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Journal articles on the topic 'Liver cancer'

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Published: 4 June 2021
Last updated: 28 July 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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

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8

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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9

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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10

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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11

Aguayo, Alvaro, and Yehuda Z. Patt. "LIVER CANCER." Clinics in Liver Disease 5, no. 2 (May 2001): 479–508. http://dx.doi.org/10.1016/s1089-3261(05)70175-6.

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12

Steinfeld, Alan D. "Liver Cancer." Radiology 160, no. 3 (September 1986): 626. http://dx.doi.org/10.1148/radiology.160.3.626.

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13

Peate, Ian. "Liver cancer." British Journal of Healthcare Assistants 13, no. 7 (July 2, 2019): 322–28. http://dx.doi.org/10.12968/bjha.2019.13.7.322.

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To understand liver cancer and to provide care that is patient-centred, safe and effective, the healthcare assistant and the assistant practitioner (HCA and AP) need to know about the normal structure and function of the liver. This article provides an overview and insight regarding primary liver cancer. A brief overview of the anatomy and physiology of the liver is provided, along with a discussion of liver cancer. The signs and symptoms of the condition are described and treatment options discussed. The HCA and AP have a role to play as members of the multidisciplinary team who offer care to those people with liver cancer and their families. A glossary of terms is provided, as well as multiple-choice questions to aid retention and recall, and 3 CPD reflective questions.
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14

Mokdad, Ali A., Amit G. Singal, and Adam C. Yopp. "Liver Cancer." JAMA 314, no. 24 (December 22, 2015): 2701. http://dx.doi.org/10.1001/jama.2015.15425.

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15

Basha, Sreenivasulu, Brady Jin-Smith, Chunbao Sun, and Liya Pi. "The SLIT/ROBO Pathway in Liver Fibrosis and Cancer." Biomolecules 13, no. 5 (May 1, 2023): 785. http://dx.doi.org/10.3390/biom13050785.

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Liver fibrosis is a common outcome of most chronic liver insults/injuries that can develop into an irreversible process of cirrhosis and, eventually, liver cancer. In recent years, there has been significant progress in basic and clinical research on liver cancer, leading to the identification of various signaling pathways involved in tumorigenesis and disease progression. Slit glycoprotein (SLIT)1, SLIT2, and SLIT3 are secreted members of a protein family that accelerate positional interactions between cells and their environment during development. These proteins signal through Roundabout receptor (ROBO) receptors (ROBO1, ROBO2, ROBO3, and ROBO4) to achieve their cellular effects. The SLIT and ROBO signaling pathway acts as a neural targeting factor regulating axon guidance, neuronal migration, and axonal remnants in the nervous system. Recent findings suggest that various tumor cells differ in SLIT/ROBO signaling levels and show varying degrees of expression patterns during tumor angiogenesis, cell invasion, metastasis, and infiltration. Emerging roles of the SLIT and ROBO axon-guidance molecules have been discovered in liver fibrosis and cancer development. Herein, we examined the expression patterns of SLIT and ROBO proteins in normal adult livers and two types of liver cancers: hepatocellular carcinoma and cholangiocarcinoma. This review also summarizes the potential therapeutics of this pathway for anti-fibrosis and anti-cancer drug development.
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16

Steffen, R., P. Neuhaus, G. Blumhardt, and W. O. Bechstein. "Liver Transplantation for Liver Cancer." Oncology Research and Treatment 14, no. 2 (1991): 100–106. http://dx.doi.org/10.1159/000216957.

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17

Nasrin Jafari and Roya Dolatkhah. "Molecular epidemiology of liver cancer: Liver cancer incidence and mortality pattern worldwide." International Journal of Life Science Research Archive 1, no. 1 (August 30, 2021): 018–23. http://dx.doi.org/10.53771/ijlsra.2021.1.1.0046.

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Primary liver cancer was the sixth most prevalent cancer and third leading cause of cancer mortality worldwide. The highest rates of incidence and mortality were reported in Eastern Asia and it was 2 to 3 times more common than females in most regions. The summary estimates of the global trends in incidence rates of liver cancer indicated decreasing trends in many Asian high-risk countries, however increasing trends for North American and European countries. Understanding the several involved cells signaling pathways in liver cancer pathogenesis provide an opportunity to identify novel targets that can be utilized for therapeutic and diagnostic modalities. At this time there are only a few effective strategies to prevent or treat liver cancer, and, therefore, a great deal of research is being conducted on liver cancer early detection and prevention. There are no widely recommended screening tests for liver cancer in people who are at average risk at this time. But, testing might be recommended for some people at higher risk. However researchers are studying ways to prevent or treat hepatitis infections before they cause liver cancers. Research into developing a vaccine to prevent hepatitis C is ongoing. Since population-based methods for screening the disease have not been introduced, the greatest focus should be placed on the predominant risk factors for the disease in older men, further studies should be conducted and high-risk provinces should be spotlighted.
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18

Akanksha, Akanksha, Vandana Vandana, Komal Kaushik, Gunjan Choudhary, Runjhun Mathur, and Abhimanyu Kumar Jha. "Possible Treatment of Liver Cancer using Natural Compounds-Review." SSR Institute of International Journal of Life Sciences 7, no. 4 (July 2021): 2827–33. http://dx.doi.org/10.21276/ssr-iijls.2021.7.4.1.

