Relevant bibliographies by topics / Hepatocellular Carcinoma HSC

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Academic literature on the topic 'Hepatocellular Carcinoma HSC'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Hepatocellular Carcinoma HSC"

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Wang, Pei-Wen, Tung-Yi Lin, Pei-Ming Yang, Chau-Ting Yeh, and Tai-Long Pan. "Hepatic Stellate Cell Modulates the Immune Microenvironment in the Progression of Hepatocellular Carcinoma." International Journal of Molecular Sciences 23, no. 18 (September 15, 2022): 10777. http://dx.doi.org/10.3390/ijms231810777.

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Hepatocellular carcinoma (HCC) is a major cause of increases in the mortality rate due to cancer that usually develops in patients with liver fibrosis and impaired hepatic immunity. Hepatic stellate cells (HSCs) may directly or indirectly crosstalk with various hepatic cells and subsequently modulate extracellular remodeling, cell invasion, macrophage conversion, and cancer deterioration. In this regard, the tumor microenvironment created by activated HSC plays a critical role in mediating pathogenesis and immune escape during HCC progression. Herein, intermediately differentiated human liver cancer cell line (J5) cells were co-cultured with HSC-conditioned medium (HSC-CM); changes in cell phenotype and cytokine profiles were analyzed to assess the impact of HSCs on the development of hepatoma. The stage of liver fibrosis correlated significantly with tumor grade, and the administration of conditioned medium secreted by activated HSC (aHSC-CM) could induce the expression of N-cadherin, cell migration, and invasive potential, as well as the activity of matrix metalloproteinases in J5 cells, implying that aHSC-CM could trigger the epithelial-mesenchymal transition (EMT). Next, the HSC-CM was further investigated and network analysis indicated that specific cytokines and soluble proteins, such as activin A, released from activated HSCs could remarkably affect the tumor-associated immune microenvironment involved in macrophage polarization, which would, in turn, diminish a host’s immune surveillance and drive hepatoma cells into a more malignant phenotype. Together, our findings provide a novel insight into the integral roles of HSCs to enhance hepatocarcinogenesis through their immune-modulatory properties and suggest that HSC may serve as a potent target for the treatment of advanced HCC.
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Mailloux, Adam, and Pearlie Epling-Burnette. "Collagen matrix deposition by hepatic stellate cells protects hepatocellular carcinoma from NK-mediated cytotoxicity (P2013)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 53.7. http://dx.doi.org/10.4049/jimmunol.190.supp.53.7.

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Abstract Liver fibrosis (LF), a leading risk factor for hepatocellular carcinoma (HCC), is caused by collagen-producing hepatic stellate cells (HSC) activated during chronic inflammation secondary to hepatitis-C infection, or alcohol liver disease (ALD). NK cells promote disease resolution via RAE1-dependant HSC clearance. A defect in NK function by an ill-defined mechanism contributes to a pro-fibrotic response. Using an engineered bioartifical collagen matrix, the expression of inhibitory leukocyte associated IgG-like receptor-1 (LAIR-1) was increased on dividing NK cells and IL-2-induced NK proliferation was inhibited. Thus, we hypothesized that the accumulation of HSC-derived collagen directly inhibits NK activity and protects both HSC and HCC from innate clearance. We found that deposition of native collagen matrix for 72h protected HSCs from NK lysis in Cr51 cytotoxicity assays. A HCC cell line (HEPG2), which produced no collagen when cultured in the absence of HSCs, was susceptible to activated NK killing and was unaffected by collagenase. To test if HSC-derived collagen protects HEPG2 cells, the populations were differentially labeled with ipophilic dyes and co-cultured for 72h for use in flow-based assays. Collagen matrix protected both targets, while collagenase pretreatment restored NK sensitivity. These results suggest that HSC-derived collagen may contribute to NK dysfunction in LF and HCC, and identifies LAIR-1 as a potential mediator of tumor-induced immune suppression.
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Jia, Shu-Qin, Jian-Jun Ren, Pei-De Dong, and Xing-Kai Meng. "Probing the Hepatic Progenitor Cell in Human Hepatocellular Carcinoma." Gastroenterology Research and Practice 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/145253.

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Objective. The intrahepatic stem cells, also known as hepatic progenitor cells (HPCs), are able to differentiate into hepatocytes and bile duct epithelia. By exposure of different injuries and different hepatocarcinogenic regimens, the mature hepatocytes can no longer effectively regenerate; stem cells are involved in the pathogenesis of hepatocellular carcinoma.Methods. Immunohistochemistry was performed on 107 paraffin-embedded hepatocellular carcinoma specimens with the marker of hepatocyte and hepatocellular carcinoma (HepPar1), biliary differentiation (CK7,CK19), haemopoietic stem cell (HSC) (c-kit/CD117, CD34, and Thy-1/CD90), HPC specific markers (OV-6), and Ki-67, p53 protein.Results. HPCs can be identified in the tumor nodules, around the edge of tumor nodules, and in the portal tracts of the paracirrhosis nodules being positive in HepPar1, CK7, CK19, and OV-6, but they failed to immunostain with CD117, CD34, and CD90. The HPCs positive in Ki-67 are observed in the tumor and paracirrhosis tissues. In 107 specimens, 40.2% (43/107) HCC tissues expressed p53 protein, lower than that of the HPCs around the tumor nodules (46.7%, 50/107) and much higher than that of the HPCs around the paracirrhosis nodules (8.41%, 9/107).Conclusion. Human hepatocellular carcinogenesis may be based on transformation of HPCs, not HSCs, through the formation of the transitional cells (hepatocyte-like cells and bile ductal cells).
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Wu, Mengna, Huajie Miao, Rong Fu, Jie Zhang, and Wenjie Zheng. "Hepatic Stellate Cell: A Potential Target for Hepatocellular Carcinoma." Current Molecular Pharmacology 13, no. 4 (November 2, 2020): 261–72. http://dx.doi.org/10.2174/1874467213666200224102820.

