Table of Contents
1
UI - 11715839
AU - Lin FS; Chen SC; Lin ZY; Hsieh MY; Wang LY; Chuang WL; Chang WY
TI -
Ultrasonic characteristics of periportal collateral circulation in
hepatocellular carcinoma with portal vein invasion.
SO - Kaohsiung J Med Sci 2001 Aug;17(8):401-7
AD - Hepatobiliary Division, Department of Internal Medicine, Kaohsiung
Medical University Hospital, No. 100, Shih-Chuan 1st Road, Kaohsiung
City, 807 Taiwan.
Real-time ultrasound (US) was used to analyze the morphological
characteristics of periportal collateral circulation (PPCC) and the
hepatic artery in hepatocellular carcinoma (HCC) patients with portal
vein invasion (PVI). During a 5-year interval, a total of 17 HCC
patients with main portal vein thrombosis and detectable periportal
vessels were collected: 14 men and 3 women, aged 27 to 76 years old. We
examined these patients' periportal vessels by real-time US, then
differentiated PPCC from hepatic artery by duplex Doppler US. We
analyzed the morphological appearances of real-time US imaging of PPCC
and the hepatic artery. Our results showed that the PPCC was always
torturously worm-like in appearance on real-time US, and the hepatic
artery usually had a linear channel appearance on real-time US. When
these two kinds of vessels were seen simultaneously along the pathway of
a thrombosed portal vein, the inner vessel was always the hepatic artery
with linear channel structure, and the outer vessel was always PPCC with
a torturously worm-like structure. In conclusion, real-time US is a
useful and reliable modality in detecting periportal vessels and
differentiating PPCC from the hepatic artery.
2
UI - 11875189
AU - Casey W; Anderson S; Fox T; Dold K; Colton H; Morgan K
TI -
Transcriptional and physiological responses of HepG2 cells exposed to
diethyl maleate: time course analysis.
SO - Physiol Genomics 2002 Feb 28;8(2):115-22
AD - Toxicogenomics, GlaxoSmithKline, Research Triangle Park, North Carolina
27709, USA. wmc22442@gsk.com
Expression levels of 767 genes were measured in HepG2 cells at eight
time points (0, 0.5, 1, 6, 12, 16, 20, and 24 h) following exposure to
the oxidizing agent, diethyl maleate (DEM). DEM treatment caused an
immediate and sustained loss of intracellular GSH, with a concomitant
increase in GSSG. From 6-12 h after exposure, there was a substantial
increase in the percentage of cells undergoing S phase arrest and
apoptosis. Expression profiles of approximately 90% of the genes fell
into one of five clusters generated using hierarchical-clustering
software, indicating the well-ordered nature of the stress response. The
directional movement and timing of induction for many genes matched
closely the known physiological role of the proteins they encode.
Inhibitors of the cell cycle (CDKN1, CDKN4D, ATM) were induced, whereas
cyclins [proliferating cell nuclear antigen (PCNA), cyclin A, cyclin D1,
cyclin K] were downregulated during the period from 6--20 h. Likewise,
pro-apoptotic genes such as the caspases (CASP9, CASP3, CASP2) and
apoptotic protease activating factor (APAF) were induced during the same
period. Results of this study indicate that there is a good correlation
between time-dependent physiological, biochemical, and gene expression
data.
3
UI - 11906173
AU - Jong HS; Lee HS; Kim TY; Im YH; Park JW; Kim NK; Bang YJ
TI -
Attenuation of transforming growth factor beta-induced growth inhibition
in human hepatocellular carcinoma cell lines by cyclin D1
overexpression.
SO - Biochem Biophys Res Commun 2002 Mar 29;292(2):383-9
AD - Cancer Research Institute, Seoul National University College of
Medicine, Chongno-gu, Seoul 110-799, Korea.
Transforming growth factor-beta1 (TGF-beta1) causes growth inhibition in
many cell types. Since its role in the outgrowth of human hepatocellular
carcinoma (HCC) is not clearly understood, we investigated the growth
inhibitory effects of TGF-beta1, the genetic and molecular integrity of
TGF-beta receptors, and the expression levels of cell cycle regulating
proteins in 11 human HCC cell lines. Of 11 cell lines, 3 (27%) showed
growth inhibition to TGF-beta1, whereas the other 8 cell lines did not.
We performed Southern and Northern analysis of TGF-beta type I and II
receptors and examined poly-adenine track mutation of the TGF-beta type
II receptor, but failed to find any genetic mutation. The
transcriptional induction of plasminogen activator inhibitor-1 and
p21(WAF1/CIP1) by TGF-beta were detected in all HCC cell lines, implying
that the molecular integrity of the TGF-beta receptors might be intact.
The amplification and overexpression of cyclin D1 gene was detected in 4
(50%) of 8 HCC cells that showed resistance to TGF-beta1. The
suppression of cyclin D1 expression with antisense cyclin D1 facilitated
the TGF-beta1-triggered growth inhibition in a TGF-beta1 resistant HCC
cell line containing amplified cyclin D1 gene. In conclusion, the
overexpression of cyclin D1 may be responsible for the attenuation of
TGF-beta1 induced growth inhibition in some HCC cells. (c)2002 Elsevier
Science (USA).
4
UI - 11867783
AU - Koyama T; Fletcher JG; Johnson CD; Kuo MS; Notohara K; Burgart LJ
TI -
Primary hepatic angiosarcoma: findings at CT and MR imaging.
SO - Radiology 2002 Mar;222(3):667-73
AD - Department of Diagnostic Imaging and Nuclear Medicine, School of
Medicine, Kyoto University, Japan.
