Individualized Therapy for Hepatocellular Carcinoma
판매가격 : 120,000120,000
적립금 :2,400
ISBN :978-4-939-02838-0
출판사 :WILEY
저자 :Young-Hwa Chung
출판일 :2017-04-25
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Book Introduction


 


              The predisposition of HCC development and progression might be caused by the genetic diversity of the patients. The Patients with HCC also have quite different clinical presentations and diverse outcomes even in spite of the similar managements. Therefore, by clarifying and exactly understanding the hepatocarcinogenetic mechanisms, we can obtain the insights to establish more effective diagnostic, therapeutic and preventive measures for patients with HCC. Thus, utilizing relevant basic and clinical investigations, we need to set up ‘individualized’ and ‘personalized’ guidelines for early diagnosis, effective treatment and prevention of HCC.


              During the past 20 years, my research team has had interests in establishing effective diagnostic, therapeutic and preventive measures for HCC. We have tried to clarify the carcinogenic mechanism of HCC, to improve the efficacies of treatments for HCC, and also to find novel therapeutic and preventive measures of HCC at the laboratory and clinic. Especially, our researches have been focused on the clarification of the diversity of HCC, and thus we have tried to establish useful diagnostic and therapeutic modalities. Also, we have tried to find new molecular targets to be applicable to the managements of HCC patients.


              This book is an introduction and summary of our research works for twenty years. I collected and edited the relevant articles, which have been recently published in celebrated medical journals and books. Indeed, I believe this book would be a valuable reference to many clinicians and basic researchers who are interested in HCC.


             


 


Keywords:


 


Hepatocellular carcinoma, HCC, HBV, HCV, Molecular targeted therapy, TACE, Individualized therapy


 


 


 


Author introduction:


 


Professor Young-Hwa Chung graduated Seoul National University College of Medicine in 1981. After then, he had accomplished residency and clinical and research fellowship at Seoul National University Hospital from 1981 to 1988. In 1992, he had been involved in the clinical works regarding liver transplantation at the Klinik fur Viszeral- und Transplantationschirurgie in Medizinische Hochschule Hannover as a visiting researcher. From 1993 to 1994, he had also worked as a research fellow at Liver Unit, NIDDK, National Institute for Health in USA. Now, he is the professor of the Department of Hepatology and Gastroenterology in University of Ulsan college of Medicine and Asan Medical Center, Seoul, Korea.


Professor Chung has published about 200 international scientific papers and about 10 textbooks in the field of hepatology. He has served as an Executive Council Member of several academic societies. From 2006 to 2007, he had served as the Secretary General of Korean Association for the Study of the Liver (KASL). He had also worked as an associate editor of Liver International from 2007 to 2012. And he is now serving as an editorial board member of several international medical journals. His major research interests are hepatic hepatocarcinogenesis and fibrogenesis. He is also very interested in the diagnosis and treatment of hepatocellular carcinoma. 



Preface


Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The prognosis of HCC is still disappointing despite recent considerable advances in its diagnostic and therapeutic techniques. The poor clinical outcomes of HCC have been known to be caused by frequent vascular invasions followed by insidious hematogenous metastasis, in addition to poor hepatic reserve functions of the patients at the time of diagnosis.


Furthermore, frequent recurrence after surgery is the major limitation to longterm survival of the patients. Therefore, to improve the clinical outcomes of HCC patients, it is essential to establish effective and safe diagnostic, therapeutic, and preventive measures in the future.


The most common causes of HCC were hepatitis viruses, especially hepatitis B virus (HBV) and hepatitis C virus (HCV). In most Asian countries except Japan, chronic HBV infection is the most common cause of HCC. It has been reported that chronic HBV infection increases the risk of HCC development by 100fold.


However, patients with chronic HBV infection have very diverse clinical courses. Some of them remain to be inactive healthy carriers, whereas some progress to cirrhosis, and others develop HCC during their life. Such diverse clinical presentations may result from viral factors such as viral replicative activity and viral genotype, which is supported by the fact that persistently high levels of serum HBVDNA is associated with higher occurrence rate of HCC. On the other hand, the predisposition of HCC development and progression might be caused by the genetic diversity of the patients. Patients with HCC also have quite different clinical presentations and diverse outcomes in spite of similar managements.


Therefore, by clarifying and exactly understanding the hepatocarcinogenetic mechanisms, we can obtain the insights to establish more effective diagnostic, therapeutic, and preventive measures for patients with HCC.