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: Liver cancer is a leading cause of cancer-related death worldwide, in which hepatocellular carcinoma (HCC) accounts for the majority. Despite the progression in treatment, the prognosis remains extremely poor for HCC patients. The mechanisms of hepatocarcinogenesis are complex, of which fibrosis is acknowledged as the pre-cancerous stage of HCC. Approximately, 80-90% of HCC develops in the fibrotic or cirrhotic livers. Hepatic stellate cells (HSCs), the main effector cells of liver fibrosis, could secret various biological contents to maintain the liver inflammation. By decades, HSCs are increasingly correlated with HCC in the tumor microenvironment. : In this review, we summarized the underlying mechanisms that HSCs participated in the genesis and progression of HCC. HSCs secrete various bioactive contents and regulate tumor-related pathways, subsequently contribute to metastasis, angiogenesis, immunosuppression, chemoresistance and cancer stemness. The study indicates that HSC plays vital roles in HCC progression, suggesting it as a promising therapeutic target for HCC treatment.
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Liu, Man, Jingying Zhou, Xiaoyu Liu, Yu Feng, Weiqin Yang, Feng Wu, Otto Ka-Wing Cheung, et al. "Targeting monocyte-intrinsic enhancer reprogramming improves immunotherapy efficacy in hepatocellular carcinoma." Gut 69, no. 2 (May 10, 2019): 365–79. http://dx.doi.org/10.1136/gutjnl-2018-317257.

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ObjectiveHepatocellular carcinoma (HCC), mostly developed in fibrotic/cirrhotic liver, exhibits relatively low responsiveness to immune checkpoint blockade (ICB) therapy. As myeloid-derived suppressor cell (MDSC) is pivotal for immunosuppression, we investigated its role and regulation in the fibrotic microenvironment with an aim of developing mechanism-based combination immunotherapy.DesignFunctional significance of MDSCs was evaluated by flow cytometry using two orthotopic HCC models in fibrotic liver setting via carbon tetrachloride or high-fat high-carbohydrate diet and verified by clinical specimens. Mechanistic studies were conducted in human hepatic stellate cell (HSC)-peripheral blood mononuclear cell culture systems and fibrotic-HCC patient-derived MDSCs. The efficacy of single or combined therapy with anti-programmed death-1-ligand-1 (anti-PD-L1) and a clinically trialled BET bromodomain inhibitor i-BET762 was determined.ResultsAccumulation of monocytic MDSCs (M-MDSCs), but not polymorphonuclear MDSCs, in fibrotic livers significantly correlated with reduced tumour-infiltrating lymphocytes (TILs) and increased tumorigenicity in both mouse models. In human HCCs, the tumour-surrounding fibrotic livers were markedly enriched with M-MDSC, with its surrogate marker CD33 significantly associated with aggressive tumour phenotypes and poor survival rates. Mechanistically, activated HSCs induced monocyte-intrinsic p38 MAPK signalling to trigger enhancer reprogramming for M-MDSC development and immunosuppression. Treatment with p38 MAPK inhibitor abrogated HSC-M-MDSC crosstalk to prevent HCC growth. Concomitant with patient-derived M-MDSC suppression by i-BET762, combined treatment with anti-PD-L1 synergistically enhanced TILs, resulting in tumour eradication and prolonged survival in the fibrotic-HCC mouse model.ConclusionOur results signify how non-tumour-intrinsic properties in the desmoplastic microenvironment can be exploited to reinstate immunosurveillance, providing readily translatable combination strategies to empower HCC immunotherapy.
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Subramanian, Pallavi, Jochen Hampe, Frank Tacke, and Triantafyllos Chavakis. "Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)." International Journal of Molecular Sciences 23, no. 13 (June 23, 2022): 6996. http://dx.doi.org/10.3390/ijms23136996.

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The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re-defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non-alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH-related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte–HSC and macrophage–HSC crosstalk.
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Wang, Wen-Hung, Kuo-Yu Hsuan, Ling-Ya Chu, Chia-Ying Lee, Yu-Chang Tyan, Zong-Shiow Chen, and Wan-Chi Tsai. "Anticancer Effects of Salvia miltiorrhiza Alcohol Extract on Oral Squamous Carcinoma Cells." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/5364010.

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Researchers have reported significant effects from Danshen (Salvia miltiorrhiza) in terms of inhibiting tumor cell proliferation and promoting apoptosis in breast cancer, hepatocellular carcinomas, promyelocytic leukemia, and clear cell ovary carcinomas. Here we report our data indicating that Danshen extracts, especially alcohol extract, significantly inhibited the proliferation of the human oral squamous carcinoma (OSCC) cell lines HSC-3 and OC-2. We also observed that Danshen alcohol extract activated the caspase-3 apoptosis executor by impeding members of the inhibitor of apoptosis (IAP) family, but not by regulating the Bcl-2-triggered mitochondrial pathway in OSCC cells. Our data also indicate that the extract exerted promising effects in vivo, with HSC-3 tumor xenograft growth being suppressed by 40% and 69% following treatment with Danshen alcohol extract at 50 and 100 mg/kg, respectively, for 34 days. Combined, our results indicate appreciable anticancer activity and significant potential for Danshen alcohol extract as a natural antioxidant and herbal human oral cancer chemopreventive drug.
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MAN, LIU, Jingying Zhou, John Wong, Anthony W. H. Chan, Zhiwei Chen, and Alfred S. L. Cheng. "Delineating the epigenetic regulation of myeloid derived suppressor cell generation in hepatocellular carcinoma associated with cirrhosis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 205.14. http://dx.doi.org/10.4049/jimmunol.198.supp.205.14.

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Abstract Hepatocellular carcinoma (HCC) is the most common liver tumor with dismal prognosis. Since most liver tumors arise in a context of chronic inflammation associated with fibrosis, tumor microenvironment plays a critical role in liver carcinogenesis. Myeloid derived suppressor cell (MDSC) is a population of immature myeloid cells that undermine immune surveillance and facilitate tumor immune escape. As a key driver of liver fibrosis, activated hepatic stellate cell (HSC) has been recently shown to induce MDSC generation through cell-cell contact and/or secreted soluble factors. Given the crucial role of epigenetics in cell lineage specification, we aim to elucidate the chromatin regulation of MDSC in the immunosuppressive liver tumor microenvironment. Using human PBMCs from healthy donors, we have successfully recapitulated the immunomodulatory effect of HSCs on monocytic MDSC generation. Comprehensive epigenetic drug screening and expression analysis indicated that accumulation of histone H3 lysine 27 acetylation (H3K27ac), an active enhancer histone mark, is involved in the process of HSC-induced MDSC generation. We further demonstrated that inhibitors of BET family, which disrupts BRD4 association with H3K27ac-enriched active enhancers, abrogates MDSC generation. These results highlight the importance of epigenetic regulation in MDSC accumulation in the fibrotic microenvironment. Ongoing work is directed towards the identification of HSC-activated enhancers that orchestrate MDSC identity and functions. As we showed high level of monocytic MDSC accumulation in patients with cirrhotic HCC, our study may provide novel therapeutic targets to restore effective anti-tumor immune response in this dreadful disease.
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Iwahashi, Shuichi, Mitsuo Shimada, Yuji Morine, Satoru Imura, Tetsuya Ikemoto, Yu Saito, Shinichiro Yamada, and Feng Rui. "The effect of hepatic stellate cells on hepatocellular carcinoma progression." Journal of Clinical Oncology 37, no. 4_suppl (February 1, 2019): 265. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.265.