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19

Li, Heliang, Linbin Yang, and Erwei Song. "Abstract 628: Liver macrophages promote breast cancer liver metastasis through migrating neutrophils and initiating NETosis." Cancer Research 83, no. 7_Supplement (April 4, 2023): 628. http://dx.doi.org/10.1158/1538-7445.am2023-628.

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Abstract Neutrophils extracellular traps (NETs), which are DNA scaffolds in complex with granule proteins, could be detected in the pre-metastatic liver niches and were associated with a poor survival in breast cancer patients. However, the mechanisms of neutrophils infiltration and NETs formation in the pre-metastatic liver tissues remain poorly understood. Here, we dynamically characterized the liver micro-environment of normal and 4T1-bearing BALB/C mouse models with or without liver metastasis by the single cell RNA sequencing. Interestingly, we found that CXCL1 and CXCL2, derived from the liver macrophages, were dramatically elevated in pre-metastatic livers and induced the infiltration of peripheral neutrophils by CXCR2. Besides, liver macrophages were educated by cancer cells-derived cathepsin C to secrete the CXCL1 and CXCL2. Furthermore, we identified that the complement signals were over-activated in pre-metastatic livers and induced neutrophils to NETosis. Therapeutically, targeting CXCL1, CXCL2 and complement signals could inhibit the NET formation and effectively reduce breast cancer liver metastasis. Citation Format: Heliang Li, Linbin Yang, Erwei Song. Liver macrophages promote breast cancer liver metastasis through migrating neutrophils and initiating NETosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 628.
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20

Caligiuri, Alessandra, Stefano Gitto, Giulia Lori, Fabio Marra, Maurizio Parola, Stefania Cannito, and Alessandra Gentilini. "Oncostatin M: From Intracellular Signaling to Therapeutic Targets in Liver Cancer." Cancers 14, no. 17 (August 30, 2022): 4211. http://dx.doi.org/10.3390/cancers14174211.

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Primary liver cancers represent the third-most-common cause of cancer-related mortality worldwide, with an incidence of 80–90% for hepatocellular carcinoma (HCC) and 10–15% for cholangiocarcinoma (CCA), and an increasing morbidity and mortality rate. Although HCC and CCA originate from independent cell populations (hepatocytes and biliary epithelial cells, respectively), they develop in chronically inflamed livers. Evidence obtained in the last decade has revealed a role for cytokines of the IL-6 family in the development of primary liver cancers. These cytokines operate through the receptor subunit gp130 and the downstream Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathways. Oncostatin M (OSM), a member of the IL-6 family, plays a significant role in inflammation, autoimmunity, and cancer, including liver tumors. Although, in recent years, therapeutic approaches for the treatment of HCC and CCA have been implemented, limited treatment options with marginal clinical benefits are available. We discuss how OSM-related pathways can be selectively inhibited and therapeutically exploited for the treatment of liver malignancies.
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21

Moroney, James, Juan Trivella, Ben George, and Sarah B. White. "A Paradigm Shift in Primary Liver Cancer Therapy Utilizing Genomics, Molecular Biomarkers, and Artificial Intelligence." Cancers 15, no. 10 (May 17, 2023): 2791. http://dx.doi.org/10.3390/cancers15102791.

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Primary liver cancer is the sixth most common cancer worldwide and the third leading cause of cancer-related death. Conventional therapies offer limited survival benefit despite improvements in locoregional liver-directed therapies, which highlights the underlying complexity of liver cancers. This review explores the latest research in primary liver cancer therapies, focusing on developments in genomics, molecular biomarkers, and artificial intelligence. Attention is also given to ongoing research and future directions of immunotherapy and locoregional therapies of primary liver cancers.
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22

Rosa-Caldwell, Megan E., Jacob L. Brown, David E. Lee, Michael P. Wiggs, Richard A. Perry Jr., Wesley S. Haynie, Aaron R. Caldwell, Tyrone A. Washington, Wen-Juo Lo, and Nicholas P. Greene. "Hepatic alterations during the development and progression of cancer cachexia." Applied Physiology, Nutrition, and Metabolism 45, no. 5 (May 2020): 500–512. http://dx.doi.org/10.1139/apnm-2019-0407.

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Cancer-associated bodyweight loss (cachexia) is a hallmark of many cancers and is associated with decreased quality of life and increased mortality. Hepatic function can dramatically influence whole-body energy expenditure and may therefore significantly influence whole-body health during cancer progression. The purpose of this study was to examine alterations in markers of hepatic metabolism and physiology during cachexia progression. Male C57BL/6J mice were injected with 1 × 106 Lewis Lung Carcinoma cells dissolved in 100 μL PBS and cancer was allowed to develop for 1, 2, 3, or 4 weeks. Control animals were injected with an equal volume of phosphate-buffered saline. Livers were analyzed for measures of metabolism, collagen deposition, protein turnover, and mitochondrial quality. Animals at 4 weeks had ∼30% larger livers compared with all other groups. Cancer progression was associated with altered regulators of fat metabolism. Additionally, longer duration of cancer development was associated with ∼3-fold increased regulators of collagen deposition as well as phenotypic collagen content, suggesting increased liver fibrosis. Mitochondrial quality control regulators appeared to be altered before any phenotypic alterations to collagen deposition. While induction of Akt was noted, downstream markers of protein synthesis were not altered. In conclusions, cancer cachexia progression is associated with hepatic pathologies, specifically liver fibrosis. Alterations to mitochondrial quality control mechanisms appear to precede this fibrotic phenotype, potentially suggesting mitochondrial mechanisms for the development of hepatic pathologies during the development and progression of cancer cachexia. Novelty Cachexia progression results in liver collagen deposition and fibrosis. Alterations in mitochondrial quality control may precede liver pathologies during cachexia.
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23

Kaps, Leonard, and Detlef Schuppan. "Targeting Cancer Associated Fibroblasts in Liver Fibrosis and Liver Cancer Using Nanocarriers." Cells 9, no. 9 (September 3, 2020): 2027. http://dx.doi.org/10.3390/cells9092027.