PURPOSE: To evaluate and describe cross-sectional imaging findings in
patients with pathologically confirmed primary hepatic angiosarcoma.
MATERIALS AND METHODS: Findings from imaging examinations in 13 patients
with pathologically confirmed primary hepatic angiosarcoma were
retrospectively reviewed (computed tomographic [CT] images obtained in
10 patients and magnetic resonance [MR] images obtained in five patients
were available for review). Two gastrointestinal radiologists evaluated
lesion number, size, attenuation and signal intensity characteristics,
and the pattern and degree of contrast material enhancement. Medical
records were reviewed for clinical features associated with
angiosarcoma. RESULTS: Angiosarcoma appeared as multiple nodules (n =
6), as dominant masses (n = 6), or as a diffusely infiltrating lesion (n
= 1). Multiple nodules were hypoattenuating at unenhanced and contrast
material--enhanced CT (six of six patients). When dominant masses were
encountered at MR imaging, T2-weighted MR imaging demonstrated
heterogeneous internal architecture (four of four patients) similar to
that of hepatocellular carcinoma. Multiphase contrast-enhanced CT and MR
images showed dominant masses to have heterogeneous and progressive
enhancement (three of three patients). Clinical features associated with
angiosarcoma included splenic metastases (six of 13 patients),
thrombocytopenia (seven of 13 patients), disseminated intravascular
coagulation (four of 13 patients), and hemolytic anemia (three of 13
patients). CONCLUSION: Primary hepatic angiosarcoma exhibits a spectrum
of appearances that reflect its varied pathologic features.
5
UI - 11867787
AU - Kassarjian A; Dubois J; Burrows PE
TI -
Angiographic classification of hepatic hemangiomas in infants.
SO - Radiology 2002 Mar;222(3):693-8
AD - Department of Radiology, Children's Hospital, Boston, MA, USA.
akassarjian@hotmail.com
PURPOSE: To review the angiograms in patients with hepatic hemangiomas
referred to two North American children's hospitals to determine the
variability in angiographic findings and to propose a classification
system that is based on these findings. MATERIALS AND METHODS:
Angiograms obtained in 15 infants with a diagnosis of hepatic hemangioma
who were examined at or referred to two tertiary pediatric hospitals in
North America from 1981 through 2000 were reviewed. The angiographic
findings were then used to classify hemangiomas into types on the basis
of a number of features, including high-flow nodules, early filling of
veins, and the type of direct shunt present. Clinical data, including
age at presentation, presence of cardiac insufficiency, and treatment,
were also recorded. RESULTS: Lesions were classified into five types on
the basis of angiographic findings. In three of 15 patients, angiograms
demonstrated the classic appearance of hepatic hemangiomas, with early
filling of abnormal vascular channels, stagnation of contrast material,
and no evidence of a direct shunt (type 1). In four patients, images
showed high-flow nodules without direct shunts (type 2). In eight
patients, direct shunts were demonstrated: arteriovenous shunts (type 3)
in one, portovenous shunts (type 4) in three, and both arteriovenous and
portovenous shunts (type 5) in four. CONCLUSION: Hepatic hemangioma in
infants is a heterogeneous lesion with variable angioarchitecture and a
spectrum of angiographic findings.
6
UI - 11819746
AU - Xu J; Mei MH; Zeng SE; Shi QF; Liu YM; Qin LL
TI -
Expressions of ICAM-1 and its mRNA in sera and tissues of patients with
hepatocellular carcinoma.
SO - World J Gastroenterol 2001 Feb;7(1):120-5
AD - 95 Leque Road, Department of Hepatobiliary Surgery, Guilin Medical
College, Guilin 541001, Guangxi, China. Jxu@gliet.edu.cn
7
UI - 11819750
AU - Cui J; Yang DH; Bi XJ; Fan ZR
TI -
Methylation status of c-fms oncogene in HCC and its relationship with
clinical pathology.
SO - World J Gastroenterol 2001 Feb;7(1):136-9
AD - Department of Gastroenterology, Zhujiang Hospital, The First Military
Medical University, Guangzhou 510282, Guangdong Province, China.
fanzr@fimmu.edu.cn
8
UI - 11867205
AU - Park WS; Lee JH; Park JY; Jeong SW; Shin MS; Kim HS; Lee SK; Lee SN; Lee
TI -
SH; Park CG; Yoo NJ; Lee JY
Genetic analysis of the liver putative tumor suppressor (LPTS) gene in
hepatocellular carcinomas.
SO - Cancer Lett 2002 Apr 25;178(2):199-207
AD - Department of Pathology, College of Medicine, The Catholic University of
Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, South Korea.
Recently, a novel liver-related putative tumor suppressor (LPTS), which
has a growth inhibitory function in the hepatocellular carcinoma (HCC)
cell line, has been identified at chromosome 8p23. To determine the
relationship of the LPTS with the development or progression of HCC, we
analyzed the genetic alterations and the expression pattern of the LPTS
gene in a series of 80 HCCs, six dysplastic nodules, and eight large
regenerating nodules, determining the genomic structures. We identified
a total of seven exons, of which two were alternative, and three LPTS
isoforms, short (LPTS-S), medium (LPTS-M), and long-sizes (LPTS-L). In
the genetic alteration study of the LPTS gene, no mutation was detected
in the large regenerating nodules, dysplastic nodules, and HCC, whereas
ten (34.5%) of 29 informative cases at one or more intragenic
polymorphic sites showed loss of heterozygosity (LOH). Interestingly,
LOH was identified only in HCC samples with hepatitis B virus (HBV)
infection and the frequency of LOH was not statistically related with
histologic grade and clinical stage, suggesting that allelic loss of the
LPTS gene may occur as an early event in the development of HCC,
especially in the cases with HBV infection.