Thus, utilizing relevant basic and clinical investigations, we need to set up individualized and personalizedguidelines for early diagnosis, effective treatment, and prevention of HCC.


 


Recently, the knowledge of genomic technologies has been progressing at a rapid pace. Especially, the establishment of microarray methods for largescale analysis of gene expressions has made it possible to identify molecules involved in the development of HCC and the outcome of HCC patients. Accordingly, a large number of novel molecular therapeutics targeting these signaling components, especially in the process of neovascularization, are in clinical development. Among these promising trials, molecular targeted therapy using sorafenib is located at the farmost front line. Also, in a number of largescale clinical trials, some other molecular targeted therapeutic agents have been proved to be safe and effective in the treatment of HCC patients.


HCC is also clinically characterized by its frequent postoperative recurrence, which may require adjuvant therapy in selected cases in order to prevent recurrence and prolong the patient survival period. Although a number of adjuvant therapies have been attempted, there is no universally accepted single therapy due to the heterogeneity of the HCC features. Many recent studies have focused on the molecular targets involved in the diverse pathways of hepatocarcinogenesis in order to complement such limitations of the given adjuvant therapies.


Recently, as a result, several molecular targeted therapies have been under phase II or III clinical study.


During the past 20 years, my research team has had interests in establishing effective diagnostic, therapeutic, and preventive measures for HCC, especially for HBVassociated HCC. We have tried to clarify the carcinogenic mechanism of HCC, to improve the efficacies of treatments for HCC, and also to find novel therapeutic and preventive measures of HCC at the laboratory and clinic. We have collaborated with basic scientists to look for novel molecular targets to establish new diagnostic and therapeutic methods. Especially, our research has been focused on the clarification of the diversity of HCC, and thus we have tried to establish useful diagnostic and therapeutic  odalities. Also, we have tried to find new molecular targets to be applicable to the management of HCC patients.


 


This book is an introduction and summary of our research works for twenty years. I collected and edited the relevant articles, which have been recently published in celebrated medical journals and books, under the title of Individualized Therapy for Hepatocellular Carcinoma: Present and Future. Indeed, I believe this book will be a valuable reference for many clinicians and basic researchers who are interested in HCC.


I think I am very lucky to have been working with many outstanding researchers in this field during my academic career. They have been the members of Research Meeting for Liver Diseases in Asan Medical Center for 20 years whom I call my family. I have been very happy to enjoy my academic life with them for a long time. We have had regular meetings for the past 20 years to share our knowledge and inspire each other. I would like to express my gratitude to all the authors of the articles in this book for their contributions. I really hope this book can provide us with a pleasant memory as well as an opportunity to talk to our readers about our concerns.


First of all, I would like to thank my mentors Prof. Chung Yong Kim and Prof. Adrian M. Di Bisceglie for giving me a lot of inspiration during my academic career. I also remember my patients who continuously gave me questions and insights on my research projects. I also thank my son and daughter, JieHoon and JieSun, for tolerating their busy father generously for a long time. Finally, I would like to express my deepest thanks to my wife, KyungRan. Without her love and warm support, I could not devote myself solely to my academic career and also complete this book.


 


YoungHwa Chung, MD, PhD.


Professor


Department of Gastroenterology & Hepatology


University of Ulsan College of Medicine


Asan Medical Center


Seoul, Korea



Contents

Foreword viii

Preface ix

Part I Hepatocarcinogenesis 1

Molecular mechanisms of hepatocarcinogenesis

1.1 Chronic hepatitis B in hepatocarcinogenesis 3

Effects of hepatitis B virus

1.2 Synergistic effects of A1896, T1653 and T1762/A1764 mutations in

genotype C2 hepatitis B virus on development of hepatocellular carcinoma 16

Aberrant epigenetic modifications

1.3 Aberrant epigenetic modifications in hepatocarcinogenesis induced by

hepatitis B virus X protein 23

Histology of chronic liver diseases

1.4 Histological characteristics predisposing development of hepatocellular

carcinoma in patients with chronic hepatitis B 43

Response to antiviral therapy

1.5 Biochemical rather than virologic response to interferon therapy may be more closely associated

with decrease of hepatocellular carcinoma incidence in patients with chronic hepatitis B 53

