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Biological Basis of Alcohol-Induced Cancer

Overview of attention for book
Cover of 'Biological Basis of Alcohol-Induced Cancer'

Table of Contents

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    Book Overview
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    Chapter 1 Introduction
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    Chapter 2 Alcohol and Breast Cancer: Reconciling Epidemiological and Molecular Data.
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    Chapter 3 Genetic-epidemiological evidence for the role of acetaldehyde in cancers related to alcohol drinking.
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    Chapter 4 Alcohol and Cancer: An Overview with Special Emphasis on the Role of Acetaldehyde and Cytochrome P450 2E1
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    Chapter 5 Implications of Acetaldehyde-Derived DNA Adducts for Understanding Alcohol-Related Carcinogenesis.
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    Chapter 6 The Role of Iron in Alcohol-Mediated Hepatocarcinogenesis
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    Chapter 7 Alcoholic Cirrhosis and Hepatocellular Carcinoma
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    Chapter 8 TLR4-Dependent Tumor-Initiating Stem Cell-Like Cells (TICs) in Alcohol-Associated Hepatocellular Carcinogenesis.
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    Chapter 9 Synergistic Toxic Interactions Between CYP2E1, LPS/TNFα, and JNK/p38 MAP Kinase and Their Implications in Alcohol-Induced Liver Injury.
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    Chapter 10 Understanding the Tumor Suppressor PTEN in Chronic Alcoholism and Hepatocellular Carcinoma.
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    Chapter 11 Alcohol Consumption, Wnt/β-Catenin Signaling, and Hepatocarcinogenesis
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    Chapter 12 Alcohol and HCV: Implications for Liver Cancer.
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    Chapter 13 Application of mass spectrometry-based metabolomics in identification of early noninvasive biomarkers of alcohol-induced liver disease using mouse model.
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    Chapter 14 Alcohol metabolism by oral streptococci and interaction with human papillomavirus leads to malignant transformation of oral keratinocytes.
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    Chapter 15 Genetic Polymorphisms of Alcohol Dehydrogense-1B and Aldehyde Dehydrogenase-2, Alcohol Flushing, Mean Corpuscular Volume, and Aerodigestive Tract Neoplasia in Japanese Drinkers
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    Chapter 16 Acetaldehyde and Retinaldehyde-Metabolizing Enzymes in Colon and Pancreatic Cancers
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    Chapter 17 Alcohol, Carcinoembryonic Antigen Processing and Colorectal Liver Metastases.
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    Chapter 18 Alcohol Consumption and Antitumor Immunity: Dynamic Changes from Activation to Accelerated Deterioration of the Immune System.
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    Chapter 19 A Perspective on Chemoprevention by Resveratrol in Head and Neck Squamous Cell Carcinoma
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    Chapter 20 The Effects of Alcohol and Aldehyde Dehydrogenases on Disorders of Hematopoiesis
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    Chapter 21 The Effect of Alcohol on Sirt1 Expression and Function in Animal and Human Models of Hepatocellular Carcinoma (HCC).
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    Chapter 22 Transgenic mouse models for alcohol metabolism, toxicity, and cancer.
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    Chapter 23 Fetal Alcohol Exposure Increases Susceptibility to Carcinogenesis and Promotes Tumor Progression in Prostate Gland
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    Chapter 24 Fetal alcohol exposure and mammary tumorigenesis in offspring: role of the estrogen and insulin-like growth factor systems.
Attention for Chapter 8: TLR4-Dependent Tumor-Initiating Stem Cell-Like Cells (TICs) in Alcohol-Associated Hepatocellular Carcinogenesis.
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Chapter title
TLR4-Dependent Tumor-Initiating Stem Cell-Like Cells (TICs) in Alcohol-Associated Hepatocellular Carcinogenesis.
Chapter number 8
Book title
Biological Basis of Alcohol-Induced Cancer
Published in
Advances in experimental medicine and biology, January 2015
DOI 10.1007/978-3-319-09614-8_8
Pubmed ID
25427905
Book ISBNs
978-3-31-909613-1, 978-3-31-909614-8
Authors

Keigo Machida, Douglas E Feldman, Hidekazu Tsukamoto, Douglas E. Feldman, Machida, Keigo, Feldman, Douglas E., Tsukamoto, Hidekazu

Abstract

Alcohol abuse predisposes individuals to the development of hepatocellular carcinoma (HCC) and synergistically heightens the HCC risk in patients infected with hepatitis C virus (HCV). The mechanisms of this synergism have been elusive until our recent demonstration of the obligatory role of ectopically expressed TLR4 in liver tumorigenesis in alcohol-fed HCV Ns5a or Core transgenic mice. CD133+/CD49f+ tumor-initiating stem cell-like cells (TICs) isolated from these models are tumorigenic in a manner dependent on TLR4 and NANOG. TICs' tumor-initiating activity and chemoresistance are causally associated with inhibition of TGF-β tumor suppressor pathway due to NANOG-mediated expression of IGF2BP3 and YAP1. TLR4/NANOG activation causes p53 degradation via phosphorylation of the protective protein NUMB and its dissociation from p53 by the oncoprotein TBC1D15. Nutrient deprivation reduces overexpressed TBC1D15 in TICs via autophagy-mediated degradation, suggesting a possible role of this oncoprotein in linking metabolic reprogramming and self-renewal.

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X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
 Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 18%
Professor 2 12%
Student > Postgraduate 2 12%
Student > Bachelor 1 6%
Student > Master 1 6%
Other 3 18%
Unknown 5 29%
Readers by discipline Count As %
Medicine and Dentistry 5 29%
Agricultural and Biological Sciences 2 12%
Biochemistry, Genetics and Molecular Biology 1 6%
Immunology and Microbiology 1 6%
Computer Science 1 6%
Other 2 12%
Unknown 5 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 March 2015.
All research outputs
#20,243,777
of 22,771,140 outputs
Outputs from Advances in experimental medicine and biology
#3,956
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Outputs of similar age
#295,628
of 352,911 outputs
Outputs of similar age from Advances in experimental medicine and biology
#189
of 272 outputs
Altmetric has tracked 22,771,140 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,928 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.0. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 272 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.

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