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265 Background: The hepatic stellate cells (HSCs) localize at the space of Disse in the liver and have multiple functions. They are identified as the major contributor to hepatic fibrosis. Some manuscripts mentioned that activated HSCs predicted prognoses of hepatocellular carcinoma. The aim of this study is to investigate the effect of HSCs and the role of IL-6 / Stat3 pathway on HCC progression. Methods: HCC cells (Hep G2 and Huh 7) were co-cultured with HSC (LX2 and Li90). The viability and migration ability of cancer cells were detected. Also, the expression of epithelial–mesenchymal transition marker (E-cadherin), stem cell marker (EpCAM and CD44), TGF-b and p-STAT3 of cancer cells were evaluated. Then the IL-6 neutralization was performed during HCC cells and HSCs co-culture. The viability and migration ability of cancer cells were detected. Also, the expression of epithelial–mesenchymal transition marker (E-cadherin), stem cell marker (EpCAM and CD44) and p-STAT3 of cancer cells were evaluated. Results: Co-culture with hepatic stellate cell increased cancer cell viability and migration ability. The expression of E-cadherin, EpCAM and CD44 of cancer cells also increased after co-culture with HSCs. The IL-6 expression and secretion of HSCs were elevated by cancer cell stimulation. The over-expressed IL-6 activated STAT3 of cancer cell showed as the level of phosphorylated STAT3 increased. Neutralized IL-6 during co-culture significantly decrease the viability and migration ability of cancer cells. Also, the expression of E-cadherin, EpCAM and CD44 of cancer cells decreased. Conclusions: HSCs might promote HCC progression through IL-6 / STAT3 pathway.
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Santamato, Angela, Emilia Fransvea, Francesco Dituri, Alessandra Caligiuri, Michele Quaranta, Tomoaki Niimi, Massimo Pinzani, Salvatore Antonaci, and Gianluigi Giannelli. "Hepatic stellate cells stimulate HCC cell migration via laminin-5 production." Clinical Science 121, no. 4 (April 28, 2011): 159–68. http://dx.doi.org/10.1042/cs20110002.

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Activated HSCs (hepatic stellate cells) are the main source of extracellular matrix proteins present in cirrhotic liver on which HCC (hepatocellular carcinoma) commonly develops. HCC cells behave differently according to differences in the surrounding microenvironment. In the present study, we have investigated a mechanism whereby HSCs modulate the migratory activity of HCC cells. We used primary cultures of human HSCs to investigate their effect on Hep3B, Alexander, HLE and HLF HCC cells. The expression of Ln-5 (laminin-5) was documented at transcript and protein levels both in vitro and in vivo. HCC cells strongly adhere, migrate and spread in the presence of HSC-conditioned medium and of co-culture. HSCs produce and secrete Ln-5 in the CM (conditioned medium). The electrophoretic pattern of secreted Ln-5 is consistent with that of a migratory substrate, showing the presence of the γ2x fragment. Blocking antibodies against Ln-5 inhibit HCC migration in the presence of HSC-CM. HCC cells migrate very poorly in the presence of Ln-5 immunodepleted HSC-CM. HCC migration in the presence of HSCs is dependent on the MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK pathway, but not the PI3K (phosphoinositide 3-kinase)/Akt pathway. HSC-CM, as well as Ln-5, activates the MEK/ERK but not the PI3K/Akt pathway. In human HCC tissues, Ln-5 is mainly distributed along α-SMA (smooth muscle actin)-positive cells, whereas in peritumoural tissues, Ln-5 is absent. HSCs stimulate HCC migration via the production and secretion of Ln-5.
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Dissertations / Theses on the topic "Hepatocellular Carcinoma HSC"

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龔衍峰 and Hin-fung Tony Kung. "The impact of heat on hepatocellular carcinoma (HCC)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B4073867X.

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Kung, Hin-fung Tony. "The impact of heat on hepatocellular carcinoma (HCC)." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B4073867X.

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Wu, Guang. "Role of Notch Signaling in Hepatocellular Carcinoma (HCC)." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18718.

