Relevant bibliographies by topics / Liver cancer

Academic literature on the topic 'Liver cancer'

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Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "Liver cancer"

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Ozaki, Michelle K., Yi Zhang, Zheng Xi, and Pepper Schedin. "Abstract A046: Liver involution generates a pro-metastatic niche in a murine model of postpartum breast cancer liver metastasis." Cancer Research 84, no. 3_Supplement_1 (February 1, 2024): A046. http://dx.doi.org/10.1158/1538-7445.advbc23-a046.

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Abstract Postpartum breast cancer (PPBC), cases diagnosed within 10 years of childbirth, has increased risk of liver metastases. Our lab has shown that the liver undergoes growth during pregnancy and lactation to support milk production, and upon weaning, undergoes involution. We have previously shown the actively involuting liver supports breast cancer liver metastasis in rodent models of PPBC, yet the mechanisms are poorly understood. Here, we performed RNAseq analysis in mouse livers across a lactation/wean cycle, and identify stromal alterations that may contribute to the “involution-educated” metastatic niche. During involution, RNA seq analysis reveals increased signatures for apoptotic cell death, catabolic metabolism, regulatory immune cell abundance, and extracellular matrix remodeling consistent with fibroblast activation. Using liver perfusion methods in live animals, we isolated viable stromal cells from livers of nullip or involution mice and validated these cells as highly enriched for fibroblasts by quantitative PCR. Liver fibroblasts were then mixed 1:1 with mouse mammary tumor cells, and injected into host mice at the flank site. We found fibroblasts from involuting livers generated larger tumors (n=28 tumors/group p=0.013), with decreased caspase 3 staining. Further, involution fibroblast tumors had increased ECM deposition as measured by trichrome staining, consistent with involution liver fibroblasts being more activated. Combined these data suggest that involution liver fibroblasts support tumor growth by suppressing tumor cell death, and by providing a pro-tumor collagen matrix when compared to nulliparous liver fibroblasts. These data implicate fibroblasts as components of the involution-educated metastatic niche in the postpartum liver. RNAseq analysis of involuting livers also identified gene signatures correlated with immature myeloid cells that associate with immune suppression and worse prognosis in numerous cancers. We thus evaluated for immature myeloid cells by multiplex immunohistochemistry in healthy mouse livers across a reproductive cycle, and identified increased abundance of immature myeloid cells (CD45+, CD11b+, Gr-1+) specifically during involution (n=6/group, p<0.05). Further, our data suggest liver involution may have a durable impact on immune composition of breast cancer liver metastases, as we find evidence for increased immature myeloid cells (CD45+, CD11b+, CD33+, CD68-, CD66b-, Cd56-, CD11c-, CD20-) in liver metastases of PPBC patients compared to non-PPBC patients. These data implicate immature myeloid cells as another component of the involution-educated liver metastatic niche. In sum, we find physiological involution of the liver post-wean alters the liver stromal microenvironment in a manner consistent with establishing a metastatic niche. Our findings may lead to the identification of liver stromal targets that can be exploited for prevention and or treatment strategies for PPBC liver metastasis. Citation Format: Michelle K Ozaki, Yi Zhang, Zheng Xi, Pepper Schedin. Liver involution generates a pro-metastatic niche in a murine model of postpartum breast cancer liver metastasis [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Advances in Breast Cancer Research; 2023 Oct 19-22; San Diego, California. Philadelphia (PA): AACR; Cancer Res 2024;84(3 Suppl_1):Abstract nr A046.
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Thorgeirsson, Snorri S. "Stemness in Liver Cancer." Digestive Diseases 35, no. 4 (2017): 387–89. http://dx.doi.org/10.1159/000456592.

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Cancer cells possessing “stemness,” or stem-cell properties, are referred to as cancer stem cells (CSC) or cancer-initiating cells. The concept that these cells rest at the apex of the cancer hierarchy is an evolving theme in cancer research. These cells are by definition primarily responsible for the initiation and propagation of tumors as well as relapse after therapy, and they are therefore of major scientific interest. Several studies indicate that hepatocellular carcinomas that harbor phenotypic features of stem cells and progenitor cells constitute a subclass of therapeutically challenging cancers that are associated with a particularly poor prognosis. We recently demonstrated that any cell type in the mouse hepatic lineage can undergo oncogenic reprogramming into a CSC by activating different cell type-specific pathways [<citeref rid="ref1">1</citeref>]. Identification of common and cell of origin-specific phenotypic and genetic changes could provide new therapeutic targets for liver cancer.
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Barber, Fedricker Diane, and Jenenne P. Nelson. "Liver Cancer." American Journal of Nursing 100, no. 4 (April 2000): 41. http://dx.doi.org/10.2307/3521935.