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Cancer associated fibroblasts (CAF) and the extracellular matrix (ECM) produced by them have been recognized as key players in cancer biology and emerged as important targets for cancer treatment and drug discovery. Apart from their presence in stroma rich tumors, such as biliary, pancreatic and subtypes of hepatocellular cancer (HCC), both CAF and certain ECM components are also present in cancers without an overt intra-tumoral desmoplastic reaction. They support cancer development, growth, metastasis and resistance to chemo- or checkpoint inhibitor therapy by a multitude of mechanisms, including angiogenesis, ECM remodeling and active immunosuppression by secretion of tumor promoting and immune suppressive cytokines, chemokines and growth factors. CAF resemble activated hepatic stellate cells (HSC)/myofibroblasts, expressing α-smooth muscle actin and especially fibroblast activation protein (FAP). Apart from FAP, CAF also upregulate other functional cell surface proteins like platelet-derived growth factor receptor β (PDGFRβ) or the insulin-like growth factor receptor II (IGFRII). Notably, if formulated with adequate size and zeta potential, injected nanoparticles home preferentially to the liver. Several nanoparticular formulations were tested successfully to deliver dugs to activated HSC/myofibroblasts. Thus, surface modified nanocarriers with a cyclic peptide binding to the PDGFRβ or with mannose-6-phosphate binding to the IGFRII, effectively directed drug delivery to activated HSC/CAF in vivo. Even unguided nanohydrogel particles and lipoplexes loaded with siRNA demonstrated a high in vivo uptake and functional siRNA delivery in activated HSC, indicating that liver CAF/HSC are also addressed specifically by well-devised nanocarriers with optimized physicochemical properties. Therefore, CAF have become an attractive target for the development of stroma-based cancer therapies, especially in the liver.
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24

Kocarnik, Jonathan M., Miranda May, Alistair Acheson, Kayleigh Bhangdia, Kelly Compton, Frances Dean, Weijia Fu, et al. "The global burden of primary liver cancer and underlying etiologies from 1990 to 2021." Journal of Clinical Oncology 42, no. 16_suppl (June 1, 2024): 10573. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.10573.

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10573 Background: Liver cancer is a leading cause of global health burden, and was the seventh leading cause of cancer death in 2021. The most common type of liver cancer in adults is hepatocellular carcinoma, which can be due to alcohol, hepatitis B, hepatitis C, non-alcoholic steatohepatitis (NASH), or other causes. In children the most common type of liver cancer is hepatoblastoma. Comprehensive and comparative estimation of liver cancer burden can inform policy decisions and public health interventions to reduce incidence, morbidity, and mortality. This study provides updated liver cancer estimates from 1990 to 2021, and for the first time includes hepatoblastoma. Methods: Using estimation methods from the Global Burden of Diseases, Injuries, and Risk Factors Study 2021 (GBD 2021) we comprehensively estimated total liver cancer incidence, mortality, prevalence, years lived with disability (YLDs), years of life lost (YLLs), and disability adjusted life-years (DALYs). Etiologic proportions from meta-analyses of literature review data were applied to the total. Liver cancers under age 10 were attributed to hepatoblastoma. YLLs were calculated using life expectancy estimates. Prevalence and YLDs were calculated from expected survival, disease sequelae, and disability weights. DALYs were the sum of YLLs and YLDs. Results are presented with 95% Uncertainty Intervals (95% UI). Results: Globally, there were an estimated 529,000 (95% UI 480,000 – 594,000) liver cancer cases and 484,000 (437,000 – 538,000) deaths in 2021, contributing to 12,900,000 (11,600,000 – 14,400,000) DALYs. Since 1990, these represented increases of 114.3% (87.0 – 145.3%) in cases, 102.5% (76.4 – 132.0%) in deaths, and 70.6% (48.7 – 96.8%) in DALYs. For liver cancer etiologies (excluding hepatoblastoma), 37.4% (32.6 – 42.6%) of deaths were due to hepatitis B, 30.3% (26.3 – 34.8%) hepatitis C, 19.1% (15.8 – 22.8%) alcohol, 8.5% (6.9 – 10.3%) NASH, and 4.3% (3.6 – 5.1%) other causes in 2021. Conclusions: These GBD 2021 estimates provide comprehensive estimates of the substantial health burden of liver cancer, highlighting a continued need for public health efforts targeting prevention, vaccination, treatment, or behavioral change.[Table: see text]
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25

Lee, Ai Qi, Yan Li, and Zhiyuan Gong. "Inducible Liver Cancer Models in Transgenic Zebrafish to Investigate Cancer Biology." Cancers 13, no. 20 (October 14, 2021): 5148. http://dx.doi.org/10.3390/cancers13205148.