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Liver cancer is the 6th most common cancer worldwide and Australia’s fastest growing malignancy both in incidence and mortality. Although great improvement in early diagnosis and treatment approach have been achieved during last two decades, patients with HCC still have a dismal prognosis with a mortality-to-incidence ratio close to 1, meaning that the disease is almost uniformly fatal. One of explanations for such a dismal prognosis for HCC is the existence of heterogeneity in HCC, in which HCC is composed of liver cancer stem cells and mature HCC cells. Previous data suggested that liver cancer stem cells are responsible for HCC initiation, early metastasis and treatment resistance. However, accurate characterization of liver cancer stem cells is still required as the reliability of those reported approaches in identify liver cancer stem cells is variable. To better characterization of liver cancer stem cells, we found by qPCR and western blotting that Oct4, a stem cell gene associated with a range of functions in HCC cells with stem cell feature, is ubiquitously expressed in all HCC tumors in our cohort, whereas other liver cancer stem cell markers had high variability in their expression. By utilizing a human Oct4 promoter driving an enhanced green fluorescent protein reporter, we successfully established OCT4+EGFP reporter HCC cells. More importantly, Oct4+ cells had all the classic features of liver cancer stem cells including increased sphere formation in vitro, tumor forming potential in vivo, along with up-regulated expression of stemness genes and increased resistance towards Sorafenib, the only drug approved for advanced HCC. Upon success in characterization for liver cancer stem cell, we, for the first, demonstrated by western blotting that JAG2, one of the five ligands in Notch signaling, is significantly increased in liver cancer stem cells. Moreover, JAG2 is the only Notch ligands aberrantly expressed in liver cancer stem cells characterized by qPCR and western blotting. In addition, Sorafenib resistant HCC cells, which are enriched for liver cancer stem cells, also have profound increase in the expression of JAG2 at both RNA and protein level. Since the reported functions of Notch signaling in HCCs are conflicting and an effective approach targeting Notch signaling with tolerable side effect is missing, we then studied the expression profile of Notch signaling components in HCC by qPCR and western blotting. We found that JAG2 is significantly increased in 65% of HCC tissues in our cohort, which is in consistence with microarray data extracted from NCBI and RNA sequence results provided by TCGA. More importantly, we showed that patients with hyper-Notch activity had worse prognosis than that with hypo-Notch activity demonstrated by immunohistochemical staining and Kaplan-Meier survival assay. These results indicate an important biological role of JAG2 mediated Notch signaling in regulation of liver cancer stem cells and HCC. Using Compound E, a selective γ-secretase inhibitor, we demonstrated that inhibition of Notch signaling leads to slowed cell proliferation and decreased liver cancer stem frequency, which were testified by Brdu assay and flow cytometry respectively. Moreover, selective inhibition of JAG2 alone by shRNA in HCC cells results in a similar phenotype along with impaired function in liver cancer stem cells. We also demonstrated a great translational potential of selective targeting JAG2 in HCC as verified by colony-forming assay that JAG2 knockdown HCC cells became significantly sensitive to the killing effect of Sorafenib. In term of mechanism, we identified that Notch2, one of the four Notch signaling receptors, is solo responsive to JAG2 mediated signaling testified by western blotting and immunofluorescence analysis. Inhibition of Notch2-dependent JAG2 signaling leads to a mature HCC phenotype including less liver cancer stem cells with impaired biological function. Targeting JAG2-initiated Notch2 signaling in HCC would greatly improve prognosis of patients with HCC.
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Mckiver, Bryan D. "SND1-Targeted Gene Therapy for Hepatocellular Carcinoma." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5676.

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Staphylococcal nuclease and tudor-domain containing 1 (SND1) is an oncogene for a wide variety of cancers, including hepatocellular carcinoma (HCC). SND1 is a multifunctional protein regulating gene expression of proto-oncogenes and tumor suppressor genes, making SND1 a prime target for developing cancer therapeutics. This notion is especially attributed to HCC as most patients are diagnosed in advanced stages and the therapeutic options available for these patients are severely limited. In this study, we evaluated the therapeutic potential of a replication-defective adenovirus vector delivering SND1 shRNA (Ad.SND1sh) to human HCC cell lines, HepG3, HuH-7, and Hep3B. Adenovirus infection in HCC cells was confirmed by Western blotting and immunofluorescence. The efficacy of Ad.SND1sh to knockdown SND1 expression was confirmed via Western blot, qRT-PCR, and immunofluorescence. Ad.SND1sh did not significantly affect proliferation of the three human HCC cells but significantly inhibited their invasive and migratory capacities, as determined by wound healing and Matrigel invasion assays, respectively. As a corollary, Ad.SND1sh treatment resulted in a decrease in mesenchymal markers, such as N-cadherin, Twist, Snail, and Slug, without affecting levels of epithelial marker E-Cadherin, indicating that SND1 knockdown induces mesenchymal conversion in HCC cells. Additionally, reductions in liver cancer stem cell marker CD133 and HCC marker α-fetoprotein (AFP) were observed with SND1 knockdown. HCC cells with aberrant expression of these markers are associated with tumor initiation, recurrence, and multi-drug resistance. Our findings indicate that Ad.SND1sh may potentially be an effective therapy for advanced HCC and needs to be studied further for its clinical application.
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Chan, Chun-Fai. "Study of cancer vaccine candidates for human hepatocellular carcinoma (HCC) /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202004%20CHAN.

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Tam, Hoy-kam Aegean, and 譚凱琴. "Epigenetic dysregulation of microRNA-9 (miRNA-9) in hepatocellular carcinoma (HCC)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46455425.

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Khan, Maheen. "AEG-1 KNOCKOUT SENSITIZES HEPATOCELLULAR CARCINOMA (HCC) CELLS TO IONIZING RADIATION." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5853.

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Liver cancer is the fourth leading cause of cancer-associated deaths globally, and among primary liver cancers, hepatocellular carcinoma (HCC) encompasses 75-85% of all cases. HCC is a highly lethal disease due to limited treatment options – only a small subset of patients qualify for surgical resection or transplantation; the remaining patients often display resistance to radiation therapy or chemotherapy. Overexpression of the oncogene astrocyte elevated gene-1 (AEG-1) is associated with poorer survival and increased tumor recurrence in HCC, and numerous studies show its role in initiation of hepatocarcinogenesis. A prior study also demonstrated AEG-1 expression inhibits senescence by diminishing the ATM/Chk1/Chk2/p53/p21 DNA damage response (DDR) pathway. The aim of this study is to understand if AEG-1 expression promotes radioresistance in HCC. A CRISPR/Cas9 plasmid system was used to delete AEG-1 in the QGY-7703, HuH7 and DihXY cell lines, which model HCC. The cell lines were then treated with ionizing radiation (IR). We find that knockout of AEG-1 in these cell lines induces sensitivity to IR at 2.5 Gy. In response to radiation, AEG-1 wildtype cells more profoundly upregulate ATR, Chk1, and Chk2 signaling; and also more rapidly induce γH2AX, ATM, and BRCA1 signaling, which sense dsDNA breaks to initiate homologous recombination repair. We conclude that AEG-1 expression protects HCC cells from IR through two mechanisms: 1) rapidly initiating the DNA damage response; and 2) increasing replication fork stabilization. These findings indicate AEG-1 can be a therapeutic target in combination with radiation treatment to improve outcomes for HCC patients who demonstrate radioresistance.
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Kienlein, Andreas. "Lebertransplantation bei Patienten mit hepatozellulärem Karzinom. Eine retrospektive Studie am Universitätsklinikum Leipzig im Zeitraum von 1994 bis 2010. Charakterisierung des Patientenkollektivs und Analyse von Einflussfaktoren auf Überleben und Outcome." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205991.

