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Titolo:
Hepatocellular carcinoma
Autore:
Okuda, K;
Indirizzi:
Chiba Univ, Sch Med, Dept Med, Chiba, Japan Chiba Univ Chiba JapanChiba Univ, Sch Med, Dept Med, Chiba, Japan
Titolo Testata:
JOURNAL OF HEPATOLOGY
, volume: 32, anno: 2000, supplemento:, 1
pagine: 225 - 237
SICI:
0168-8278(2000)32:<225:HC>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEPATITIS-C VIRUS; PERCUTANEOUS ETHANOL INJECTION; CARBON-DIOXIDE MICROBUBBLES; PRIMARY LIVER-CANCER; ADENOMATOUS HYPERPLASTIC NODULE; LECTIN AFFINITY ELECTROPHORESIS; LARGE REGENERATIVE NODULES; FETOPROTEIN MESSENGER-RNA; TUMOR-SUPPRESSOR GENE; CONTRAST-ENHANCED US;
Keywords:
adenomatous hyperplasia; hepatitis B virus; hepatitis C virus; hepatocellular carcinoma;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
160
Recensione:
Indirizzi per estratti:
Indirizzo: Okuda, K Chiba Univ, Sch Med, Dept Med, Chiba, Japan Chiba Univ Chiba Japan a Univ, Sch Med, Dept Med, Chiba, Japan
Citazione:
K. Okuda, "Hepatocellular carcinoma", J HEPATOL, 32, 2000, pp. 225-237

Abstract

Hepatocellular carcinoma (HCC) is increasing in many countries as a resultof an increase in hepatitis C virus (HCV) infection since World War II. The epidemiology of HCC varies with the global region. There have been conflicting observations from different parts of the world concerning the frequency of HCC in patients who in the distant past had posttransfusion non-A, non-B hepatitis. The genetic basis of hepatocarcinogenesis is still poorly understood. In hepatitis B virus (HVB) associated HCC, codon 249 mutation in the p 53 gene seems more related to exposure to aflatoxin B1 than to hepatocarcinogenesis itself. HCC that occurs in children in high HBV endemic regions could be associated with germ-line mutations, but little information isavailable; not much is known about chemical hepatocarcinogens in the environment other than aflatoxins. The X gene of HBV seems to play an important role in HBV-associated hepatocarcinogenesis. There are preliminary observations on the molecular mechanism of HCV-associated HCC, such as HCV core protein inducing HCC in transgenic mice and the NS3 genome transforming NIH 3T3 cells. Pathological distinction between preneoplastic and very early transformed lesions still depends on classical morphology, and a more genetically oriented differential diagnosis is required. Clinical diagnosis based onmodern imaging has improved greatly, but is still unsatisfactory in the differential diagnosis of preneoplastic and early transformed nodules, because the vasculature changes that occur within the nodule are not accurately discerned with the current imaging. Use of sensitive des-gamma-carboxy prothrombin (PIVKA II) assay, and lectin affinity chromatography separating HCC specific subspecies of AFP molecules with a more practical biochemical technique will further improve diagnosis. Early diagnosis and transplantation are the best treatment at the moment, but transplantation is not widely available because of the donor shortage. Despite successful resection, the remnant cirrhotic liver frequently develops new HCC lesions, seriously curtailing long-term survival. All-out efforts should be directed to the preventionof HCC, through prevention of viral hepatitis, prevention of acute hepatitis from becoming chronic, prevention of chronic hepatitis from progressing to cirrhosis, and prevention of the cirrhotic liver from developing HCC (chemoprevention). At the moment, very few such studies exist.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 14:58:02