9
UI - 11965049
AU - Kairemo KJ; Lindahl H; Merenmies J; Fohr A; Nikkinen P; Karonen SL;
TI -
Makipernaa A; Hockerstedt K; Goldenberg DM; Heikinheimo M
Anti-alpha-fetoprotein imaging is useful for staging hepatoblastoma.
SO - Transplantation 2002 Apr 15;73(7):1151-4
AD - Children's Hospital and Department of Radiology, University of Helsinki,
Helsinki, Finland.
BACKGROUND: Liver transplantation (Tx) has become an alternative
treatment of malignant childhood liver tumors, and the importance of
careful pretransplantation evaluation has been emphasized.
Anti-alpha-fetoprotein (AFP) imaging has been suggested for evaluation
of adult patients with AFP-positive tumors. METHODS: Antibody imaging
utilizing Tc-99 m-labeled monoclonal anti-AFP Fab' fragments was used to
demonstrate pathologic uptake in hepatoblastoma (HB). RESULTS: Radical
operation or liver Tx was not possible after four cycles of chemotherapy
in a child with HB because of a single extrahepatic metastasis.
Chemotherapy was continued, and reevaluation with anti-AFP imaging
demonstrated a pathologic uptake only in the liver. Subsequently, a
right liver lobe resection was performed. Along with a new rise in serum
AFP, repeated anti-AFP imaging revealed active liver tumor but no
metastases. A liver Tx was performed, and the child is well with a
normal serum AFP level 18 months after the operation. CONCLUSION: This
is the first case of pediatric HB in which anti-AFP imaging has been
successfully used for patient management.
10
UI - 11407669
AU - Cimino L; Oriani G; D'Arienzo A; Manguso F; Loguercio C; Ascione A;
TI -
Caporaso N; Del Vecchio Blanco C; Budillon G
Interactions between metabolic disorders (diabetes, gallstones, and
dyslipidaemia) and the progression of chronic hepatitis C virus
infection to cirrhosis and hepatocellular carcinoma. A cross-sectional
multicentre survey.
SO - Dig Liver Dis 2001 Apr;33(3):240-6
AD - Department of Clinical and Experimental Medicine, Federico II University
of Naples, Italy.
BACKGROUND: Diabetes, gallstones and dyslipidaemia are widespread,
metabolically related, disorders that can affect the liver, often in a
clinically silent fashion. AIM: To investigate whether the presence of
these disorders may worsen chronic viral disease by inducing additional
liver damage, revealed by variations in serum increases of
aminotransferase, alkaline phosphatase and gamma-glutamyl-transpeptidase
activities. PATIENTS AND METHODS: This retrospective, cross-sectional
study involved 1,195 patients with chronic hepatitis C virus infection:
47.2% chronic hepatitis, 45.2% cirrhosis, and 7.6% hepatocellular
carcinoma. 14.9% of patients had enzymatic cholestasis, defined as
combined increase of alkaline phosphatase and
gamma-glutamyl-transpeptidase. A Log-linear statistical model was
applied to the following variables: stages of liver disease, diabetes,
cholelithiasis, hypertriglyceridaemia, hypercholesterolaemia, and
enzymatic cholestasis. RESULTS: Log-linear analysis, applied to
categorical variables, revealed, for the first time, a three-way
interaction between the stages of chronic liver disease, diabetes, and
enzymatic cholestasis. Two-way interactions demonstrated that liver
disease stages correlated directly to the prevalence of cholelithiasis
and inversely to hypercholesterolaemia. Irrespective of the liver
disease stage, hypertriglyceridaemia correlated to
hypercholesterolaemia. CONCLUSIONS: This study discloses a synergistic
liver damaging effect of diabetes and hepatitis C virus. The three-way
interaction obtained by our analysis suggests that diabetes is a risk
factor for the progression of viral liver disease and that it
contributes to disease evolution, at least in part, by induction of
cholestasis.
11
UI - 11859720
AU - Cheng H; Xu A; Chen D
TI -
[Relation between transcatheter arterial chemoembolization and time of
death in patients with hepatic carcinoma]
SO - Zhonghua Zhong Liu Za Zhi 2001 Nov;23(6):497-9
AD - Department of Radiology, Eastern Hepatobiliary Surgery Hospital, PLA
Second Military Medical University, Shanghai 200438, China.
OBJECTIVE: To evaluate the relationship between transcatheter arterial
chemoembolization (TACE) and time of death in hepatic carcinoma
patients. METHODS: One hundred and ninety-five patients (male 188,
female 7) with liver cancer underwent TACE with patients dying at
different intervals after treatment. Dose of antitumor drugs, amount of
iodized oil, liver function, size, recurrence of surgical resection,
pattern of tumor, metastasis, presence of portal vein thrombosis, post
TACE relapse, post TACE liver function and AFP, etc, altogether 15
variables were subjected to statistical analysis with the Cox's hazard
proportional model. RESULTS: According to univariate and forward
stepwise regression analysis, factors associated with significantly
worse survival were diffused type, multi-nodular growth of tumor, and
tumor embolus in the portal vein (P < 0.0001). Before death, most
patients had symptoms of chest oppression, shortness of breath, ascites,
abdominal distension, jaundice, hepatic failure and hematemesis. Causes
of death were hepatic coma (27.2%, n = 53), hepatic failure (23.1%, n =
45), hemorrhage from the digestive tract (36.9%, n = 72), multiple organ
failure (5.1%, n = 10) and others (7.2%, n = 14). CONCLUSION: Several
factors of TACE may lead to failure in liver function and death. TACE
may hasten death in patients with severe liver functional embarrassment.