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Primary liver cancer is one of the most prevalent and deadly cancers, which incidence continues to increase while treatment response remains poor; thus, in-depth understanding of tumour events is necessary to develop more effective therapies. Animal models for liver cancer are powerful tools to reach this goal. Over the past decade, our laboratory has established multiple oncogene transgenic zebrafish lines that can be robustly induced to develop liver cancer. Histological, transcriptomic and molecular analyses validate the use of these transgenic zebrafish as experimental models for liver cancer. In this review, we provide a comprehensive summary of our findings with these inducible zebrafish liver cancer models in tumour initiation, oncogene addiction, tumour microenvironment, gender disparity, cancer cachexia, drug screening and others. Induced oncogene expression causes a rapid change of the tumour microenvironment such as inflammatory responses, increased vascularisation and rapid hepatic growth. In several models, histologically-proven carcinoma can be induced within one week of chemical inducer administration. Interestingly, the induced liver tumours show the ability to regress when the transgenic oncogene is suppressed by the withdrawal of the chemical inducer. Like human liver cancer, there is a strong bias of liver cancer severity in male zebrafish. After long-term tumour progression, liver cancer-bearing zebrafish also show symptoms of cancer cachexia such as muscle-wasting. In addition, the zebrafish models have been used to screen for anti-metastasis drugs as well as to evaluate environmental toxicants in carcinogenesis. These findings demonstrated that these inducible zebrafish liver cancer models provide rapid and convenient experimental tools for further investigation of fundamental cancer biology, with the potential for the discovery of new therapeutic approaches.
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26

Lee, Ai Qi, Yan Li, and Zhiyuan Gong. "Inducible Liver Cancer Models in Transgenic Zebrafish to Investigate Cancer Biology." Cancers 13, no. 20 (October 14, 2021): 5148. http://dx.doi.org/10.3390/cancers13205148.

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Primary liver cancer is one of the most prevalent and deadly cancers, which incidence continues to increase while treatment response remains poor; thus, in-depth understanding of tumour events is necessary to develop more effective therapies. Animal models for liver cancer are powerful tools to reach this goal. Over the past decade, our laboratory has established multiple oncogene transgenic zebrafish lines that can be robustly induced to develop liver cancer. Histological, transcriptomic and molecular analyses validate the use of these transgenic zebrafish as experimental models for liver cancer. In this review, we provide a comprehensive summary of our findings with these inducible zebrafish liver cancer models in tumour initiation, oncogene addiction, tumour microenvironment, gender disparity, cancer cachexia, drug screening and others. Induced oncogene expression causes a rapid change of the tumour microenvironment such as inflammatory responses, increased vascularisation and rapid hepatic growth. In several models, histologically-proven carcinoma can be induced within one week of chemical inducer administration. Interestingly, the induced liver tumours show the ability to regress when the transgenic oncogene is suppressed by the withdrawal of the chemical inducer. Like human liver cancer, there is a strong bias of liver cancer severity in male zebrafish. After long-term tumour progression, liver cancer-bearing zebrafish also show symptoms of cancer cachexia such as muscle-wasting. In addition, the zebrafish models have been used to screen for anti-metastasis drugs as well as to evaluate environmental toxicants in carcinogenesis. These findings demonstrated that these inducible zebrafish liver cancer models provide rapid and convenient experimental tools for further investigation of fundamental cancer biology, with the potential for the discovery of new therapeutic approaches.
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27

Han, Xi. "Analysis of treatment methods for liver cancer." Highlights in Science, Engineering and Technology 102 (July 11, 2024): 46–50. http://dx.doi.org/10.54097/922vgn71.

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Cancer is a challenging disease to treat and has resulted in numerous fatalities. Among these cancers, liver cancer accounts for an important proportion of deaths from cancer and has become one of the main causes of human death. To this end, the treatment of liver cancer is of utmost importance, and scholars worldwide are exploring ways to cure it. Currently, several liver cancer treatment methods have significantly advanced. Different regions have varying treatment methods for liver cancer patients, including targeted drug therapy like sorafenib and the use of viruses to destroy cancer tissue. It is crucial to summarize the advantages and disadvantages of different treatment plans as they are suitable for different patients. This research will analyze existing therapies used in the treatment of liver cancer, highlighting their present situation with deficiencies. The relevant achievements of scholars from different countries are discussed to function as a reference for the subsequent development of liver cancer treatment.
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28

Yosra, Yahyaoui, Ghorbel Achref, Charfi Lamia, Gamoudi Ahmed, Gabsi Azza, and Mezlini Amel. "Low Grade Abdominal Leiomyosarcoma with Liver Metastasis: A Second Cancer Twenty Years after Treatment for Nasopharyngeal Cancer." Clinical Oncology Research and Reports 1, no. 2 (November 16, 2020): 01–03. http://dx.doi.org/10.31579/2693-4787/015.

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Background: leiomyosarcoma is one of the most frequent soft tissues and abdominal-pelvic sarcomas however intra-abdominal leiomyosarcoma with liver metastasis remain a very rare disease. Case presentation: A 61 year-old man presented in February 2019 a recent history of abdominal pain and weight loss. Imagery showed a 5 cm abdominal mass with multiples liver lesions. Biopsy of the liver lesions concluded to a metastases of a low grade leiomyosarcoma. Surgical resection was deemed not possible due to anatomical restrictions and the patient received 6 cycles of systemic mono-chemotherapy with epirubicin. A CT scan performed after the chemotherapy showed a stable disease using RECIST criteria. Conclusions: In case of an unresectable liver metastasis palliative chemotherapy can be offered although it is widely recognized that leiomyosarcoma show moderate sensitivity to chemotherapy.
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29

Lee, Na-Hyun, So Jung Kim, and Jeongeun Hyun. "MicroRNAs Regulating Hippo-YAP Signaling in Liver Cancer." Biomedicines 9, no. 4 (March 30, 2021): 347. http://dx.doi.org/10.3390/biomedicines9040347.