Genetic predispositions

1.6 Genetic variations at loci involved in the immune response are risk factors

for hepatocellular carcinoma 60

1.7 Polymorphisms of DNA repair genes in Korean hepatocellular carcinoma

patients with chronic hepatitis B: Possible implications on survival 71

1.8 Expression of transforming growth factor‐α mRNA in livers of patients

with chronic viral hepatitis and hepatocellular carcinoma 80

1.9 p16 Hypermethylation in the early stage of hepatitis B virusassociated hepatocarcinogenesis 86

1.10 Expression of DNA methyltransferases in multistep hepatocarcinogenesis 93

Part II Serologic markers for early diagnosis of hepatocellular carcinoma 101

Alpha-fetoprotein

2.1 Specificities of serum α‐fetoprotein in HBsAg+ and HBsAg patients in the

diagnosis of hepatocellular carcinoma 103

Transforming growth factor-β1

2.2 Transforming growth factor ‐β1 as a useful serologic marker of small

hepatocellular carcinoma 109

 

Part III Systemic therapy for hepatocellular carcinoma 117

Interferon therapy

3.1 Combined therapy consisting of intraarterial cisplatin infusion and systemic

interferon‐α for hepatocellular carcinoma patients with major portal vein

thrombosis or distant metastasis 119

Molecular targeted therapy

3.2 Angiogenic factors as molecular targets for hepatocellular carcinoma 125

3.3 Clinical trials of molecular targeted therapies in hepatocellular carcinoma:

Efficacies and toxicities 138

Combined therapy

3.4 Interim analysis of START: Study in Asia of the combination of TACE

(transcatheter arterial chemoembolization) with sorafenib in patients with

hepatocellular carcinoma trial 150

3.5 The combination of transcatheter arterial chemoembolization and sorafenib is

well tolerated and effective in Asian patients with hepatocellular carcinoma:

Final results of the START trial 164

Adverse effects of molecular targeted therapy

3.6 Genetic predisposition of handfoot skin reaction after sorafenib therapy in

patients with hepatocellular carcinoma 176

Part IV Recurrences of hepatocellular carcinoma 185

Factors associated with recurrence after curative resection

4.1 Effects of genomic changes in hepatitis B virus on postoperative recurrence and

survival in patients with hepatocellular carcinoma 187

Factors associated with recurrence following locoregional therapy

4.2 Recurrences of hepatocellular carcinoma following initial remission by

transcatheter arterial chemoembolization 195

4.3 Predisposing factors of hepatocellular carcinoma recurrence following complete

remission in response to transarterial chemoembolization 202

4.4 Recurrences of hepatocellular carcinoma following complete remission by transarterial

chemoembolization or radiofrequency therapy: Focused on the recurrence patterns 211

Mediators associated with invasiveness of hepatocellular carcinoma

4.5 Metastatic tumor antigen 1 is closely associated with frequent postoperative

recurrence and poor survival in patients with hepatocellular carcinoma 220

4.6 Clinical implications of arrestdefective protein 1 expression in hepatocellular carcinoma:

A novel predictor of microvascular invasion 229

4.7 Association between insulinlike growth factor2 and metastases after transcatheter arterial

chemoembolization in patients with hepatocellular carcinoma: A prospective study 235

Adjuvant therapy to prevent hepatocellular carcinoma recurrence

4.8 Safety and efficacy of adjuvant pegylated interferon therapy for metastatic

tumor antigen 1positive hepatocellular carcinoma 244

 

Part V Prognostic indicators of hepatocellular carcinoma 253

MicroRNAs

5.1 Roads towards a new tailored therapy for hepatocellular carcinoma: Diagnostic,

therapeutic and prognostic implications of microRNAs 255

Metastatic tumor antigens

5.2 Metastatic tumor antigen in hepatocellular carcinoma: Golden roads toward

personalized medicine 258

5.3 Factors predisposing metastatic tumor antigen 1 overexpression in hepatitis B virus

associated hepatocellular carcinoma 276

5.4 Single nucleotide polymorphisms associated with metastatic tumour antigen 1

overexpression in patients with hepatocellular carcinoma 284

5.5 Overexpression of metastasisassociated protein 2 is associated with hepatocellular

carcinoma size and differentiation 296

Tumor necrosis factor-alpha

5.6 Clinical aspects of tumor necrosis factor‐α signaling in hepatocellular carcinoma 303

Telomerase maintenance gene

5.7 Prognostic impact of telomere maintenance gene polymorphisms on hepatocellular

carcinoma patients with chronic hepatitis B 317

Index 329


 



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