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Oberfield, R. A., G. Steele, J. L. Gollan, and D. Sherman. "Liver Cancer." CA: A Cancer Journal for Clinicians 39, no. 4 (July 1, 1989): 206–18. http://dx.doi.org/10.3322/canjclin.39.4.206.

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Susman, Ed. "Liver Cancer." Oncology Times 37, no. 12 (June 2015): 59–60. http://dx.doi.org/10.1097/01.cot.0000467337.34244.33.

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Laino, Charlene. "Liver Cancer." Oncology Times 29, no. 5 (March 2007): 26–27. http://dx.doi.org/10.1097/01.cot.0000267756.88700.06.

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Gravitz, Lauren. "Liver cancer." Nature 516, no. 7529 (December 2014): S1. http://dx.doi.org/10.1038/516s1a.

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Blum, Hubert E. "Liver cancer." European Journal of Gastroenterology & Hepatology 17, no. 5 (May 2005): 475–76. http://dx.doi.org/10.1097/00042737-200505000-00001.

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Venook, Alan P. "Liver Cancer." American Journal of Gastroenterology 93, no. 3 (March 1998): 489–90. http://dx.doi.org/10.1111/j.1572-0241.1998.488_2.x.

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Barber, Fedricker Diane, and Jenenne P. Nelson. "Liver Cancer." AJN, American Journal of Nursing &NA;, Supplement (April 2000): 41–46. http://dx.doi.org/10.1097/01.naj.0000370637.48055.17.

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Dissertations / Theses on the topic "Liver cancer"

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Clèries, Soler Ramon. "Geographic Variability in Liver Cancer." Doctoral thesis, Universitat Autònoma de Barcelona, 2006. http://hdl.handle.net/10803/4627.