Before instituting TACE, careful weighing the pros and cons of the
general condition and liver function is important for patients with
portal vein embolism, multiple tumors or diffused lesions. Tolerance of
liver to the drug, time, dose and method of treatment should be
meticulously and carefully planned. Post TACE protection of liver is
also very important.
12
UI - 11926561
AU - Lonardo A; Loria P
TI -
Is insulin resistance a pathogenic co-factor in hepatitis C
virus-related disease and hepatocellular carcinoma?
SO - Dig Liver Dis 2002 Feb;34(2):151
13
UI - 11958138
AU - Liu SL; Liu GZ; Cheng J; Shi DY; Chen HL; Zhang YD
TI -
[Influence of PKB on ROS regulation of proliferation in human 7721
hepatoma cells]
SO - Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2002
Jan;34(1):67-72
AD - Department of Biochemistry, Medical Center of Fudan University, Shanghai
200032, China. slliu@shmu.edu.cn
In the present study, the relationship between PKB signaling and
reactive oxygen species (ROS) during the course of exogenous and
endogenous ROS or antioxidants regulating human 7721 hepatoma cell
proliferation was studied. To change endogenous ROS levels, 7721 cells
were transfected with human manganese superoxide dismutase (MnSOD)
construct containing sense or antisense MnSOD cDNA. Low level of
exogenous ROS H2O2(1-10 mumol/L) significantly stimulated PKB activity
and c-fos/c-jun expression and cell growth, which could be abolished by
antioxidant danshensu (40 mg/L). It was observed that overexpression of
MnSOD inhibited 7721 cell growth by inhibiting PKB activity and
c-fos/c-jun expression; the PKB activity and c-fos/c-jun expression,
however, were stimulated by down-regulated MnSOD expression. In
addition, PKB-7721 cells (transfected with sense PKB cDNA) promoted
c-fos/c-jun expression by stimulating PKB activity. These results
suggest that the redox state stimulated hepatoma cell growth through PKB
pathway, which modulates AP-1 expression.
14
UI - 11943133
AU - Wong LL
TI -
Current status of liver transplantation for hepatocellular cancer.
SO - Am J Surg 2002 Mar;183(3):309-16
AD - Transplant Institute, Department of Surgery, St. Francis Medical Center,
2226 Liliha St., Suite 402, Honolulu, Hawaii 96817, USA.
hepatoma@aol.com
The incidence of hepatocellular cancer is increasing in the United
States and is one of the most common cancers worldwide. Traditionally,
the gold standard treatment for hepatocellular cancer has been surgical
resection, but most patients were not suitable candidates due to
advanced disease. Other treatments include locally ablative techniques
(cryosurgery, radiofrequency ablation and various injection therapies),
chemotherapeutic options and rarely, radiation therapies. In the 1980s,
liver transplant emerged as the treatment of choice for end-stage liver
disease and also became an option for patients with hepatocellular
cancer. When comparing liver transplant with resection in retrospective
studies, liver transplant patients had better survival and reduced
recurrence. However, not all patients with hepatocellular cancer will be
candidates for liver transplant. Size, stage, and histological grade of
tumor all affect prognosis after transplant. Use of chemotherapeutic
treatments and locally ablative techniques may be beneficial prior to
liver transplant, but larger controlled studies are needed. Liver
transplant is the most effective treatment for hepatocellular cancer in
the subgroup of smaller tumors, but ultimately we are limited by the
number of available donors. Future goals in this area include increasing
the donor pool and determining optimal management to allow patients to
wait for an appropriate donor.
15
UI - 10460371
AU - Helmberger TK; Ros PR; Mergo PJ; Tomczak R; Reiser MF
TI -
Pediatric liver neoplasms: a radiologic-pathologic correlation.
SO - Eur Radiol 1999;9(7):1339-47
AD - Institute of Diagnostic Radiology, Klinikum Grosshadern,
Ludwig-Maximilians-Universitat, Marchioninistrasse 15, D-81366 Munich,
Germany.
Only 1-2 % of all pediatric tumors occur in the liver. Two thirds of
these tumors are malignant and almost all of the tumors cause clinical
symptoms due to their mass effects. Besides the poor prognosis in most
of the malignant tumors, for further treatment the origin and nature of
the neoplasm has to be known. Due to the mostly unimpeded growth into
the peritoneal cavity, the origin of the tumors is primarily often
unclear and can non-invasively only be determined by advanced imaging
techniques. The display of the macro- and microhistological key features
of primary pediatric liver neoplasms, including hepatoblastoma (HB),
infantile hemangioendothelioma (IHE), mesenchymal hamartoma (MH),
undifferentiated (embryonal) sarcoma (UES), and hepatocellular carcinoma
(HCC), together with their imaging representation by ultrasound,
computed tomography, and magnetic resonance imaging, may deepen the
understanding of the underlying pathology and its imaging appearance.
Furthermore, in many cases sufficient information may be provided not
only to differentiate benign from malignant tumors, but also to guide
for adequate treatment.
16
UI - 11287540
AU - Rose SC; Hassanein TI; Easter DW; Gamagami RA; Bouvet M; Pretorius DH;
TI -
Nelson TR; Kinney TB; James GM
Value of three-dimensional US for optimizing guidance for ablating focal
liver tumors.