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Liver cancer is one of the most common cancers worldwide, and its prevalence and mortality rate are increasing due to the lack of biomarkers and effective treatments. The Hippo signaling pathway has long been known to control liver size, and genetic depletion of Hippo kinases leads to liver cancer in mice through activation of the downstream effectors yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ). Both YAP and TAZ not only reprogram tumor cells but also alter the tumor microenvironment to exert carcinogenic effects. Therefore, understanding the mechanisms of YAP/TAZ-mediated liver tumorigenesis will help overcome liver cancer. For decades, small noncoding RNAs, microRNAs (miRNAs), have been reported to play critical roles in the pathogenesis of many cancers, including liver cancer. However, the interactions between miRNAs and Hippo-YAP/TAZ signaling in the liver are still largely unknown. Here, we review miRNAs that influence the proliferation, migration and apoptosis of tumor cells by modulating Hippo-YAP/TAZ signaling during hepatic tumorigenesis. Previous findings suggest that these miRNAs are potential biomarkers and therapeutic targets for the diagnosis, prognosis, and treatment of liver cancer.
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30

Saada, J., S. Bhattacharya, A. P. Dhillon, R. Dick, A. K. Burroughs, K. Rolles, and B. R. Davidson. "Detection of small hepatocellular carcinomas in cirrhotic livers using iodised oil computed tomography." Gut 41, no. 3 (September 1, 1997): 404–7. http://dx.doi.org/10.1136/gut.41.3.404.

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Background—The detection of hepatocellular cancers (HCC) is a major role of preoperative imaging in patients with end stage liver disease being considered for orthotopic liver transplantation (OLT).Aims—To assess the sensitivity of iodised oil computed tomography (IOCT).Patients and methods—A prospective evaluation in 50 consecutive patients undergoing OLT included ultrasound scan, contrast enhanced CT, angiography (with intra-arterial injection of iodised oil), and a second CT (IOCT) 10 days later. Following transplantation the explant liver was serially sectioned for pathological evaluation. Soft tissue radiographs of the liver slices were used to match histological lesions with CT findings.Results—Eleven patients were excluded due to protocol violations. Of the remaining 39, histological evaluation revealed no cancers in 33 explant livers, in keeping with negative preoperative imaging. Six explant livers contained 55 HCCs, 84% of which were less than 1 cm in diameter. Pretransplant IOCT detected 3/6 patients with cancer (50%) but only 7% of cancerous lesions. Ultrasound, contrast CT, and angiography each detected 2/6 patients with cancer and 4% of cancerous lesions.Conclusion—IOCT is an insensitive method for the detection of small HCCs in livers with advanced cirrhosis but in this study was slightly superior to ultrasound, CT, and angiography.
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Gerardo-Ramírez, Monserrat, Vanessa Giam, Diana Becker, Marco Groth, Nils Hartmann, Helen Morrison, Helen L. May-Simera, et al. "Deletion of Cd44 Inhibits Metastasis Formation of Liver Cancer in Nf2-Mutant Mice." Cells 12, no. 9 (April 26, 2023): 1257. http://dx.doi.org/10.3390/cells12091257.

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Primary liver cancer is the third leading cause of cancer-related death worldwide. An increasing body of evidence suggests that the Hippo tumor suppressor pathway plays a critical role in restricting cell proliferation and determining cell fate during physiological and pathological processes in the liver. Merlin (Moesin-Ezrin-Radixin-like protein) encoded by the NF2 (neurofibromatosis type 2) gene is an upstream regulator of the Hippo signaling pathway. Targeting of Merlin to the plasma membrane seems to be crucial for its major tumor-suppressive functions; this is facilitated by interactions with membrane-associated proteins, including CD44 (cluster of differentiation 44). Mutations within the CD44-binding domain of Merlin have been reported in many human cancers. This study evaluated the relative contribution of CD44- and Merlin-dependent processes to the development and progression of liver tumors. To this end, mice with a liver-specific deletion of the Nf2 gene were crossed with Cd44-knockout mice and subjected to extensive histological, biochemical and molecular analyses. In addition, cells were isolated from mutant livers and analyzed by in vitro assays. Deletion of Nf2 in the liver led to substantial liver enlargement and generation of hepatocellular carcinomas (HCCs), intrahepatic cholangiocarcinomas (iCCAs), as well as mixed hepatocellular cholangiocarcinomas. Whilst deletion of Cd44 had no influence on liver size or primary liver tumor development, it significantly inhibited metastasis formation in Nf2-mutant mice. CD44 upregulates expression of integrin β2 and promotes transendothelial migration of liver cancer cells, which may facilitate metastatic spreading. Overall, our results suggest that CD44 may be a promising target for intervening with metastatic spreading of liver cancer.
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Kim, Dong-Sik. "Surgical Perspectives of Hepatocellular Carcinoma beyond the Barcelona Clinical Liver Cancer Guideline; Focusing on Liver Resection." Journal of Liver Cancer 15, no. 1 (March 31, 2015): 1–3. http://dx.doi.org/10.17998/jlc.15.1.1.