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At the beginning of the 21st century, primary liver cancer (PLC) remains the fifth most common malignancy in men worldwide, and the eighth in women. Central Africa and South East of Asia are high risk geographic areas for PLC, whereas developed countries appear to be generally low risk. Infections with hepatitis B (HBV) and C (HCV) viruses are the main risk factors for PLC, accounting for well over 80% of PLC cases detected worldwide. The recently detected increase in both incidence and mortality by PLC in developed countries is strongly related to these viral infections. The evaluation of PLC time trends needs to take into consideration the geographic distribution and effect of these viruses. This thesis presents three studies which the aim to describe PLC incidence and mortality issues in different geographic areas, each addressing several epidemiological and methodological issues. For each study, different statistical methods on the basis of the Bayesian inference have been proposed, evaluated and discussed in order to cope with extra-Poisson variability.
The first study, entitled "Meta-analysis of cohort studies of risk of liver cancer death among HBV carriers", evaluates the variability in PLC mortality reported in 11 cohort studies of male HBV carriers, taking into consideration the effects of geographic area and the choice of the general population versus a more comparable group such as HBV-negative workers or blood donors as the comparison group. The statistical methods of this study focuses on mixtures of Poisson distributions. The "stickbreaking" method has been used to estimate the number of components of the mixture of Poisson distributions, and, thus to obtain a pooled relative risk (RR) of death for PLC among male HBV carriers. The pooled RR of death by PLC related to HBV infection was 23.5 (95% Credibility Interval (CRI): 14.9 - 44.5). Studies carried out in high risk areas for PLC (China and Taiwan) showed RRs 2 to 5-fold higher than those of studies carried out in Europe, Japan and the U.S.. In low risk areas for PLC, studies which used workers or blood donors as comparison groups had RRs 1.9-fold higher (95% CRI: 1.2 - 3.1) than studies which used the general population. However, in high risk areas, the ratio of RRs was 5.3-fold (95% CRI: 3.4 - 7.9). This is the first time that a "healthy donor effect" has been quantified in longitudinal studies.
The second study, entitled "Geographic distribution of primary liver cancer in Europe in 2002" evaluates the effect of HBV and HCV seroprevalence in 38 European countries on PLC incidence and mortality. Mixed Poisson models based on Bayesian inference have been used to smooth Standardized Incidence (SIR) and Mortality (SMR) ratios for PLC accounting for the effect of HBV and HCV prevalences. This approach enabled us to both examine the effect of different levels of HBV and HCV, and to identify remaining variability in PLC after accounting for infection rates. Bayesian inference allowed the determination of posterior probabilities for the somoothed SIRs and SMRs (hereafter RRs). The Deviance Information Criterion (DIC) and the "effective number of parameters" (pD) have been used as tools for model choice. The highest mortality and incidence PLC RRs were found in Southern European countries (RR range 0.9-2.4), whereas Northern European countries showed the lowest RRs (RR range: 0.3-0.9). The effect of HBV infection was not found to be statistically significant in the model which accounted for both HBV and HCV prevalence. Countries with a prevalence of HCV higher than 2% (e.g.: Italy and Spain) had a higher risk of incidence and mortality (RR range: 1.28 - 1.78) than countries with HCV prevalence below 1%. Thus, the high risk of PLC detected in Southern Europe appears to be explained, in part, by HCV infection. The high HCV seroprevalence in this area could be associated with exposure 30-50 years ago. There may be an underestimation of PLC incidence and mortality rates in Eastern European countries given the low PLC RRs reported, despite high HBV and HCV seroprevalences observed. The implementation of population-based cancer registries in Eastern European countries is warranted, as well as HCV prevalence studies across Europe, to better determine the distribution of PLC in Europe and its relationship with that virus.
The last study, entitled "Time trends in liver disease in Spain during the period 198397", describes incidence and mortality trends in hepatocellular carcinoma and cholangiocarcinoma as well as mortality trends in liver cirrhosis in Spain. Autoregressive age-period-cohort (APC) models have been used to evaluate the time trends. We found that APC models performed well for those liver diseases with large number of cases, whereas the age-period models did for those liver diseases with low number of cases. We found an increase in incidence and mortality of hepatocellular carcinoma in Spain (annual percent change (APCH) in men's incidence: 6.6%, 95% CRI: 5.8, 8.1: APCH in women's incidence: 4.5%, 95% CRI: 1.4%, 7.3%; APCH in men's mortality: 6.8%, 95% CRI: 5.8%, 8.1%; APCH in women's mortality: 5.1%, 95% CRI: 3.5%, 6.3%), that appear to be related to HCV exposure 30 years ago, as described in other studies of PLC. We also found an increasing trend in cholangiocarcinoma mortality (APCH in men: 17.1%, 95% CRI: 13.5%, 21.2%; APCH in women: 15.0%, 95% CRI: 11.5%, 19.5%) similar to that found in some developed countries, that could be attributed to improvement in diagnosis resulting from better imaging and diagnostic techniques. However, we did not detect a significant increasing trend in cholangiocarcinoma incidence, perhaps due to the low number of cases reported by the Spanish cancer registries. We have observed a decreasing trend in cirrhosis mortality in both sexes during the study period (APCH in men: -3.1%, 95% CRI: -5.1, -1.9%; APCH in women: -2.9%; 95% CRI: -6.2%, -1.3%), although younger cohorts did not show this pattern. This cohort effect suggests the possibility that younger cohorts could be exposed to some additional risk factors besides alcohol consumption. HIV and HCV or HBV co-infection and intravenous drug addiction could explain the increase in liver cirrhosis mortality among younger cohorts.
The flexibility of the Bayesian approach allowed us to cope with extra-Poisson variability in three statistical analyses, applying different models, and addressing relevant methodological aspects specific to each problem. Challenging statistical issues in the framework of Bayesian applied modelling are: i) the selection of prior distributions for model parameters, which is related to convergence of the model; and ii) model selection procedures, and these remain important considerations for future research.
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Ng, Oi-lin Irene, and 呂愛蓮. "Patho-biological prognostic factors in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31981537.

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黎卓先 and Cheuck-seen Edward Lai. "Resection margin for hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1992. http://hub.hku.hk/bib/B30257529.

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Urdzik, Jozef. "Colorectal Cancer Liver Metastases : Effects of Chemotherapy on Liver Parenchyma and Resections." Doctoral thesis, Uppsala universitet, Institutionen för kirurgiska vetenskaper, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-233790.