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Für Lebertransplantationen bei Patienten mit hepatozellulärem Karzinom stellt sich angesichts der defizitären Organspendesituation die berechtigte Frage, unter welchen Bedingungen diese Form der Therapie ein gutes Outcome für die Patienten verspricht und somit keine Verschwendung der ohnehin knappen Ressourcen darstellt. Ziel dieser Arbeit war es, ein Kollektiv aus 98 Patienten, die an einem hepatozellulären Karzinom erkrankten und im Zeitraum von 1994 bis einschließlich 2010 am Universitätsklinikum Leipzig eine Lebertransplantation erhielten, retrospektiv zu charakterisieren und den Einfluss mehrerer Faktoren auf das Outcome der Patienten zu untersuchen. Bei den Faktoren handelte es sich um die Wartezeit, den präoperativen Einsatz der TACE, den präoperativen AFP-Serumspiegel, sowie die Tumorzahl und -größe. Der Nachbeobachtungszeitraum lag bei 3 Jahren. Die Charakterisierung des Kollektivs erbrachte folgende Ergebnisse: Das Kollektiv bestand zu rund 80% aus Männern. Das mediane Alter zum Zeitpunkt der Transplantation lag bei 59 Jahren. Die Transplantationszahlen bei HCC-Patienten sind am UKL seit Einführung des MELD-Scores 2006 deutlich angestiegen. Die mediane Wartezeit hat sich seit Einführung des MELD-Scores nicht wesentlich verändert. Sie betrug 7,3 Monate in der Prä-MELD-Ära und 6,9 Monate in der MELD-Ära. Mit über 60% war der Alkoholabusus die häufigste Ursache für die Entstehung des hepatozellulären Karzinoms. An zweiter Stelle stand die Hepatitis-C-Infektion. In der Diagnostik des HCC spielte die Computertomographie die größte Rolle. Die Sensitivität des AFP zur Erfassung des HCC (>400 ng/ml) war mit Werten unter 30% sehr niedrig. Die TACE war die mit Abstand am häufigsten durchgeführte, neoadjuvante Maßnahme. Zum Zeitpunkt der Transplantation befanden sich rund 75% der Patienten in einem Stadium bis maximal T2. Das Auftreten von solitären und multifokalen HCCs war in etwa gleich häufig (46,9% vs. 53,1%). Die Milan-Kriterien waren bei knapp 39% der Patienten im postoperativen Explantat-Befund überschritten. Nach Transplantation traten bei 26 Patienten Abstoßungsreaktionen auf. 8 Patienten mussten aufgrund eines Transplantatversagens retransplantiert werden. Das postoperative Überleben (intention-to-treat) betrug 75,5% (6 Monate), 71,4% (1 Jahr) und 63,3% (3 Jahre). Die entsprechenden Rezidivraten lagen bei 11,2%, 14,3% und 22,4%. Rezidiven traten am häufigsten in der Spenderleber auf, gefolgt von einem Befall der Lymphknoten und Knochen. Ein signifikanter Einfluss auf das Outcome der Patienten konnte für das AFP, die Tumorzahl und die Milan-Kriterien nachgewiesen werden: Präoperative AFP-Spiegel unter 100 ng/ml zeigten eine signifikant niedrigere Rezidivrate. Multifokale Tumoren waren mit einem signifikant schlechteren 3-Jahres-Überleben verknüpft. Bei Erfüllung der Milan-Kriterien (im postoperativen Explantat-Befund) war die Rezidivrate signifikant und die Überlebensrate deutlich besser. Für die Wartezeit konnte seit Einführung des MELD-Scores eine positive Entwicklung festgestellt werden. Das 3-Jahresüberleben hat sich bei Wartezeiten unter 12 Monaten um 22,5% verbessert. Die Rezidivrate ist bei Wartezeiten über 12 Monate um 15,3% gesunken. Für den Einfluss der TACE auf das Outcome der Patienten konnten keine signifikanten Unterschiede festgestellt werden. Auch andere Studien belegten bisher lediglich einen Vorteil für das erfolgreiche Downstaging gegenüber Patienten, bei denen die TACE erfolglos blieb. Für die Untersuchung des tatsächlichen Nutzens einer TACE vor Transplantation werden daher Studien mit höherem Evidenzgrad benötigt.
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Shinozuka, Ken. "Effectiveness of Radiofrequency Ablation of Initial Recurrent Hepatocellular Carcinoma after Hepatectomy: Long-Term Results and Prognostic Factors." Kyoto University, 2018. http://hdl.handle.net/2433/231012.

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Peng, Chengyuan. "Diagnosis of Steatosis, Precancerous Lesions and Hepatocellular Carcinoma Using Infrared Microspectroscopy." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T032.