SO - J Vasc Interv Radiol 2001 Apr;12(4):507-15
AD - Department of Radiology, University of California Medical Center, 200
West Arbor Drive, San Diego, CA 92103, USA. scrose@ucsd.edu
PURPOSE: To determine if three-dimensional ultrasound (3D US), by nature
of its ability to simultaneously evaluate structures in three orthogonal
planes and to study relationships of devices to tumor(s) and surrounding
anatomic structures from any desired orientation, adds significant
additional information to real-time 2D US used for placement of devices
for ablation of focal liver tumors. MATERIALS AND METHODS: Sixteen
patients underwent focal ablation of 23 liver tumors during two
intraoperative cryoablation (CA) procedures, three intraoperative
radiofrequency ablation (RFA) procedures, 11 percutaneous ethanol
injections (PEI) procedures, and six percutaneous RFA procedures. After
satisfactory placement of the ablative device(s) with 2D US guidance, 3D
US was used to reevaluate adequacy to device position. Information added
by 3D US and resultant alterations in device deployment were tabulated.
RESULTS: 3D US added information in 20 of 22 (91%) procedures and caused
the operator to readjust the number or position of ablative devices in
10 of 22 (45%) of procedures. Specifically, 3D US improved visualization
and confident localization of devices in 13 of 22 (59%) procedures,
detected unacceptable device placement in 10 of 22 (45%), and determined
that 2D US had incorrectly predicted device orientation to a tumor in
three of 22 (14%). CONCLUSIONS: Compared to conventional 2D US, 3D US
provides additional relationship information for improved placement and
optimal distribution of ablative agents for treatment of focal liver
malignancy.
17
UI - 11775432
AU - Curley SA
TI -
Diagnosis and management of intrahepatic and extrahepatic
cholangiocarcinoma.
SO - Cancer Treat Res 2001;109():117-44
AD - University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
18
UI - 11775443
AU - Reynolds M
TI -
Pediatric liver tumors.
SO - Cancer Treat Res 2001;109():299-312
AD - Children's Memorial Hospital, Chicago, IL, USA.
19
UI - 11935085
AU - Teo EK; Fock KM
TI -
Hepatocellular carcinoma: an Asian perspective.
SO - Dig Dis 2001;19(4):263-8
AD - Department of Medicine, Changi General Hospital, Singapore.
eng_kiong_teo@cgh.com
Hepatocellular carcinoma (HCC) is one of the most frequently occurring
malignancies in Asia. The incidence exceeds 30 cases/100,000/year in the
east Asian region. Worldwide, it accounts for almost 1 million
deaths/year. The high incidence in Asia is due to the high prevalence of
chronic viral hepatitis, mainly chronic hepatitis B. With the
introduction of universal vaccination for hepatitis B in some Asian
countries in the mid 1980s, some of these countries are experiencing a
decline in the incidence of HCC. This probably underscores the point
that HCC caused by hepatitis B is a malignancy preventable by vaccine.
Due to the relative paucity of symptoms in the early stages and the
rapid doubling time of the tumor, most HCCs are discovered late in
advanced stages at presentation. Most Asian countries have adopted a
screening program for patients at risk. Earlier and smaller HCCs are
detected through such programs but these programs have yet to
demonstrate improved patient survival. Physicians managing patients with
HCC are faced with two main challenges, the malignancy itself and the
underlying liver disease. The extent of the tumor and the existing liver
function limits the therapeutic choices available. Hepatic resection
remains the treatment of choice. However, the majority of patients
present with nonresectable tumors. Transarterial chemoembolization,
percutaneous ethanol injection and radiofrequency ablation are the other
treatment modalities. In patients with small tumors (<5 cm) and poor
liver function, liver transplant offers a viable treatment alternative.
In summary, the risk factor for HCC in Asia is predominantly chronic
hepatitis B. Universal vaccination against hepatitis B is likely to
reduce the incidence. The prognosis and outcome of treatment remains
poor with a 5-year survival of 35% for patients treated surgically and
less than 10% for nonresectable tumors. Current management is aimed at
earlier detection and more effective treatment of early HCC. In future,
the challenge will be managing HCC in the premalignant stage. Copyright
2002 S. Karger AG, Basel
20
UI - 11935088
AU - Abdel-Rahim AY
TI -
Parasitic infections and hepatic neoplasia.
SO - Dig Dis 2001;19(4):288-91
AD - Tropical Medicine Department and Gastrointestinal Endoscopy and Liver
Unit, Cairo University, Cairo, Egypt. aymanyoussry@hotmail.com
Parasitic infections are highly prevalent in the general population.
Detecting a relationship between a parasitic infection and cancer is not
an easy task; it requires epidemiological, microbiological and molecular
biology techniques. In this article the important mechanisms by which
parasitic infections may induce carcinogenesis are reviewed. The
association between Schistosoma japonicum, Schistosoma mansoni and
hepatocellular carcinoma is covered. The cause-and-effect relationship
between the liver flukes Opisthorchis viverrini, Opisthorchis felineus,
Clonorchis sinensis, and cholangiocarcinoma is also reviewed. The
evidence supporting the role of schistosomes and liver flukes in
carcinogenesis is discussed. Finally the importance of the primary
prevention of these parasitic infections with oncogenic potentials is
emphasized. Copyright 2002 S. Karger AG, Basel
21
UI - 11935095
AU - Hellerbrand C; Hartmann A; Richter G; Knoll A; Wiest R; Scholmerich J;
TI -
Lock G
Hepatocellular carcinoma in southern Germany: epidemiological and
clinicopathological characteristics and risk factors.