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Current multimodal treatment of colorectal cancer liver metastasis often combines liver resections with preoperative chemotherapy with a 5-year survival of 40-50%. Preoperative chemotherapy includes conversion of initially non-resectable situation and control of micrometastatic disease. Despite its potential advantages also problems with associated steatosis, steatohepatitis and sinusoidal injury has been discussed. Paper I focused on prospective steatosis evaluation prior to resections using proton MR spectroscopy, most sensitive non-invasive method. Proton MR spectroscopy showed high concordance with digital quantification of steatosis and was also able to predict steatohepatitis with 100% sensitivity and 89% specificity without knowing lobular inflammation or hepatocyte ballooning. Paper II focused on portal vein hemodynamics changes in patients treated with oxaliplatin-based treatment and with sinusoidal injury. Magnetic resonance imaging flowmetry demonstrated portal vein dilatation associated with oxaliplatin treatment. Patients with SI showed a tendency towards decreased mean portal flow velocity. Portal vein flow was not changed. This may indicate that SI is associated with an increased resistance to blood flow in the liver parenchyma and stasis in splanchnic system. Paper III attempted to enlighten the effects of FOLFOX treatment on human liver tissue 6 weeks after treatment cessation by quantification of protein expression changes using label-free global proteome analysis. Deep proteome analysis identified 5891 proteins, where machine learning algorithm identified 3% of classifying proteins, associated with changes in DNA replication through upregulation of the minichromosome maintenance complex and with the innate immune response. Significant changes were observed in 1% of proteins, associated with DNA replication and cell cycle entry. Results support the hypothesis that liver has already regenerated from the FOLFOX treatment injury after 6 weeks. Paper IV aimed to identify possible patient, disease and chemotherapy characteristics associated with liver specific and severe general complications in a retrospective single centre cohort composed of 516 consecutive resections. Chemotherapy with more than 4 cycles of oxaliplatin was associated with post-hepatectomy hemorrhage. Underlying liver disease and diabetes mellitus were associated with 90-day mortality. Size of resection, intraoperative blood loss and transfusions were verified as independent predictors of liver specific complications to resections.
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Poon, Tung-ping Ronnie, and 潘冬平. "Surgical strategies to improve long-term survival after hepatectomy for hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31979634.

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Farah, Yasser Abdulhamid Elskay, and L. O. Averyanova. "Technologies for prevention liver cancer in Egypt." Thesis, ХНУРЕ, 2019. http://openarchive.nure.ua/handle/document/8373.

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Deaths from liver cancer are common, especially in East Asia and Pacific, South Asia, and parts of Sub-Saharan Africa, largely as a result of infection decades ago. Controlling the risk factors would not only reduce the incidence of liver cancer; it would also reduce the incidence of cirrhosis and its other complications. This paper will discuss the clinical implications of imaging in screening, diagnosis, staging, and follow-up of patients in liver malignancies.
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Rava', M. "FUNCTIONAL DISSECTION OF ST18 IN LIVER CANCER." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/254403.

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The molecular mechanisms and pathways responsible for the progression of hepatocellular carcinoma (HCC) remain to be fully characterized. Among the genetic lesions associated with HCC progression, Shukla et al. (2013) identified insertions of the L1 transposon proximal to the gene encoding the zinc-finger DNA-binding protein ST18 (suppression of tumorigenicity 18) and suggested that this actually functions as an oncogene in HCC. However, functional evidence for a cancer-promoting activity of ST18 and insight into its mode of action are missing. Here, I pursued the functional characterization of ST18 in a mouse model of HCC based on ex vivo transformation and subcutaneous transplantation of embryonic hepatoblasts. ST18 was undetectable in either normal liver or cultured hepatoblasts, but was induced in the subcutaneous tumors. ST18 was also expressed in either chronically or acutely inflamed mouse livers (as assessed in Mdr2-/- or LPS-treated mice) as well as in human Progressive Familial Intrahepatic Cholestasis 2 (PFIC2: a condition associated with chronic inflammation), suggesting its induction by inflammatory stimuli. The knockdown of ST18 delayed tumor formation or, if induced in already formed tumors, led to rapid hemorrhage, pervasive morphological changes in the tumor cells reminiscent of an epithelial-to-mesenchymal transition (EMT) and eventually tumor regression. RNA profiling revealed that ST18 silencing caused expression of EMT-associated genes, among others. Previous studies have linked inflammation to the induction of EMT in other epithelia: we hypothesize that the concomitant activation of ST18 constitutes a safeguard against EMT, inactivation of this control mechanism causing the dramatic phenotypic switch observed in our model. These data warrant further evaluation of the mode of action of ST18 and of its potential value as a therapeutic target in HCC.
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Fung, Wai-yip. "The characterization of PAK 6 in liver cancer." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4260980X.