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Carcinome hépatocellulaire (CHC) est le sixième cancer et la deuxième cause de mortalité par cancer dans le monde. Dans la majorité des cas, le CHC se développe sur une maladie chronique associée à des étiologies variées telles que l'infection par le virus de l'hépatite B ou l’hépatite C, la consommation excessive d'alcool et des maladies métaboliques. Le développement des maladies chroniques du foie qui conduisent à la cirrhose puis au cancer induisent des modifications de la composition chimique des cellules et des tissus. En effet, la carcinogenèse hépatique est un processus en plusieurs étapes caractérisé par la progression de nodules de régénération, de nodules dysplasiques de bas grade puis de grade et enfin du CHC. Le traitement du CHC reste difficile et la transplantation du foie est la seule option thérapeutique curative à long terme. Le problème est qu'il n'y a pas de marqueur objectifs et quantifiables pour contrôler la qualité d’un greffon. Des biomarqueurs spécifiques marquant la progression du CHC font également défauts.Dans ce travail de thèse, nous avons évalué l’intérêt de la microspectroscopie infrarouge (IR) pour le diagnostic de la stéatose, qui est le facteur le plus important affectant la reprise de la fonction hépatique après greffe de foie. La microspectroscopie infrarouge permet de détecter de façon qualitative et quantitative les caractéristiques biochimiques liées aux différents constituants moléculaires présents dans l'échantillon biologique. Nos travaux ont montré que la progression de la stéatose hépatique correspond non seulement à l'accumulation de lipides, mais également à des changements spectaculaires dans la composition qualitative du tissu. En effet, le bas grade de stéatose présente une diminution de la teneur en glycogène et une augmentation concomitante de lipides par rapport au foie normal. La stéatose intermédiaire montre une augmentation de glycogène et des changements majeurs sont observés en ce qui concerne les lipides, avec une contribution significative des acides gras estérifiés, des chaînes de carbone allongées et des lipides insaturés. Ces caractéristiques sont encore plus prononcées dans les hauts degrés de stéatose. De plus, nous avons mis en évidence que des changements biochimiques majeurs se produisent dans la partie non-stéatosique du tissu malgré son aspect normal sur le plan histologique, ce qui suggère que l’organe dans son ensemble reflète le degré de la stéatose.La deuxième partie de la thèse est focalisée la carcinogenèse hépatique. Il s’agit d’un processus en plusieurs étapes qui se caractérise dans la plupart des foies cirrhotiques par la progression de nodules hyperplasiques de régénération vers des lésions précancéreuses telles que les nodules dysplasiques de bas grade puis de haut grade et enfin le CHC. Le diagnostic différentiel entre nodules dysplasiques en particulier de haut garde et CHC reste extrêmement difficile. Nous avons abordé le potentiel de la microspectroscopie IR pour le diagnostic des nodules cirrhotiques. Nous avons observé de profondes modifications de la composition biochimique du foie pathologique. En effet, des changements importants ont été détectés dans la composition des lipides, des protéines et des sucres mettant en évidence la reprogrammation métabolique dans la carcinogenèse. Les principaux changements ont été observés dans le domaine de fréquence 950-1480 cm-1 dans lequel plusieurs bandes permettaient la discrimination des nodules cirrhotiques, dysplasiques et tumoraux. Enfin, nous avons montré que le diagnostic peut être réalisé à l’aide d’un microscope de laboratoire qui peut être facilement mis en œuvre en milieu hospitalier
Hepatocellular carcinoma (HCC) is the sixth most common neoplasm and the second most common cause of death in the world. Hepatocarcinogenesis is a multistep process characterized in patients with chronic liver diseases by a spectrum of hepatic nodules that mark the progression from regenerative nodules to dysplastic lesions followed by HCC. Liver transplantation remains the curative therapeutic option able to treat both the HCC and the underlying liver disease. The issue is that there is no objective and quantifiable marker for quality control of liver graft. Specific biomarkers of early stages of HCC are also an unmet need.In this study, we have evaluated the potential of infrared (IR) microspectroscopy for the diagnosis of steatosis, one of the most important factors affecting the liver allograft function. Vibrational microspectroscopy, such as Fourier transform infrared microspectroscopy (FTIR), allows detecting spectral characteristics associated with different molecular components present in the biological sample, both qualitatively and quantitatively. Our first working hypothesis was that the progression of liver steatosis corresponds not only to the accumulation of lipids but also to dramatic changes in the qualitative composition of tissue. Indeed, a lower grade of steatosis showed a decrease in glycogen content and concomitant increase in lipids in comparison with normal liver. Intermediate steatosis exhibited an increase in glycogen and major changes in lipids, with a significant contribution of esterified fatty acids with elongated carbon chains and unsaturated lipids, and these features were more pronounced in a high grade of steatosis. Furthermore, we have shown, that FTIR approach allows a systemic discrimination of morphological features, leading to a separate investigation of steatotic vesicles and the non-steatotic counterpart of the tissue. This highlighted the fact that dramatic biochemical changes occur in the non-steatotic part of the tissue also despite its normal histological aspect, suggesting that the whole tissue reflects the grade of steatosis. The second part of the thesis focused on hepatocarcinogenesis; a multistep process that is characterized in most cirrhotic livers by the progression from hyperplastic regenerative nodules to low grade dysplastic nodules (LGDN), high grade dysplastic nodules (HGDN) and finally small HCC which corresponds either to vaguely nodular well differentiated HCC so called early HCC or to distinctly nodular moderately differentiated hepatocellular carcinomas. Since the differential diagnosis between precancerous dysplastic nodules and early HCC remains extremely difficult, we addressed the potential of FTIR microspectroscopy for grading cirrhotic nodules. The study was focused on 39 surgical specimens including normal livers as controls, dysplastic nodules, early HCC and the progressed HCC. Profound alterations of the biochemical composition of the pathological liver were demonstrated by FTIR microspectroscopy. Indeed, dramatic changes were observed in lipids, proteins and sugars highlighting the metabolic reprogramming in carcinogenesis. The major changes were observed in the frequency domain 950-1480 cm-1 in which several bands allowed significant discrimination of cirrhotic nodules, dysplastic lesions and HCC. Finally, a significant discrimination between benign, dysplastic nodules and early HCC remained possible using a FTIR microscope equipped with a laboratory-based infrared source that can be easily implemented in hospital environment. In conclusion, our study positions FTIR microspectroscopy as a versatile and powerful approach for investigating liver diseases, such as steatosis, dysplastic lesions and cancer. Further studies on larger series of patients as well as on biopsies will allow confirming the clinical reliability of such spectral signatures. Therefore, we anticipate that FTIR microspectroscopy will open new avenue in clinical diagnosis
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Books on the topic "Hepatocellular Carcinoma HSC"

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Bamia, Christina, Sherri Stuver, and Lorelei Mucci. Cancer of the Liver and Biliary Tract. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0012.

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Primary liver cancer is one of the most commonly occurring cancers globally, and is the second most common cause of cancer death worldwide. There are two major histologic forms of primary liver cancer: hepatocellular carcinoma (HCC) and cholangiocarcinoma. It is a rapidly and almost uniformly fatal disease, yet there is already sufficient knowledge about its major risk factors, many of which are modifiable, to make primary prevention effective. Primary liver cancer is one of the first common human cancer that was found to have an infectious etiology, with hepatitis B virus (HBV) and hepatitis C virus (HCV) for HCC, and parasitic liver flukes for cholangiocarcinoma. Obesity is emerging as an important risk factor, particularly in Western countries, where primary liver cancer rates appear to be increasing over time. A number of additional risk factors and potential preventive factors are considered in this chapter.
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Thomas London, W., Jessica L. Petrick, and Katherine A. McGlynn. Liver Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0033.

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Primary liver cancer is the sixth most frequently occurring cancer in the world and the second most common in terms of cancer deaths. The global burden of liver cancer is borne principally by countries in East Asia and Africa, where 80% of liver cancer arises. Incidence rates of liver cancer, however, have begun to decline in Asia, while rates are increasing in low-rate areas such as Europe and North America. The dominant histology of liver cancer in almost all countries is hepatocellular carcinoma (HCC). The major risk factors for HCC—chronic infection with either hepatitis B virus (HBV) or hepatitis C virus (HCV), aflatoxin B1 (AFB1) contamination of foodstuffs, excessive alcohol consumption, and diabetes/obesity/fatty liver disease—all result in chronic inflammation in the liver. HBV infection is preventable by immunization, and HCV infection is largely preventable by public health measures and now is curable with new antiviral therapies.
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Keshav, Satish, and Palak Trivedi. Liver cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0218.

