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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Liver Cancer - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
UI - 11734333
AU - Qin LF; Ng IO
TI -
Induction of apoptosis by cisplatin and its effect on cell cycle-related
proteins and cell cycle changes in hepatoma cells.
SO - Cancer Lett 2002 Jan 10;175(1):27-38
AD - Department of Pathology and Centre for the Study of Liver Disease, The
University of Hong Kong, Room 127B, University Pathology Building, Queen
Mary Hospital, Pokfulam, Hong Kong.
We investigated cisplatin-induced apoptosis and the effects on cell
cycle-related proteins and cell cycle changes. Two human hepatoma cell
lines, HepG2 (with wild-type p53) and Hep3B (with deleted p53), were
treated with different concentrations of cisplatin. Cisplatin induced
apoptosis in both cell lines as assessed by cell morphology, DNA
fragmentation analysis,TdT-mediated dUTP nick end labeling assay and
flow cytometry. HepG2 cells were more sensitive to cisplatin than Hep3B.
Low-dose cisplatin induced a transient G(1) arrest, S phase block and
upregulation of p53 and p21(WAF1/CIP1) expression in HepG2, but not in
Hep3B cells. With cisplatin at a high dose, both cell lines underwent
apoptosis that was accompanied by downregulation of p27(KIP1) and
Bcl-x(L). In HepG2, upregulation of p53 and p21(WAF1/CIP1) was observed
before apoptosis occurred, suggesting that cisplatin-induced apoptosis
in HepG2 might be p53-dependent. Expression of Fas was also increased
following cisplatin treatment in HepG2. However, there was no induction
of p53, p21(WAF1/CIP1) and Fas observed in Hep3B cells. In conclusion,
cisplatin induced apoptosis in hepatoma cells via both p53-dependent and
-independent pathways.
2
UI - 11778551
AU - Lu Y; Zhou R
TI -
[Mechanism of enhanced invasiveness of human hepatocellular carcinoma by
integrin alpha 6 beta 1]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):287-9
AD - Department of Cell Biology, Beijing Medical University, Beijing 100083,
China.
OBJECTIVE: To study the mechanism of enhanced invasiveness of human
hepatocellular carcinoma (HCC) by laminin (LN) receptor integrin alpha 6
beta 1. METHODS: A stable transfectant of HCC Bel 7402 cell line, the
alpha 6 beta 1 receptors of which were replaced by non-functional LN
receptor alpha 6 beta 4-TR using dominant negative strategy, was used.
Motility of the non-transfected, mock transfected and transfected tumor
cells was assessed by the number of cells migrated to an area scratched
out of cells on tumor cell monolayer. Tumor cell invasion was examined
by cell penetration through a Matrigel layer in Boyden chamber. Matrix
metalloproteinases (MMPs) secretion was detected by gelatin zymography.
RESULTS: The migration of HCC Bel 7402 cells expressing dominant
negative alpha 6 beta 1 was significantly decreased. Their invasive
capability was decreased by 46.7%. The secretion of MMP-9 was almost
totally inhibited and the activated MMP-2 was decreased by 43.9%.
CONCLUSION: The decrease in cell motility, invasiveness and MMPs
secretion of HCC cells expressing dominant negative alpha 6 beta 4 TR
implies that LN-integrin interaction plays important role in HCC
progression.
3
UI - 11778560
AU - Chen Y; Li H
TI -
[Imaging findings of intrahepatic peripheral cholangiocarcinoma]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):318-20
AD - Cancer Institute (Hospital), Chinese Academy of Medical Sciences, Peking
Union Medical College, Beijing 100021, China.
OBJECTIVE: To study the imaging features of intrahepatic peripheral
cholangiocarcinoma. METHODS: The imaging features of 11 cases of
surgically and pathologically confirmed intrahepatic peripheral
cholangiocarcinoma were retrospectively reviewed. B-ultrasonic
scanning(BUS) was performed in all patients. CT was done in 8 patients,
including conventional unenhanced scanning followed by enhanced scanning
in 4 patients, dynamic double-stage scanning in 2 patients, and dynamic
double-stage scanning followed by delayed scanning in the other 2
patients. Of the 3 patients received MRI, conventional SE series, T1WI
and T2WI were performed in 2 patients, conventional SE series and
dynamic scanning in the other one. RESULTS: All lesions were hypo-echoic
in BUS, homogeneous or heterogeneous. On unenhanced CT, the lesions were
of low density with ill-defined border. On enhanced scanning, moderate
enhancement was observed at the edge of the lesions. MRI was of low
intensity in T1WI and moderately high intensity in T2WI. Dynamic MRI and
double-stage CT scanning showed characteristic enhancement from the
periphery toward the center of the lesion. Focal dilatation of the
intrahepatic bile ducts around the tumor was seen in 6 cases and
retraction of liver capsule in 3 cases. CONCLUSION: To some extent, the
imaging features of intrahepatic peripheral cholangiocarcinoma are
characteristic. They are useful for differentiating these tumors from
other space-occupying lesions in the liver.