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Lilienberg, Elsa. "Biopharmaceutical Evaluation of Intra-arterial Drug-Delivery Systems for Liver Cancer : Investigations in healthy pigs and liver cancer patients." Doctoral thesis, Uppsala universitet, Institutionen för farmaci, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-267396.

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There are currently two types of intra-arterial drug-delivery system (DDS) in clinical use in the palliative treatment of primary liver cancer. The chemotherapeutic drug doxorubicin (DOX) can be formulated into a drug-in-lipiodol emulsion (LIPDOX) or a microparticulate drug-eluting bead system (DEBDOX). To facilitate development of future DDSs, we need to understand the release and local distribution of drug from these DDSs into the complex, in vivo, pathological environment. The overall aim of this project was to assess and improve understanding of the in vivo release of DOX from LIPDOX and DEBDOX and its local disposition in the liver. These processes were investigated in detail in a multisampling-site, healthy pig model and in human patients with liver cancer. The mechanisms involved in DOX disposition were studied by examining potential interactions between DOX and lipiodol and/or cyclosporine A (CsA) in pigs.   In this project, the main elimination pathway for DOX and its primary metabolite doxorubicinol (DOXol) was via bile; their extensive canalicular carrier-mediated transport (e.g. ATP-binding cassette transporters ABCB1, ABCC1, ABCC2 and ABCG2) was inhibited by CsA. CsA had no effect on the carbonyl and aldo-keto reductases responsible for the metabolism of DOX into DOXol. LIPDOX released DOX more rapidly and to a greater extent into the circulation than DEBDOX, which had only released 15% of the dose in patients after 24 hrs. The systemic exposure to DOX was lower for DEBDOX than for LIPDOX. Greater fractions of DOXol were formed in blood and bile with LIPDOX than with DEBDOX. This may have been because DOX was more widely distributed into regions with increased metabolic capacity or because of increased intracellular uptake when DOX was delivered in LIPDOX. The excipient lipiodol in the LIPDOX formulation did not interact with transporters, enzymes or membranes that would explain the increased cellular uptake of DOX. In conclusion, the release of DOX from DEBDOX is more controlled in vivo than that from LIPDOX, indicating that DEBDOX is a more robust pharmaceutical product. The formulations for future optimized DDSs should therefore be more similar to DEBDOX than to LIPDOX.
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Liu, Ming, and 劉銘. "Identification and characterization of novel genetic alterations in the progression of hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196441.