SO - Dig Dis 2001;19(4):345-51
AD - Department of Internal Medicine I, University of Regensburg, Germany.
claus.hellerbrand@klinik.uni-regensburg.de
The aetiology of chronic liver disease leading to hepatocellular
carcinoma (HCC) and the clinical characteristics of patients with HCC
vary considerably internationally and intranationally. This study
analyses the characteristics of HCC patients in southern Germany, a low
endemic area of HCC. METHODS: The files of 118 consecutive patients with
HCC observed in a single tertiary care hospital between 1994 and 2000
have been reviewed. Epidemiological and clinicopathological
characteristics such as age at presentation, ethanol consumption,
serological hepatitis virus markers, and fibrosis were studied.
Additionally, serum levels of alpha-fetoprotein (AFP) were analysed at
the time of diagnosis in 77 patients. RESULTS: The male:female ratio was
4:1 and the mean age at presentation was 61.8 years. Alcohol abuse
(49.2%) and chronic hepatitis C infection (17.8%) were the most frequent
risk factors. Histologically proven liver cirrhosis in the surrounding
non-tumorous tissue was present in only 59.0% of cases. AFP levels were
elevated in 78% of cases, but only 34% reached >500 ng/ml, a value
considered to be significant for the diagnosis of HCC. AFP levels
correlated with the stage of fibrosis. SUMMARY AND CONCLUSIONS: The
sensitivity of AFP serum levels as a tumour marker is poor but might
help to detect at least a minority of cases. As in other populations
within Europe, chronic alcohol abuse is frequently associated with HCC
in southern Germany, confirming that alcohol is still the most important
risk factor for hepatocarcinogenesis in areas with low hepatitis virus
prevalence. Considering the poor prognosis of HCC, prevention is of
pivotal importance, particularly for patients with chronic liver disease
and other risk factors for the development of HCC. Copyright 2002 S.
Karger AG, Basel
22
UI - 11935096
AU - Schluter V; Rabe C; Meyer M; Koshy R; Caselmann WH
TI -
Intracellular accumulation of middle hepatitis B surface protein
activates gene transcription.
SO - Dig Dis 2001;19(4):352-63
AD - Department of Virus Research, Max Planck Institute of Biochemistry,
Martinsried, Germany.
While the natural intact protein does not possess any transactivator
function, C-terminal truncation of the middle hepatitis B surface (MHBs)
protein yields a novel transactivator function. We have previously found
that the truncated transactivator protein, MHBs(t167), is not secreted
but retained within the secretory pathway. Here, we provide evidence
that when full-length MHBs is coexpressed with the truncated MHBs(t167)
protein, the secretion of the full-length protein is inhibited and both
proteins accumulate within the cell. We further show that MHBs, forcibly
retained in the cell by C-terminal fusion to the endoplasmic reticulum
retention signal KDEL (MHBsKDEL), mimics the effects of MHBs(t167) in
enhancing the nuclear-binding activity of transcription factors NFkappaB
and AP-1, and activation of NFkappaB- and AP-1-dependent transcription
of reporter genes. As is the case for MHBs(t167), MHBsKDEL-dependent
activation of NFkappaB is inhibited by the antioxidant
N-acetyl-L-cysteine indicating the involvement of reactive oxygen
intermediates and suggesting a similar mechanism of activation. This
study suggests that the intracellular retention and accumulation of the
normally secreted MHBs leads to oxidative stress and activation of
transcription. This may be an important but not exclusive mechanism in
hepatocarcinogenesis. Copyright 2002 S. Karger AG, Basel
23
UI - 11960222
AU - Efremidis SC; Hytiroglou P
TI -
The multistep process of hepatocarcinogenesis in cirrhosis with imaging
correlation.
SO - Eur Radiol 2002 Apr;12(4):753-64
AD - Department of Radiology, University Hospital of Ioannina, Medical
School, P.O. Box 1186, 45110 Ioannina, Greece. sefremid@cc.uoi.gr
Hepatocarcinogenesis in the cirrhotic liver has recently become a
subject of intense investigation. The development of hepatocellular
nodules demonstrating varying degrees of cellular and architectural
atypia suggests that these nodular lesions represent a pathway of
carcinogenesis in cirrhosis of different etiologies. This pathway
involves processes, such as capillarization and neoangiogenesis, leading
to a gradual change in blood supply from portal to arterial, as a
dysplastic nodule becomes hepatocellular carcinoma. These changes in
intranodular blood supply create different enhancement patterns in the
two phases of liver circulation after an intravenous contrast injection
on multi-phase helical CT or dynamic gadolinium-enhanced MRI. This
article reviews the current concepts regarding the vascular changes
occurring in dysplastic nodules in the multistep process of
hepatocarcinogenesis, along with the associated imaging manifestations.
Some practical issues and dilemmas regarding the follow-up and biopsy of
these lesions are also discussed.
24
UI - 11950923
AU - Wilkens L; Bredt M; Flemming A; Mengel M; Klempnauer J; Kreipe H;
TI -
Flemming P
Detection of chromosomal aberrations in well-differentiated
hepatocellular carcinoma by bright-field in situ hybridization.
SO - Mod Pathol 2002 Apr;15(4):470-5
AD - Department of Pathology, Medizinische Hochschule, Hannover, Germany.
Differentiation between well-differentiated hepatocellular carcinoma
(HCC) and nonmalignant lesions with increased cellular proliferation may
be difficult in needle biopsies. Based on recurrent chromosome
aberrations known for HCC, we developed a nonfluorescent in situ
hybridization technique that allows combination with morphological
analysis in bright-field microscopy. Fourteen biopsies of HCC and 31
samples of regenerative nodules (n = 10), chronic hepatitis (n = 10),
fibrosis or cirrhosis of unknown origin (n = 5), focal nodular
hyperplasia (n = 2), primary biliary cirrhosis (n = 2), steatosis (n =
1), and adenomatous hyperplasia (n = 1) were analyzed with probes
specific for the centromeric regions of chromosomes 1, 6, 7, and 8.
