat Hepatic Carcinogenesis and liver regeneration on Northern blot, localization of alpha-TTP mRNA in HCC of rats and humans by in situ hybridization, and we analyzed the correlation between alpha-TTP mRNA and alpha-tocopherol. alpha-TTP mRNA concentrations of the rats were decreased at the early stage of Hepatic Carcinogenesis, and remained 3-5-fold reduced as the tumor progressed. In parallel, serum alpha-tocopherol concentrations were significantly decreased to 40% of those in the controls at the early stages of rat Hepatic Carcinogenesis (p < 0.01). The 2 data sets were strongly correlated (r = 0.834, p < 0.001). In situ hybridization revealed that a decrease of alpha-TTP mRNA was preferentially localized in the tumor nodules of rats and humans with HCC. Our data suggest that repressed transcription of alpha-TTP is associated with a decrease of serum alpha-tocopherol and with Hepatic Carcinogenesis.

  • Overexpression of Prothymosin Alpha, Concomitant with c-myc, during Rat Hepatic Carcinogenesis
    Biochemical and biophysical research communications, 1997
    Co-Authors: W. Boers, P. R. Reitsma, S. J. H. Van Deventer, Robert A. F. M. Chamuleau
    Abstract:

    By using a subtraction-enhanced display technique, we identified a cDNA clone representing alpha-prothymosin, from rat hepatocellular carcinoma (HCC). alpha-Prothymosin has been reported to be involved in cell proliferation and regulated by c-myc gene in vitro. In the present study, we investigated the gene expression pattern of alpha-prothymosin and analyzed its correlation with c-myc during rat Hepatic Carcinogenesis and liver regeneration. Hepatic alpha-prothymosin mRNA levels, concomitant with c-myc, were increased at the early stage of Hepatic Carcinogenesis (6 weeks), and remained nearly 10 fold higher as the tumor progressed. In comparison, alpha-prothymosin mRNA levels were only slightly and moderately increased at early (3-6 hr) and at later stage (24-30 hr) of liver regeneration after 70% partial hepatectomy. In situ hybridization revealed that overexpressed alpha-prothymosin mRNA was restricted to the tumor nodules and to tumor cells invading blood vessels. These data provide evidence that overexpression of alpha-prothymosin, concomitant with c-myc, is related to rat Hepatic Carcinogenesis.

Sun Young Choi - One of the best experts on this subject based on the ideXlab platform.

  • Magnetic resonance imaging of hepatocellular carcinoma using contrast media.
    Oncology, 2008
    Co-Authors: Myeong-jin Kim, Jin-young Choi, Yong Eun Chung, Sun Young Choi
    Abstract:

    Magnetic resonance imaging (MRI) has been widely used for evaluation of focal lesions associated with Hepatic Carcinogenesis including hepatocellular carcinoma (HCC). By providing better tissue contrast compared to ultrasonography and computed tomography, MRI is considered the most sensitive modality for diagnosis of HCC. Dynamic MRI using gadolinium-based extracellular fluid (ECF) agents is useful for detection of hypervascular tumors and lesion characterization but has limitations in the diagnosis of hypovascular HCCs and lesion characterization of nonhypervascular tumors. MRI using superparamagnetic iron oxide agents may be useful for detecting and characterizing lesions that were not seen on dynamic MRI using ECF agents, but finding well-differentiated HCC and differentiating it from a dysplastic nodule can be difficult in some cases. Hepatobiliary agents that can be used in both dynamic MRI and delayed hepatobiliary phase imaging have great potential for improving characterization of focal lesions associated with Hepatic Carcinogenesis. Further studies are necessary to determine their roles in evaluation and management of HCCs.

  • Magnetic resonance imaging of hepatocellular carcinoma using contrast media.
    Oncology, 2008
    Co-Authors: Myeong-jin Kim, Jin-young Choi, Yong Eun Chung, Sun Young Choi
    Abstract:

    Magnetic resonance imaging (MRI) has been widely used for evaluation of focal lesions associated with Hepatic Carcinogenesis including hepatocellular carcinoma (HCC). By providing better tissue contra

Lopa Mishra - One of the best experts on this subject based on the ideXlab platform.

  • Liver stem cells and tgf-Beta in Hepatic Carcinogenesis.
    Gastrointestinal cancer research : GCR, 2008
    Co-Authors: Rupen Amin, Lopa Mishra
    Abstract:

    Hepatocellular carcinoma is the fifth most common malignancy worldwide. Recent trends indicate a rising incidence in the United States, with a 5-year survival rate of less than 5%. New therapeutics targeting advanced-stage hepatocellular carcinoma, such as sorafenib, have marginally improved the median overall survival by 3 months. There is an urgent need for new targeted agents that are associated with minimal local and systemic toxicities. Up to 40% of hepatocellular carcinomas are clonal, potentially arising from stem cells and increased activation of multiple pathways including IL-6/STAT3, WNT, CDK4, and hedgehog, as well as loss of response to the transforming growth factor-beta (TGF-beta) signaling pathway. Our hypothesis has been that these "cancer stem cells" or cancer sustaining cells may prove to be strong genetic and therapeutic targets. Modulating stem cell renewal factors such as STAT3, NANOG, and OCT4 may reduce hepatocellular carcinoma formation. These points are discussed in detail in this review.

Goberdhan P. Dimri - One of the best experts on this subject based on the ideXlab platform.

  • bmi1 functions as an oncogene independent of ink4a arf repression in Hepatic Carcinogenesis
    Molecular Cancer Research, 2009
    Co-Authors: Susie A. Lee, Prashant V Bommi, Goberdhan P. Dimri, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

  • Bmi1 Functions as an Oncogene Independent of Ink4A/Arf Repression in Hepatic Carcinogenesis
    Molecular Cancer Research, 2009
    Co-Authors: Chuanrui Xu, Prashant V Bommi, Goberdhan P. Dimri, Coral Ho, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in HCC development has not been well studied. In this manuscript, we report that Bmi1 is over-expressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. T o investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, co-expression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study demonstrates that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

  • Bmi1 Functions as an Oncogene Independent of Ink4A/Arf Repression in Hepatic Carcinogenesis
    Molecular cancer research : MCR, 2009
    Co-Authors: Susie A. Lee, Prashant V Bommi, Goberdhan P. Dimri, Siu Tim Cheung, Shiang Huang, Xin Chen
    Abstract:

    Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote Hepatic Carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.