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O’Brien, April, Tianhao Zhou, Christopher Tan, Gianfranco Alpini, and Shannon Glaser. "Role of Non-Coding RNAs in the Progression of Liver Cancer: Evidence from Experimental Models." Cancers 11, no. 11 (October 25, 2019): 1652. http://dx.doi.org/10.3390/cancers11111652.

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Liver cancer is a devastating cancer that ranges from relatively rare (around 2% of all cancers in the United States) to commonplace (up to 50% of cancers in underdeveloped countries). Depending upon the stage of pathogenesis, prognosis, or functional liver tissue present, transplantation or partial hepatectomy may be the only available treatment option. However, due to the rise in metabolic syndrome and the increasing demand for livers, patients often wait months or years for available organs. Due to this shortage, doctors must have other treatment options available. One promising area of cancer research lies in understanding the role of regulatory non-coding RNAs (ncRNAs) as oncogenic drivers and potential targets for prospective therapies. While the role of these ncRNAs was not initially clear, many of them have since been recognized to function as important players in the regulation of gene expression, epigenetic modification, and signal transduction in both normal and cancer cell cycles. Dysregulation of these different ncRNA subtypes has been implicated in the pathogenesis and progression of many major cancers including hepatocellular carcinoma. This review summarizes current findings on the roles noncoding RNAs play in the progression of liver cancer and the various animal models used in current research to elucidate those data.
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Sindhi, Rakesh, Vinayak Rohan, Andrew Bukowinski, Sameh Tadros, Jean de Ville de Goyet, Louis Rapkin, and Sarangarajan Ranganathan. "Liver Transplantation for Pediatric Liver Cancer." Cancers 12, no. 3 (March 19, 2020): 720. http://dx.doi.org/10.3390/cancers12030720.

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Unresectable hepatocellular carcinoma (HCC) was first removed successfully with total hepatectomy and liver transplantation (LT) in a child over five decades ago. Since then, children with unresectable liver cancer have benefitted greatly from LT and a confluence of several equally important endeavors. Regional and trans-continental collaborations have accelerated the development and standardization of chemotherapy regimens, which provide disease control to enable LT, and also serve as a test of unresectability. In the process, tumor histology, imaging protocols, and tumor staging have also matured to better assess response and LT candidacy. Significant trends include a steady increase in the incidence of and use of LT for hepatoblastoma, and a significant improvement in survival after LT for HCC with each decade. Although LT is curative for most unresectable primary liver sarcomas, such as embryonal sarcoma, the malignant rhabdoid tumor appears relapse-prone despite chemotherapy and LT. Pediatric liver tumors remain rare, and diagnostic uncertainty in some settings can potentially delay treatment or lead to the selection of less effective chemotherapy. We review the current knowledge relevant to diagnosis, LT candidacy, and post-transplant outcomes for these tumors, emphasizing recent observations made from large registries or larger series.
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O’Rourke, Colin, Shiva Jayaraman, Robert H. El-Maraghi, Amit G. Singal, and Ania Z. Kielar. "Chronic Liver Disease and Liver Cancer." Magnetic Resonance Imaging Clinics of North America 29, no. 3 (August 2021): 269–78. http://dx.doi.org/10.1016/j.mric.2021.05.001.

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36

Yang, Ke. "Precise liver resection in liver cancer." World Chinese Journal of Digestology 22, no. 26 (2014): 3990. http://dx.doi.org/10.11569/wcjd.v22.i26.3990.

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37

Wan, Ling-Feng. "Chronic liver inflammation and liver cancer." World Chinese Journal of Digestology 22, no. 31 (2014): 4757. http://dx.doi.org/10.11569/wcjd.v22.i31.4757.

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38

Balabaud, Charles. "Liver biopsy interpretation in liver cancer." Hepatology 54, no. 2 (June 27, 2011): 750. http://dx.doi.org/10.1002/hep.24320.

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39

Gandhi, Armin Aabish, Filipe Araujo Hoffmann, Michael LaPorte II, Aaron Havas, Adarsh Rajesh, Andrew Davis, Marcos G. Teneche, Jessica Proulx, Susan Kaech, and Peter D. Adams. "Abstract 1407: Investigating the effect of an aged liver microenvironment on immune surveillance and predisposition to cancer​." Cancer Research 84, no. 6_Supplement (March 22, 2024): 1407. http://dx.doi.org/10.1158/1538-7445.am2024-1407.

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Abstract The incidence of liver cancer is increasing and there is an urgent need for new therapies and preventative strategies. Age is a major risk factor for liver cancer, the reasons for which are not well defined. One of the hallmarks of aging is immune dysfunction which affects liver homeostasis potentially making it prone to cancer. To understand the role of immune dysfunction in aging liver, we analyzed immune cells from young and old livers. As is reported before, in aged livers we observed an increase in CD101+PD1+CD8+ T cell population as well as an increase in an IFNγ+TNFα+ population suggesting an increase in T cell response in an aging liver. We next sought to understand the cause of T cell exhaustion in aged livers. Cell cluster analysis of the young (4-month-old) and old (22 month old) livers by scRNA seq revealed a cell population unique to the aged livers, showing increased expression of immune checkpoint ligands as well as tumor-initiating cell markers. We validated this data by flow cytometry. We next functionally probed the immune environment of aged liver, by testing the effect of cognate antigen expression in young and old hepatocytes on adoptively transferred activated P14 CD8+ T cells isolated from a young P14 mouse. Analysis of the ex vivo activated P14 CD8+ T cells from young and old antigen-expressing livers by flow cytometry and scRNA sequencing revealed increased exhaustion and cytokine-deficiency in old mice as compared to the young mice. This study explores the age-associated alterations in the immune cells in the liver, aiming to alter liver-resident immune cells and their metabolic states in a way that promotes anti-tumor immunity in an aging liver. Citation Format: Armin Aabish Gandhi, Filipe Araujo Hoffmann, Michael LaPorte II, Aaron Havas, Adarsh Rajesh, Andrew Davis, Marcos G. Teneche, Jessica Proulx, Susan Kaech, Peter D. Adams. Investigating the effect of an aged liver microenvironment on immune surveillance and predisposition to cancer​ [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1407.
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Hao, Shuang, Liqun Chen, Wenhui Du, and Huiyan Sun. "A Comprehensive Comparison between Primary Liver Cancer and Liver Metastases through scRNA-Seq Data Analysis." Metabolites 14, no. 2 (January 26, 2024): 90. http://dx.doi.org/10.3390/metabo14020090.