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Primary hepatocellular carcinoma (HCC) arises from hepatocytes and is one of the commonest solid-organ malignancies in the world, particularly in the Far East and in sub-Saharan Africa. Cholangiocarcinoma arises from the biliary epithelium. The incidence is rising in the West, and primary sclerosing cholangitis (PSC) is an important risk factor (15% lifetime risk). Other forms of liver cancer include metastatic cancer, which is much more common in the West than any primary liver cancer, accounting for 90% of liver cancers and for which common primary sites are the colon, the stomach, the breasts, and the lungs; hepatoblastoma, which is an uncommon malignancy in children, originating from immature liver cell precursors; haemangiosarcomas, which are also rare, are malignant tumours arising from the blood vessels in the liver and can be very rapidly growing; and gall bladder cancer, arising from the gall bladder epithelium. Gallstones and PSC are risk factors for gall bladder cancer; in particular, PSC confers a risk >160 times that of the control population. This chapter primarily focuses on HCC.
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Book chapters on the topic "Hepatocellular Carcinoma HSC"

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Aravalli, Rajagopal N., and Clifford J. Steer. "Pathophysiology of HCC." In Hepatocellular Carcinoma, 15–32. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09414-4_4.

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Carr, Brian I., and Srikanth Nagalla. "Medical Therapy of HCC." In Hepatocellular Carcinoma, 527–68. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-376-3_20.

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Aravalli, Rajagopal N., and Clifford J. Steer. "Molecular Mechanisms of HCC." In Hepatocellular Carcinoma, 33–46. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09414-4_5.

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Carr, Brian I. "HCC and Its Microenvironment." In Hepatocellular Carcinoma, 163–66. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34214-6_11.

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Robertson, Chadia L., Devanand Sarkar, and Arun J. Sanyal. "Obesity, NASH, and HCC." In Hepatocellular Carcinoma, 275–86. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34214-6_18.

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Agnello, Francesco, and Giuseppe Brancatelli. "Computed Tomography of HCC." In Hepatocellular Carcinoma, 399–408. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34214-6_26.

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Carr, Brian I., Srikanth Nagalla, and Ravit Geva. "Medical Therapy of HCC." In Hepatocellular Carcinoma, 489–512. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34214-6_33.

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Loosen, Sven H., Christoph Roderburg, and Tom Luedde. "Gut Microbiota and HCC." In Hepatocellular Carcinoma, 149–55. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34214-6_9.

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Carr, Brian I., and Susan Kralian. "Molecular Targeted Therapies for HCC." In Hepatocellular Carcinoma, 589–614. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-376-3_22.

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Aravalli, Rajagopal N., and Clifford J. Steer. "Novel Therapeutic Strategies to Combat HCC." In Hepatocellular Carcinoma, 51–63. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09414-4_7.

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Conference papers on the topic "Hepatocellular Carcinoma HSC"

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Mohsin, Abeer. "Effects of Induced Oxidative Stress as a Therapeutic Approach Against Hepatocellular Carcinoma." In INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Jinnah University for Women, Karachi,Pakistan, 2022. http://dx.doi.org/10.37962/ibras/2022/14-16.

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Hepatocellular carcinoma is a type of primary liver cancer that accounts for 75% of all liver cancers globally. HCC is said to be the 6th most prevalent cancer and the 3rd major cause of cancer related death accounting for approximately 0.32 million annual deaths across the globe. The increasing incidence of HCC with a very high mortality rate is a major problem encountered by many regions of the world including both developing and developed countries and is a source of increasing economic burden. Therefore, effective treatment strategies for HCC are the need of the hour. Oxidative stress can be referred to as the lack of proportion between generation of reactive oxygen species and their removal by antioxidant defense mechanisms. This imbalance can have deleterious effects and contributes to the pathophysiology of several disorders including inflammation, aging cataract, diabetes and cancer. However, this controversial role of oxidative stress leading to apoptosis can be acquired as a treatment for HCC. The current study aimed to investigate the effect of induced oxidative stress via hydrogen peroxide (H2O2) on the proliferation of HCC Huh-7 cells in-vitro. The toxicity generated by H2O2 produce anti- proliferative effect on HCC Huh-7 cells and up regulates the oxidative stress markers. Proteomic studies were conducted in order to identify differential protein expression as potential therapeutic targets for the treatment of HCC.
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Lei, Ningjing, Bo Peng, Yang Li, Yurong Chai, and Jianying Zhang. "Abstract 5381: p62/IMP2 promotes hepatocellular carcinoma (HCC) progression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5381.

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Lefrère, J. J., D. Gozin, J. P. Soulier, P. Mavier, L. Bettan, and D. Dhumeaux. "SPECIFICITY OF INCREASED DES-GAMMA-CARBOXYPROTHROMBIN AS A MARKER OF HEPATOCELLULAR CARCINOMA AFTER VITAMIN K INJECTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644319.

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An elevation of des-gamma-carboxyprothrombin (DCP) has been observed in about 70 % of cases of hepatocellular carcinoma (HCC). Howewer, an increased DCP is not specific of HCC. Oral anticoagulant therapy increases the DCP level by preventing the gamma-carboxylation of prothrombin : thereafter an increased DCP can not be used as an HCC marker before three weeks have elapsed after stopping anti vitamin K therapy. Furthermore, since vitamin K is necessary for the gamma-carboxylation of vitamin K dependent factors, a vitamin K deficiency increases the DCP level long before the modification of the prothrombin time. It is thus imperative to eliminate an underlying vitamin K deficiency before attributing an increased DCP to a HCC. We used a method of DCP assay using staphylocoagulase. We studied the effect of an intravenous injection of 20 mg of vitamin K1 on DCP level in 7 patients with histologically proven HCC and in 10 patients with various disorders (5 alcoholic cirrhosis, 1 chronic hepatitis, 4 pancreatic cancer). All these 17 patients had increased DCP before vitamin K injection. In a second sampling obtained 15 days or more after injection, only the 7 patients with HCC kept increased DCP level. In patients of both categories in whom we obtained intermediary samplings, we observed that the DCP level decreased In all cases. The normalisation of the DCP level was lasting only in those patients without HCC, confirming the hypothesis of an underlying vitamin K deficiency ; this decrease was very transitory in those patients with HCC, suggesting that the elevated DCP came from a yet unexplained (but not linked to a vitamin K deficiency) mechanism. We may conclude that an increased DCP level 15 days after vitamin K injection may constitute a specific marker of HCC.
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Srivastava, Jyoti, Devaraja Rajasekaran, Ayesha Siddiq, Rachel Gredler, Chadia L. Robertson, Maaged A. Akiel, Xue-Ning Shen, et al. "Abstract 5400: A novel combinatorial therapy for hepatocellular carcinoma (HCC)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5400.