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Hepatocellular carcinoma (HCC) is one of the most frequent human malignancies worldwide with very poor prognosis. It is generally believed that accumulation of irreversible alterations in critical oncogenes and tumor suppressor genes during the long-term inflammation finally leads to the hepatocellular pathogenesis. Although under intensive investigation, the molecular pathogenesis of HCC still remains to be further elucidated. In this study, we aimed to identify novel genetic alterations critical to the pathogenesis of HCC, especially in hot regions with recurrent chromosomal instability. Amplification of broad regions of 8q is one of the most frequent genetic alterations in HCC, suggesting the existence of oncogenes in addition to MYC at 8q24. By screening the publicly available microarray database and clinical samples, we found frequent amplification and overexpression of Serum and Glucocorticoid Kinase 3 (SGK3) in clinical HCC specimens, and SGK3 genomic activation was significantly associated with poor outcome of HCC patients. Functional assays revealed that SGK3 could increase G1/S cell cycle progression, cell survival, clonogenicity, anchorage-independent growth, and tumor formation in nude mice. We provided evidences that SGK3 could promote HCC growth and survival through inactivating GSK3-β and BAD respectively. We also found that expression of SGK3, which like AKT is activated by PI3K/PDK1, has more significance than overexpression of AKT in predicting poor outcome of HCC patients. Our findings suggested the existence of an AKT-independent SGK3 pathway, which may function in parallel with AKT pathway in the pathogenesis of HCC. In addition to large chromosomal alterations, small changes in nucleotides may also make substantial contributions to carcinogenesis. Recent advances in high-throughput deep sequencing technology have provided a powerful tool to understand the whole cancer transcriptome and identify novel genetic alterations related to cancer progression. In this study, we identified a high proportion of allele imbalance in genes related to cellular stress response by sequencing the whole transcriptome of 3 paired HCC tissues. A novel nucleotide variation which resulted in a R438H amino acid change was identified in the coding region of the gene Oxidative Stress Induced Growth Inhibitor 1 (OSGIN1), and the variant 438H form of OSGIN1 was found to be specifically retained in the tumor tissues in a cohort of HCC patients. OSGIN1 was found to be closely associated with chemotherapeutic reagents and exhibited strong tumor suppressive function in HCC by directly inducing cell apoptosis. The wild type OSGIN1 was found to have stronger tumor suppressive function than the variant allele, and this might be due to their different ability to localize to mitochondria. The significantly decreased basal apoptotic index in HCC patients carrying OSGIN1 variant allele and their poor prognosis further suggested that the specific retention of 438H OSGIN1 might be important in HCC progression. In summary, we found a frequently amplified oncogenic SGK3 signaling pathway, as well as the allele-specific imbalance of tumor suppressive OSGIN1 in the pathogenesis of HCC. Further characterization of their mechanisms in hepatocarcinogenesis may help provide novel prognostic biomarkers and therapeutic targets in HCC treatment.
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Books on the topic "Liver cancer"

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A, Curley Steven, ed. Liver cancer. New York: Springer, 1998.

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Hayat, M. A. Liver Cancer. Dordrecht: Springer Netherlands, 2009.

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Curley, Steven A., ed. Liver Cancer. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-1666-7.

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Hayat, M. A., ed. Liver Cancer. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9804-8.

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Bottino, Joseph C., Richard W. Opfell, and Franco M. Muggia, eds. Liver Cancer. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2593-2.

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1947-, Bottino Joseph C., Opfell Richard W, and Muggia Franco M, eds. Liver cancer. Boston: Nijhoff, 1985.

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Chao-yu, Tʼang, Wu Meng-chʼao, and Hsia Sui-sheng, eds. Primary liver cancer. Beijing: China Academic Publishers, 1989.

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Carr, Brian I. Understanding Liver Cancer. Tarporley: Springer Healthcare Ltd., 2014. http://dx.doi.org/10.1007/978-1-910315-02-6.

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Reau, Nancy, and Fred Poordad, eds. Primary Liver Cancer. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-863-4.

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Gu, Jianren. Primary Liver Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28702-2.

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Book chapters on the topic "Liver cancer"

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Kono, Yoshiharu, Takeaki Ishizawa, and Kiyoshi Hasegawa. "Liver Cancer (Primary Liver Cancer, Metastatic Liver Cancer)." In Fluorescence-Guided Surgery, 93–99. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-7372-7_14.

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Mufti, Siraj I. "Liver Cancer." In Liver Pathology and Alcohol, 195–219. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0421-3_7.

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Granov, Anatoliy, Leonid Tiutin, and Thomas Schwarz. "Liver Cancer." In Positron Emission Tomography, 111–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21120-1_9.

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Stern, Robert J. "Liver Cancer." In Encyclopedia of Immigrant Health, 1021–22. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5659-0_467.

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Thomas, Joseph D., George A. Poultsides, Timothy M. Pawlick, and Melanie B. Thomas. "Liver Cancer." In Gastrointestinal Oncology, 225–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13306-0_9.

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Jin, Minghua, and He Qiang. "Liver Cancer." In Alternative and Complementary Therapies for Cancer, 153–83. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-0020-3_7.

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Shiu, W., and Z. Y. Tang. "Liver Cancer." In Manual of Clinical Oncology, 303–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85159-9_19.

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Risse, J. H. "Liver Cancer." In PET and PET-CT in Oncology, 203–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18803-9_19.

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Alvarenga, Thayse Gardini, Pamela Carvalho Muniz, Hakaru Tadokoro, Ramon Andrade De Mello, and Nora Manoukian Forones. "Liver Cancer." In International Manual of Oncology Practice, 405–20. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16245-0_20.

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De Raffele, Emilio. "Liver Cancer." In Liver Diseases, 341–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-24432-3_31.