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Metastasis is one of the leading causes of cancer-related deaths. A comprehensive comparison of the differences between primary and metastatic cancers within the same organ can aid in understanding the growth mechanisms of cancer cells at metastatic sites, thereby helping to develop more effective targeted treatment strategies. Primary liver cancer is one of the most common types of cancer, and the liver is also one of the main metastatic sites. In this paper, we utilize single-cell RNA-Seq data to compare primary liver cancer and colorectal liver metastases from multiple perspectives, including cell types and proportions, activity of various cell types, cell–cell communication, mRNA expression differences within the same types of cells, key factors associated with cell proliferation, etc. Our analysis results show the following: (i) Compared to primary tissue, metastatic tissue contains more cytotoxic T cells and exhausted T cells, and it retains some specific characteristics of the primary site. (ii) Cells of the same type exhibit functional differences between primary and metastatic cancers, with metastatic cancer cells showing lower metabolism levels and immune cells exhibiting stronger immune activity. (iii) Interactions between monocytes and hepato-associated cells are strong in primary cancer, while depleted T cells frequently communicate with hepatocytes in metastatic cancer. (iv) Proliferation-related genes in primary and metastatic cancers are mainly involved in cell energy supply and basic metabolism activity, respectively.
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Tu, Taojian, Handan Hong, Lina He, Mario Alba, Curtis T. Okamoto, and Bangyan L. Stiles. "Abstract 1350: Kupffer cells secrete CXCL5 to promote liver cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 1350. http://dx.doi.org/10.1158/1538-7445.am2023-1350.

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Abstract Liver carcinoma is the 6th most prevalent cancer worldwide in 2020. Moreover, it is the 3rd leading cause of cancer related deaths. In addition to the genomic and transcriptomic heterogeneity of liver tumor cells which is recognized as a major driver in liver cancer progression, the liver immune system is also fundamental to liver carcinogenesis and presents a promising target for therapy. The liver immune response is orchestrated by cytokines and chemokines. Recent studies suggest that chemokines not only recruit immune cells but also regulate various liver functions. In partial hepatectomy, CXCL2 has been shown to promote hepatocyte proliferation. CXCL1, 2, 5 and 8 can induce endothelial cells chemotaxis to promote angiogenesis through binding to CXCR2. These diverse functions suggest that chemokines could play multifaceted roles in liver cancer development. However, chemokines that are commonly associated with liver cancer is still unknown.We analyzed HCC patient data from the GEO database, and we categorized the datasets based on HCC etiologies including HBV, HCV, alcoholic and NASH. We identified CXCL5 as the only chemokine consistently upregulated in HCC with different etiologies compared to healthy or cirrhotic livers. Immunohistochemistry (IHC) analysis reveals that CXCL5 was produced by immune cells but not tumor cells in human HCC tissues. To further study HCC associated CXCL5 expression, the liver-specific Pten deletion mouse model (PM mice) that recapitulates NAFLD-NASH-HCC progression was used. A gradual increase of hepatic CXCL5 expression is observed during HCC development, reaching nearly 100-fold upregulation of CXCL5 mRNA expression in 12-month-old PM mice livers carrying tumors. Examination of liver immune cell populations showed that macrophages were significantly enriched in Pten deleted livers bearing tumors than wild type livers without tumors. Flow cytometry and IHC analysis further identified Kupffer cells (KCs), the liver resident macrophages as the source of CXCL5 in tumor bearing livers using these mice. Since increased LPS is a prominent feature in most chronic liver diseases, we isolated and treated mouse KCs with LPS and found that LPS treatment robustly increased CXCL5 expression by nearly 20-fold. Interestingly, neither murine macrophage cell lines nor primary peritoneal macrophages displayed induced CXCL5 expression in response to LPS. These data suggest that induction of CXCL5 in KCs is likely a unique function of the KCs but not of other macrophages. To explore the function of CXCL5 in HCC development, we treated mouse hepatocytes and HCC cells with CXCL5 and showed that CXCL5 induces the proliferation of these cells. This effect is further blocked by the inhibition of CXCR2, the receptor of CXCL5, demonstrating the specificity for CXCL5 mediated effects. Together we show here for the first time that CXCL5 expression is a unique property of Kupffer cells and the induction of CXCL5 promotes HCC progression. Citation Format: Taojian Tu, Handan Hong, Lina He, Mario Alba, Curtis T. Okamoto, Bangyan L. Stiles. Kupffer cells secrete CXCL5 to promote liver cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1350.
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42

Srikanth, G. "Liver Cancer Prediction Using Matlab." International Journal for Research in Applied Science and Engineering Technology 12, no. 4 (April 30, 2024): 2146–51. http://dx.doi.org/10.22214/ijraset.2024.60033.