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Rajesh, Sanapala, Nurul Amin Choudhury, and Soumen Moulik. "Hepatocellular Carcinoma (HCC) Liver Cancer prediction using Machine Learning Algorithms." In 2020 IEEE 17th India Council International Conference (INDICON). IEEE, 2020. http://dx.doi.org/10.1109/indicon49873.2020.9342443.

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Bisceglie, Adrian M. Di. "Abstract IA37: Prevention of Hepatocellular Carcinoma (HCC) with antiviral therapy." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-ia37.

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Michalski, M., E. Aschenbrenner, K. Pollinger, M. Müller-Schilling, and K. Gülow. "Induction of cell death in hepatocellular carcinoma (HCC) via energy depletion." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677219.

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Michalski, M., O. Wiesner, M. Müller-Schilling, and K. Gülow. "Dimethyl fumarate (DMF) inhibits migration and proliferation of hepatocellular carcinoma (HCC)." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402232.

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Ma, Yuxiang, Yang He, Haiyan Chen, Heng Guo, Dawei Deng, Zhiyu Qian, and Yueqing Gu. "Characteristic of a drug carrier for hepatocellular carcinoma (HCC)-selective targeting." In Bio-Optics: Design and Application. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/boda.2015.jt3a.14.

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Shen, Jing, Abby B. Siegel, Helen Remotti, Qiao Wang, Yueyue Shen, and Regina M. Santella. "Abstract 3818: Deregulated long non-coding RNAs in hepatocellular carcinoma (HCC)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3818.

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Reports on the topic "Hepatocellular Carcinoma HSC"

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Zheng, Jiaxi, and Haihua Yang. Clinical Benefits of Immune Checkpoint Inhibitors and Predictive Value of Tumor Mutation Burden in Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0008.

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Review question / Objective: Is immunotherapy associated with beneficial clinical outcomes for hepatocellular carcinoma (HCC) and how can combination immunotherapy be deployed to produce the best benefit? Is tumor mutation burden (TMB) a predictive biomarker for immune‐checkpoint inhibitors? Condition being studied: To this date, about 50 single-arm clinical trials and several randomized control trials (RCTs) presented final or interim results of investigations on the efficacy of PD-1/PD-L1 inhibitors for advanced HCC. In the CheckMate 459, IMbrave 050, and ORIENT-32, immunotherapies were found to significantly improve progression-free survival (PFS) and overall survival (OS) compared with sorafenib (a tyrosine-kinase inhibitor, as standard systemic treatment) in patients with advanced hepatocellular carcinoma. However, these clinical trials were different on clinical phases, sample size, and response evaluation criteria, and inconsistent clinical outcomes were shown in several trials.
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Jin, Hongyu, and Man Zhang. LR-5 by LI-RADS under contrast enhanced ultrasonography manifests satisfactory diagnostic performance for hepatocellular carcinoma: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0011.

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Review question / Objective: To evaluate the relative diagnostic sensitivity, specificity, and accuracy of LR-5 under contrast-enhanced ultrasonography (CEUS) LI-RADS system in the differential diagnosis of hepatocellular carcinoma (HCC). Information sources: A comprehensive and thorough search of literature was carried out through internationally acknowledged medical literature resources database, including PubMed/MEDLINE, EMBASE, Ovid, and Web of Science along with regional databases with key research words of (“hepatocellular carcinoma” OR “liver cancer” OR “liver tumor” OR “liver nodule” OR “liver mass” OR “liver lesion”) AND (“contrast-enhanced US” OR “contrast-enhanced ultrasonography” OR “contrast-enhanced ultrasound” OR “CEUS”) AND (“LI-RADS” OR “liver reporting and data system”) for studies published between January 2017 and June 2021. We limited the language used in the literature as English only.
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Chen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng, and Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, September 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.

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Objective: The aim of this study was to assess the therapeutic effects of Jianpi Liqi decoction (JPLQD) in hepatocellular carcinoma (HCC) and explore its underlying mechanisms. Methods: The characteristics and outcomes of HCC patients with intermediate stage B who underwent sequential conventional transcatheter arterial chemoembolization (cTACE) and radiofrequency ablation (RFA) only or in conjunction with JPLQD were analysed retrospectively. The plasma proteins were screened using label-free quantitative proteomics analysis. The effective mechanisms of JPLQD were predicted through network pharmacology approach and partially verified by ELISA. Results: Clinical research demonstrated that the Karnofsky Performance Status (KPS), traditional Chinese medicine (TCM) syndrome scores, neutropenia and bilirubin, median progression-free survival (PFS), and median overall survival (OS) in HCC patients treated with JPLQD were superior to those in patients not treated with JPLQD (all P<0.05). The analysis of network pharmacology, combined with proteomics, suggested that 52 compounds targeted 80 potential targets, which were involved in the regulation of multiple signaling pathways, especially affecting the apoptosis-related pathways including TNF, p53, PI3K-AKT, and MAPK. Plasma IGFBP3 and CA2 were significantly up-regulated in HCC patients with sequential cTACE and RFA therapy treated with JPLQD than those in patients not treated with JPLQD (P<0.001). The AUC of the IGFBP3 and CA2 panel, estimated using ROC analysis for JPLQD efficacy evaluation, was 0.867. Conclusion: These data suggested that JPLQD improves the quality of life, prolongs the overall survival, protects liver function in HCC patients, and exhibits an anticancer activity against HCC. IGFBP3 and CA2 panels may be potential therapeutic targets and indicators in the efficacy evaluation for JPLQD treatment, and the effective mechanisms involved in the regulation of multiple signaling pathways, possibly affected the regulation of apoptosis.
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