After microwave pretreatment and in situ hybridization, signals were
detected using a tyramine-based system and AEC as substrate. Evaluation
of signals was done by conventional bright-field microscopy. Using this
approach, aberrant counts were seen for at least one chromosome in 12/14
cases of HCC. In contrast, none of the nonmalignant lesions revealed
aberrant counts for any of the chromosomes analyzed. In conclusion, this
new combination of in situ hybridization and tyramine amplification
allows fast and reliable evaluation of chromosome aberrations in a
histomorphological context similar to paraffin immunohistochemistry.
Registration of imbalances contributes to a reliable differentiation
between malignant and nonmalignant lesions of the liver.
25
UI - 11996790
AU - Sainati L; Leszl A; Surace C; Perilongo G; Rocchi M; Basso G
TI -
Fluorescence in situ hybridization improves cytogenetic results in the
analysis of hepatoblastoma.
SO - Cancer Genet Cytogenet 2002 Apr 1;134(1):18-20
AD - Department of Pediatrics, University of Padua, Via Giustiniani 3, Padua,
Italy. laura.sainati@unipd.it
Hepatoblastoma (HB) is the most frequent malignant liver tumor in
children. Cytogenetic data indicate the presence of recurring trisomies
of the chromosomes 2, 8, and 20, but more work is needed to clarify
their incidence and prognostic significance. Cytogenetic analysis is
limited by the requirement of suitable cells in metaphase. A different
method that increases analysis sensitivity is fluorescence in situ
hybridization (FISH). We studied 20 cases of hepatoblastoma; FISH
analysis obtained results in 10 cases of HB with no informative
karyotype. In 5 of 10 of these cases at least one trisomic clone was
detected, which always coexisted with a population of diploid cells.
These results confirm that trisomy 20 and/or 2 and 8 coexisting with
diploid cells is a frequent finding in hepatoblastoma and provide
further support to the clonal evolution theory: indeed, trisomy 20 was
the most frequently detected abnormality, followed by trisomy of
chromosomes 2 and 8. In view of the high incidence of recurrent
trisomies, FISH analysis should be recommended in all the cases of HB
with no informative karyotype.
26
UI - 11030243
AU - Hanazaki K; Kajikawa S; Shimozawa N; Mihara M; Shimada K; Hiraguri M;
TI -
Koide N; Adachi W; Amano J
Survival and recurrence after hepatic resection of 386 consecutive
patients with hepatocellular carcinoma.
SO - J Am Coll Surg 2000 Oct;191(4):381-8
AD - Second Department of Surgery, Shinshu University School of Medicine,
Matsumoto, Japan.
BACKGROUND: Although hepatic resection is one of the most effective
treatments for hepatocellular carcinoma (HCC), the longterm results of
hepatic resection of this malignancy are far from satisfactory. The
potential benefits of hepatectomy for patients with HCC have not been
fully delineated. This study aimed to identify surgical outcomes of 386
consecutive patients with HCC undergoing hepatic resection. STUDY
DESIGN: The retrospective study looked at records of 293 men and 93
women. The mean age was 63.2 years. Preoperative transarterial
chemoembolizaton and portal vein embolization were performed in 138
patients (35.8%) and 8 patients (2.1%), respectively. Sixty-two patients
(16.1 %) had major hepatectomy and the other 324 (83.9%) had minor
hepatectomy. Thirty-seven of 386 patients (9.6%) had a noncurative
operation. RESULTS: The 30-day (operative) mortality rate was 4.1%, and
there were 11 additional late deaths (2.9%). Two hundred fourteen of 327
patients (65.4%) had recurrence after curative resection. Unfavorable
factors for survival and recurrence were resection between 1983 and
1990, Child class B or C, cirrhosis, a high value of indocyanine green
retention-15, a large amount of intraoperative blood loss, stage IV
disease, positive surgical margin, vascular invasion, and postoperative
complications. Preoperative transarterial chemoembolization increased
the recurrence rate and showed no contribution to prognosis. Currently,
106 patients (27.5%) are alive: 7 (1.8%) after more than 10 years and 43
(11.1%) after more than 5 years. Mean and median overall survivals after
operation were 38 months and 29 months, respectively. The 5-year and
10-year overall or disease-free survival rates after hepatic resection
were 34.4% and 10.5% or 23.3% and 7.8%, respectively. CONCLUSIONS: The
longterm survival rate after operation remains unsatisfactory mainly
because of the high recurrence rate. Preoperative transarterial
chemoembolization should be avoided because of a high risk of
postoperative recurrence. Treatment strategies for recurrent HCC may
play an important role in achieving better prognosis after operation,
especially in patients with more than Child class B, cirrhosis, high
values of indocyanine green retention-15, massive intraoperative blood
loss, stage IV disease, positive surgical margin, vascular invasion, and
postoperative complications.
27
UI - 11981340
AU - de Ledinghen V; Laharie D; Lecesne R; Le Bail B; Winnock M; Bernard PH;
TI -
Saric J; Couzigou P; Balabaud C; Bioulac-Sage P; Drouillard J
Detection of nodules in liver cirrhosis: spiral computed tomography or
magnetic resonance imaging? A prospective study of 88 nodules in 34
patients.