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Abstract: The liver is necessary for survival and is also prone to many diseases. CT examinations can be used to plan and properly administer radiation treatments for cancers and to guide biopsies and other minimally invasive procedure. The statistical and textural information are obtained from the extracted cancer using the features like mean, standard deviation and entropy of the obtained sub bands are calculated and stored in a feature vector (in format of mat file). The extracted features are fed as input to Extreme Machine Learning classifier to identify the presence of Liver cancer disease and to classify it as Malignant or Benign stage.
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PIKOULIS, EMMANOUIL, GEORGIOS A. MARGONIS, NIKOLAOS ANDREATOS, KAZUNARI SASAKI, ANASTASIOS ANGELOU, GEORGIOS POLYCHRONIDIS, ANASTASIA PIKOULI, ELENA RIZA, TIMOTHY M. PAWLIK, and EFSTATHIOS ANTONIOU. "Prognostic Role of BRAF Mutations in Colorectal Cancer Liver Metastases." Anticancer Research 36, no. 9 (September 9, 2016): 4805–12. http://dx.doi.org/10.21873/anticanres.11040.

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44

Solomon, S., N. Muruganantham, and M. M. Senthamilselvi. "ANTICANCER ACTIVITY OF ABELMOSCHUS ESCULENTUS (FLOWERS) AGAINST HUMAN LIVER CANCER." International Journal of Pharmacy and Biological Sciences 6, no. 3 (July 1, 2016): 154–57. http://dx.doi.org/10.21276/ijpbs.2016.6.3.18.

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45

Shi, Haihong, Yuxin Xu, Xin Yi, Dandan Fang, and Xia Hou. "Current Research Progress on Long Noncoding RNAs Associated with Hepatocellular Carcinoma." Analytical Cellular Pathology 2019 (June 24, 2019): 1–8. http://dx.doi.org/10.1155/2019/1534607.

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Hepatocellular carcinoma (HCC) is the second leading cause of mortality among cancers. It has been found that long noncoding RNAs (lncRNAs) are involved in many human cancers, including liver cancer. It has been identified that carcinogenic and tumor-suppressing lncRNAs are associated with complex processes in liver cancer. These lncRNAs may participate in a variety of pathological and biological activities, such as cell proliferation, apoptosis, invasion, and metastasis. Here, we review the regulation and function of lncRNA in liver cancer and evaluate the potential of lncRNA as a new goal for liver cancer.
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Ogoshi, Yumi, Kei Ito, Keiko Nemoto Murofushi, Masaya Ito, Shuichiro Kobayashi, and Fumitaka Koga. "Dramatic improvement after palliative whole-liver radiotherapy for liver damage caused by diffuse liver metastases from castration-resistant prostate cancer: A case report." Journal of Case Reports and Images in Urology 8, no. 1 (January 17, 2023): 5–9. http://dx.doi.org/10.5348/100029z15yo2023cr.

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Introduction: Whole-liver radiotherapy (WLRT) is performed for palliative purposes in patients with metastatic liver tumors. However, it remains unclear whether the benefits obtained from WLRT surpass the potential disadvantages of radiotherapy-induced liver disease in such patients, particularly those with severe liver damage. We present the case of a 76-year-old man with diffuse liver metastases from castration-resistant prostate cancer. Case Report: He was diagnosed as having prostate cancer with multiple metastases to the bone, pleura, and para-aortic lymph nodes three years and six months earlier and developed hepatic metastases following a sequence of therapies, including surgical castration, bicalutamide, enzalutamide, and 10 cycles of docetaxel. Despite administering abiraterone acetate for two months, the prostate-specific antigen (PSA) levels increased, and the patient developed symptomatic liver damage, presenting with jaundice, anorexia, and fatigue. His serum total bilirubin (9.5 mg/dL) and liver transaminase (>100 U/L) levels were markedly elevated. The patient received WLRT at 8 Gy in a single fraction for palliative intent. Symptomatic relief was achieved shortly after WLRT, and the total bilirubin and transaminase levels decreased and normalized within two months. Additionally, two months after WLRT, the PSA level decreased from 285 to 23.3 ng/mL, and a robust partial tumor response was observed on computed tomography images. Although the patient died of cancer eight months after WLRT, radiotherapy-induced liver disease was not confirmed during the follow-up period. Conclusion: In the present case, WLRT successfully relieved the symptoms and reversed the liver damage caused by diffuse metastases, and it was considered to contribute to cancer control without adverse events. Thus, WLRT can be a viable option for patients with liver damage induced by diffuse liver metastases.
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Pola, Carolina. "Liver cancer progenitors." Nature Medicine 19, no. 11 (November 2013): 1376. http://dx.doi.org/10.1038/nm.3402.

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Meyer, T. "Primary liver cancer." British Journal of Cancer 108, no. 4 (March 2013): 995–96. http://dx.doi.org/10.1038/bjc.2013.52.

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49

Croager, Emma. "OutFOXing liver cancer." Nature Reviews Cancer 4, no. 5 (May 2004): 329. http://dx.doi.org/10.1038/nrc1350.

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Alderton, Gemma. "Foxing liver cancer." Nature Reviews Cancer 7, no. 2 (February 2007): 74–75. http://dx.doi.org/10.1038/nrc2074.

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