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Conference papers on the topic "Liver cancer"

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Li, San-Qiang, Hong-Ye Meng, Shou-Min Xi, Ling-Jun Ma, and Wu-BiaoYang. "Expression of ADAM8 in Liver Cancer." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.210.

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CHARANRAJ, NALLAGIRI. "LIVER CANCER IN CHILDREN." In MOL2NET 2018, International Conference on Multidisciplinary Sciences, 4th edition. Basel, Switzerland: MDPI, 2018. http://dx.doi.org/10.3390/mol2net-04-05915.

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Dimitropoulos, Charalampos, Georgios Hillas, Ioanna Haziri, Ioanna Kostara, Ioannis Ntanos, Dimitrios Veldekis, and Fotis Vlastos. "Liver Metastases In Lung Cancer Patients." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4410.

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Marques, Lays Costa, Lizzia Rabelo Barbosa, Yasmin Batista de Paiva, Isabella Miranda Guimaraes, Luciana Ximenes Salustiano, and Danilo Araújo Gusmão. "Invasive lobular breast carcinoma presenting hepatic carcinomatosis: A case report." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1058.

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Metastatic carcinomatosis to the liver is a pattern of malignant infiltration that tends to provoke liver fibrosis. It is a rare complication of multiple types of solid tumors and often seen in the absence of a discrete tumor mass in the liver. We report the case of a patient who presented the rare diagnosis of metastatic carcinomatosis for liver from breast cancer. A woman at the age of 42 years presented invasive lobular carcinoma, pT3 pN0 M0, positive immunohistochemistry 70% for estrogen receptor and 30% progesterone, HER2 and E-cadherin negative, and Ki67 of 5%. The patient during the fourth year of adjuvant hormone therapy with tamoxifen presented an increase in serum tumor marker (CA 125: 17–130), with no evidence of systemic disease on imaging tests. Due to the slightly cirrhotic contour of the liver on a computed tomography, a liver biopsy was performed for investigation. The early diagnosis of occult and diffuse dissemination to the liver was made by means of a percutaneous liver biopsy showing invasive breast cancer cells, with immunohistochemistry compatible with metastasis of lobular breast carcinoma, positive for hormone receptors, and doubtful for HER-2, with KI67 of 20%. Metastatic carcinomatosis, unlike lesions of discrete liver masses, may not be detectable with imaging tests, and often biopsy or autopsy is needed to confirm the diagnosis. This case highlights a rare and difficult to early diagnosis pattern of hepatic carcinomatosis due to lobular breast carcinoma.
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Ramgopal, N. CH, Prabhakar Gantela, R. Rajagopal, Thamari Thankam, and R. SenthamilSelvan. "Automatic Liver Cancer Detection in Abdominal Liver Images Using Soft Optimization Techniques." In 2022 International Conference on Knowledge Engineering and Communication Systems (ICKECS). IEEE, 2022. http://dx.doi.org/10.1109/ickecs56523.2022.10060747.

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Hashemi, R. R., J. H. Early, M. Bahar, A. A. Tyler, and J. F. Young. "A signature-based liver cancer predictive system." In International Conference on Information Technology: Coding and Computing (ITCC'05) - Volume II. IEEE, 2005. http://dx.doi.org/10.1109/itcc.2005.37.

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Sriwattanapongse, Wattanavadee, and Sukon Prasitwattanaseree. "Liver cancer mortality rate model in Thailand." In INTERNATIONAL CONFERENCE ON MATHEMATICAL SCIENCES AND STATISTICS 2013 (ICMSS2013): Proceedings of the International Conference on Mathematical Sciences and Statistics 2013. AIP, 2013. http://dx.doi.org/10.1063/1.4823955.

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Zeng, Chaoying, Dong Yang, Ping Huang, Huijuan Zhang, Muyin Huang, Ji Chen, and Guorong Lu. "Ultrasound-guided interventional PDT of liver cancer." In Photonics China '96, edited by Brij M. Khorana, Junheng Li, and Michail M. Pankratov. SPIE, 1996. http://dx.doi.org/10.1117/12.251938.

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Maurya, Bhawana, Saroj Hiranwal, and Manoj Kumar. "A Review on Liver Cancer Detection Techniques." In 2020 5th IEEE International Conference on Recent Advances and Innovations in Engineering (ICRAIE). IEEE, 2020. http://dx.doi.org/10.1109/icraie51050.2020.9358362.