4
UI - 11521784
AU - Emile JF; Azoulay D; Gornet JM; Lopes G; Delvart V; Samuel D; Reynes M;
TI -
Bismuth H; Goldwasser F
Primary non-Hodgkin's lymphomas of the liver with nodular and diffuse
infiltration patterns have different prognoses.
SO - Ann Oncol 2001 Jul;12(7):1005-10
AD - Service d'anatomie pathologique, Hjpital Paul Brousse, UPRES 1596 and
IFR 89, Universite Paris Sud, France.
jean-francois.emile@pbr.ap-hop-paris.fr
BACKGROUND: Primary liver non-Hodgkin's lymphomas have peculiar clinical
and biological patterns. This study correlates these patterns with
pathology and outcome. PATIENTS AND METHODS: Clinical records and
histology of patients with primary liver non-Hodgkin's lymphoma, treated
at our institution over a 20-year period, were reviewed.
Lymphoproliferations occurring after liver transplantation were
excluded. Survival analyses were performed with patients from the other
published series (62 patients). RESULTS: Our series included eight
patients. Three patients had a nodular liver infiltration, corresponding
to a large B-cell lymphoma. Five patients had a diffuse liver
infiltration, of whom three had a T-cell lymphoma with predominant
sinusoid infiltration, and two had a large B-cell lymphoma. Patients
with diffuse liver infiltration presented with hepatomegaly, and two of
these also had acute liver failure. Diffuse infiltration had a worse
prognosis than nodular infiltration (P = 0.0033). Among these latter
patients, those treated with an anthracycline-based chemotherapy had a
better outcome (P < 0.0001). CONCLUSIONS: Patients with primary liver
lymphomas can be classified in two groups, depending on the type of
infiltration. Those with nodular infiltration may benefit from
anthracycline-based chemotherapy. Diffuse infiltration has a bad
prognosis, and should be suspected in patients presenting with altered
liver functions and hepatomegaly.
5
UI - 11776078
AU - Shao J; Li Y; Li H; Wu Q; Hou J; Liew C
TI -
Deletion of chromosomes 9p and 17 associated with abnormal expression of
p53, p16/MTS1 and p15/MTS2 gene protein in hepatocellular carcinomas.
SO - Chin Med J (Engl) 2000 Sep;113(9):817-22
AD - Cancer Center, Sun Yat-Sen University of Medical Sciences, Guangzhou
510060, China.
OBJECTIVE: Fifteen loci on chromosome 9p and 17 were analyzed to clarify
the involvement of loss of heterozygosity (LOH) in hepatocellular
carcinoma (HCC) in Chinese patients positive for hepatitis B (HBV)
and/or hepatitis C (HCV) infection. Expression of tumor suppressor genes
(TSG) of p53, p16, and p15 gene was found to correlate with a deletion
of these genes. METHODS: Immunohistochemistry and PCR-based
microsatellite polymorphism analysis techniques were used. RESULTS: A
high frequency of LOH was detected on chromosome 9p24 at locus D9S54
(61.8%) and 9p21, concentrated at loci D9S1747 (52.4%) and D9S1752
(51.8%). On chromosome 17, high frequent LOH was concentrated on 17p at
the p53 gene locus (53.8%) and locus D17S520 (52.8%). p53 protein
expression was increased in HCC, which correlated with p53 gene loss.
Expression of p16 and p15 protein decreased in HCC when LOH occurred at
locus D9S1752 (p15 gene locus) or at locus D9S1747 and D9S1748 (p16 gene
is located between these 2 loci). LOH at the p53 gene and p15 gene loci
was closely associated with HBV and HCV co-infection in HCC. No
significant relationship between LOH and HCC clinico-pathological
outcomes was observed. CONCLUSION: High frequency LOH occurs on
chromosomes 9p and 17 in HCC in Chinese patients. Such sites may contain
several putative tumor suppressor genes critically involved in the
development and/or progression of HCC. Deletion of p53, p16, or p15
tumor suppressor genes may cause abnormal expression of the protein
product of these genes. HBV and/or HCV infection may be closely
associated with LOH p53 and/or p15 gene expression.
6
UI - 11776086
AU - Ji Y; Zhu X; Sun H; Tan Y; Ma Z; Ye Q; Sujie A; Tang Z
TI -
Hepatocellular adenoma and focal nodular hyperplasia: a series of 24
patients with clinicopathological and radiological correlation.
SO - Chin Med J (Engl) 2000 Sep;113(9):852-7
AD - Department of Pathology, Zhongshan Hospital, Shanghai 200032, China.
newera.ji@yahoo.com
OBJECTIVE: To investigate two rare benign lesions, hepatocellular
adenoma (HCA) and focal nodular hyperplasia (FNH), and evaluate
differential diagnosis. METHODS: Twenty-four consecutive patients with
presumed HCA and FNH were studied at the Liver Cancer Institute from
evaluation, symptoms and laboratory tests. New imaging techniques were
prospectively appraised in addition to usual techniques. All had hepatic
resections and follow-up. Histologic examination of surgical specimens
was obtained in all cases. RESULTS: In every instance, FNH was an
incidental finding. FNH consists of nodular aggregates of cytologically
normal hepatocytes with foci of intranocular bile duct proliferation. In
this series, patients with HCA had larger tumors and more often were
symptomatic but the occurrence was unrelated to oral contraceptive
steroids (OCS) usage. Intralesional hemorrhage or necrosis is common,
and was seen in 75% of cases. The best imaging procedure in the
diagnosis of FNH was MRI. Color Doppler US was a useful adjunct, but CT
lacked specificity, making histological diagnosis mandatory. All
patients underwent tumor resected were tumor--free during the follow-up.