SO - Eur J Gastroenterol Hepatol 2002 Feb;14(2):159-65
AD - Unite de Transplantation Hepatique, Hopital Pellegrin, Bordeaux, France.
victor.deledinghen@chu-bordeaux.fr
Detection and characterization of all focal lesions in the liver are
critical for screening patients with chronic liver disease. The aim of
this prospective study was to investigate the accuracy of magnetic
resonance imaging (MRI) and spiral computed tomography for the diagnosis
of hepatic nodules in cirrhotic patients when compared with pathological
cirrhotic patients waiting for orthotopic liver transplantation (OLT)
(mean age, 53.5 +/- 9.3 years; 24 males) were included. All patients had
MRI and spiral computed tomography examinations, and findings were
matched with the histological findings. Data analyses were made using
the McNemar chi-square test. Mean time between radiological examination
(MRI or spiral computed tomography) and OLT was 43.8 +/- 39 days. A
total of 88 nodules were found in the 34 patients: 54 hepatocellular
carcinoma (HCC) (mean size, 18 +/- 10 mm) in 21 patients, 22 dysplastic
nodules (mean size, 10.7 +/- 4.3 mm) in 11 patients, and 12
macroregenerative nodules in 13 patients. Lesion-by-lesion analyses
showed that sensitivity of MRI and spiral computed tomography for
nodule, HCC or dysplastic nodule diagnosis was 44.3 and 31.8% (P =
0.02), 61.1 and 51.9% (P = 0.2), and 27.3 and 0% (P = 0.04),
respectively. Patient-by-patient analyses showed no statistical
difference between spiral computed tomography and MRI for nodule
diagnosis. In conclusion, in patients with liver cirrhosis, MRI is more
accurate than spiral computed tomography for the detection of liver
nodules and dysplastic nodules. However, tumour size is always a
restricting factor for these two techniques, which are unable to detect
small HCC in more than 60% of cases.
28
UI - 11938045
AU - Ganne-Carrie N; Mohand D; N'kontchou G; Grando-Lemaire V; Trinchet JC
TI -
[Synopsis: Diagnosis and treatment of hepatocellular carcinoma in
patients with cirrhosis]
SO - Gastroenterol Clin Biol 2002 Jan;26(1):73-7
AD - Service d'Hepato-Gastroenterologie, Hopital Jean-Verdier, AP-HP et UFR
SMBH, Universite Paris 13, 93143 Bondy Cedex, France.
29
UI - 11938047
AU - Beaugrand M
TI -
[Diagnosis and treatment of hepatocellular carcinoma. Questions for
Professor Michel Beaugrand]
SO - Gastroenterol Clin Biol 2002 Jan;26(1):84-6
AD - Service d'Hepato-Gastroenterologie, Hopital Jean-Verdier, AP-HP et UFR
SMBH, Universite Paris 13, 93143 Bondy Cedex.
30
UI - 11973655
AU - Delpuech O; Trabut JB; Carnot F; Feuillard J; Brechot C; Kremsdorf D
TI -
Identification, using cDNA macroarray analysis, of distinct gene
expression profiles associated with pathological and virological
features of hepatocellular carcinoma.
SO - Oncogene 2002 Apr 25;21(18):2926-37
AD - INSERM U370, CHU Necker/Institut Pasteur, 75015, Paris, France.
It is still unclear as to whether the gene expression profile in HCV- or
HBV-related HCC exhibits a degree of specificity and whether the
development of HCC in a context of cirrhosis influences this gene
profile. To address these issues, the expression profiles of 15 cases of
HCC were analysed using cDNA macroarray. A global analysis and
hierarchical clustering, demonstrated the heterogeneity of HCC patterns,
with a majority of down-regulated genes. Statistical analysis clearly
showed a distinction between the gene expression profiles of HCV- and
HBV-related HCC. HBV-associated HCC exhibited involvement of different
cellular pathways, those controlling apoptosis, p53 signalling and G1/S
transition. In HCV-related HCC we identified a more heterogenous pattern
with an over-expression of the TGF-beta induced gene. In HCC developing
on non-cirrhotic tissues, beta-catenin encoding gene and genes
implicated in the PKC pathway were specifically up-regulated. In
addition, our investigation highlighted a distinct profiles of TGF-beta
superfamily encoding genes in well, moderately or poorly differentiated
HCC. Overall, our study supports the hypothesis that despite the
heterogeneity of the HCC pattern, the large-scale screening of gene
expression may provide data significant to our understanding of the
mechanism of liver carcinogenesis.
31
UI - 11836602
AU - Itoh Y; Ohkubo K; Iuchi H; Michitaka K; Horiike N; Onji M
TI -
Chronological changes of causes of death and distant metastasis in
hepatocellular carcinoma.
SO - Oncol Rep 2002 Mar-Apr;9(2):331-5
AD - Third Department of Internal Medicine, Ehime University School of
Medicine, Shigenobu-Cho, Ehime 791-0295, Japan. horiike@m.ehime-u.ac.jp
The diagnostic approaches, mode of therapies, frequencies of distant
metastasis and causes of death in 139 patients with hepatocellular
carcinoma (HCC) between 1976 and 1998 were studied by dividing the total
study duration into three periods. The period between 1976-1980 (period
I) was characterized by the absence of periodic follow-up of the
patients with chronic liver diseases, and operation was the only
therapeutic choice for HCC. During 1981-1986 (period II), periodic
screening of patients with chronic liver diseases was started using
ultrasonography, and transarterial embolization became a second choice
of therapy along with operation. Period III (1986-1998) was
characterized by the availability of facilities to make definitive
diagnosis of HCC using small-gauge cutting needle biopsy under
sonographic guidance. Data from our study show that along with the
advancement of new and invasive diagnostic and therapeutic approaches,
the frequency of death due to gastrointestinal bleeding decreased,
whereas, the frequency of death due to respiratory failure resulting
from pulmonary metastasis increased. Patients treated with transcatheter
arterial embolization were more prone to develop pulmonar
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