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Musa, Musa Sani, Dilber Uzun Ozsahin, and Ilker Ozsahin. "A Comparison for Liver Cancer Treatment Alternatives." In 2019 Advances in Science and Engineering Technology International Conferences (ASET). IEEE, 2019. http://dx.doi.org/10.1109/icaset.2019.8714471.

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Reports on the topic "Liver cancer"

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Wang, Qiang, Anrong Wang, Zhen Li, Ernesto Sparrelid, and Torkel Brismar. Systematic review of the impact of sarcopenia on the future liver remnant growth after portal vein embolization and ALPPS. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0038.

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Review question / Objective: Does sarcopenia affect the future liver remnant growth after portal vein embolization/ligation (thus affect the subsequent hepatectomy in patients with liver cancers)? Condition being studied: Portal vein embolization (PVE) and Associating Liver Partition and Portal vein Ligation for Staged hepatectomy (ALPPS) are two commonly used procedures for hypertrophy of the remaining liver before major liver resection in patients with liver cancer. However, around 30% patients who undergo PVE cannot proceed to liver resection due to insufficient liver growth. Many factors may affect liver growth after PVE. This study evaluates the clinical variables affecting liver growth after portal vein embolization/ligation in patients with liver cancers.
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Travis, C., and A. Arms. Reference physiological parameters for pharmacodynamic modeling of liver cancer. Office of Scientific and Technical Information (OSTI), January 1988. http://dx.doi.org/10.2172/6145452.

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Bull, Richard J., and Brian D. Thrall. Mechanism Involved in Trichloroethylene-Induced Liver Cancer: Importance to Environmental Cleanup. Office of Scientific and Technical Information (OSTI), June 1999. http://dx.doi.org/10.2172/827051.

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Bull, Richard J., and Brian D. Thrall. Mechanisms Involved in Trichloroethylene-Induced Liver Cancer: Importance to Environmental Cleanup. Office of Scientific and Technical Information (OSTI), June 2000. http://dx.doi.org/10.2172/827059.

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Bull, Richard J., and Brain D. Thrall. MECHANISMS INVOLVED IN TRICHLOROETHYLENE INDUCED LIVER CANCER: IMPORTANCE TO ENVIRONMENTAL CLEANUP. Office of Scientific and Technical Information (OSTI), December 2001. http://dx.doi.org/10.2172/827061.

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Shen, Dong, Zhuang Xiong, Yangyang Liu, Yan Leng, Houbo Deng, Song Wang, Xiangtong Meng, and Tiejun Liu. Efficacy and safety of Chinese herbal medicine combined with Sorafenib in the treatment of primary liver cancer: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0024.

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The aim of this systematic review is to compare Chinese herbal medicine combined with Sorafenib in terms of efficacy and acceptability in the primary liver cancer to better inform clinical practice. To this end, the proposed systematic review will address the following question: Which is the best choice to reduce Efficacy and safety in Patients with primary liver cancer, Chinese herbal medicine combined with Sorafenib or Sorafenib.this systematic review and meta-analysis will evaluate the efficacy and Sorafenib combined with Chinese herbal medicine in the treatment of PLC. Information sources: We will search the following databases from inception up to September 8, 2021: PubMed, Web of Science, Embase, AMED, Cochrane Library, CNKI, VIP, CBM, and Wanfang. There will be no restrictions regarding publication date or language. We will apply a combination of medical keywords and words, including "Sorafenib", "Chinese herbal medicine" and "primary liver cancer". Additionally, we will manually search all reference lists from relevant systematic reviews to find other eligible studies.
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Liu, Wenfeng, and Keshu Hu. Prognostic significance of microRNA-221 in liver cancer: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0014.

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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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Bull, R. J. Mechanism involved in trichloroethylene-induced liver cancer: Importance to environmental cleanup. 1997 annual progress report. Office of Scientific and Technical Information (OSTI), June 1997. http://dx.doi.org/10.2172/13581.

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Bull, R. J., B. D. Thrall, L. B. Sasser, J. H. Miller, and I. R. Schultz. Mechanism involved in trichloroethylene-induced liver cancer: Importance to environmental cleanup. 1998 annual progress report. Office of Scientific and Technical Information (OSTI), June 1998. http://dx.doi.org/10.2172/13582.

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