CONCLUSIONS: FNH is a distinct histopathologic entity, and is
distinguishable from HCA. FNH is a hyperplastic response by the liver
parenchyma to a pre-existing arterial malformation. HCA is a liver
neoplasia and has the potential of malignant transformation to HCC.
Based on these findings, we believe that if the clinical suspicion of
HCA or FNH is strong, resection is usually the best approach if
technically feasible and histologic diagnosis is mandatory.
7
UI - 11778272
AU - Zhao X; Wan D; Jiang H
TI -
[Analysis on loss of heterozygosity of chromosome 17p13.3 in
hepatocellular carcinoma and construction of genomic contig in the
deleted region]
SO - Zhonghua Zhong Liu Za Zhi 2000 Sep;22(5):377-80
AD - National Laboratory for Oncogenes and Related Genes, Shanghai Cancer
Institute, Shanghai 200032, China.
OBJECTIVE: To detect the status of loss of heterozygosity (LOH) on
chromosome 17p13.3 in hepatocellular carcinoma (HCC) and determine a
minimum region of LOH as well as construct genomic contig in LOH region.
METHODS: Variable number tandem repeat (VNTR) and RFLP markers examined
by Southern hybridization were used to detect LOH of HCC. Microsatellite
markers amplified by PCR were detected for LOH by denatured PAGE. Using
microsatellite primers, 3 rounds of PCR amplification were carried out
to screen positive genomic clones. The contig was constructed by PCR
detecting the reaction between microsatellite markers and individual
genomic clone. RESULT: Fifty-four paired HCC samples were analysed with
16 polymorphic markers on chromosome 17p13.3. The data revealed that the
region between D17S5 and D17S34 had a high rate of LOH (> 63%), but
three markers (proximal to D17S5) toward centromere had low or no LOH.
TP53 marker on chromosome 17p13.1 had a LOH rate of 31% which was lower
than that on D17S5-D17S34 region. No LOH was found at D17S34, D17S1866
(proximal to telomere) and D17S5, D17S1574 (distal to telomere) in 2
cases of HCC. However, there was LOH between D17S849 and D17S1574 in
some cases. In LOH region, genomic clones relative to 18 of markers were
obtained. A contig covering 9 markers was constructed. CONCLUSION:
Determination of the minimum LOH region on chromosome 17p13.3 in HCC and
the construction of genomic clone contig provide basis for further
identification of putative new tumor suppressor gene(s) in HCC.
8
UI - 11676880
AU - Peng G; Pang Z
TI -
[In vitro modulation of the invasive and metastatic potentials of human
hepatocellular carcinoma by interlukin-2]
SO - Zhonghua Gan Zang Bing Za Zhi 2001 Oct;9(5):303-5
AD - Southwest Hospital, Third Military Medical University, Chongqing 400038,
China.
OBJECTIVE: To investigate the effects of interlukin-2 (IL-2) on the in
vitro invasiveness and the expression of several cell surface antigens
related to invasive and metastatic potentials of human hepatocellular
carcinoma (HCC) QGY-7701 cell line. METHODS: QGY-7701 cells were
incubated with high concentration of IL-2 or low concentration of IL-2
in different time. The expression of ICAM-1, CD(44) and HLA-I of the
tumor cells was determined by fluorescence-activated cell sorter (FACS)
analysis The tumor cell binding affinity to extracellular matrix
components was measured by cell attachment assay. The degree of
homotypic aggregation was quantified by cell aggregation assay. RESULTS:
IL-2 treatment exhibited enhanced expression of ICAM-1 (from 8.3% to
20.5% after high concentration of IL-2 treatment and 17.3% after low
concentration of IL-2 treatment) and HLA-I (from 9.8% to 25.4% and
22.1%, respectively after high and low concentration of IL-2 treatment),
suppression of CD(44) (from 26.4% to 12.5% and 11.6%, respectively) on
HCC cell line and decreased binding affinity to type IV collagen (from
23.5% to 12.4%, 32.3% to 13.8%, 45.7% to 19.6% at 20 min, 40 min and 60
min, respectively after high concentration of IL-2 treatment, and 9.6%,
12.5% and 17.9%, respectively after low concentration of IL-2 treatment)
and fibronectin (from 18.6% to 14.1%, 31.2% to 18.4%, 44.5% to 20.5% at
20 min, 40 min and 60 min, respectively after high concentration of IL-2
treatment, and 14.6%, 17.1% and 18.9%, respectively after low
concentration of IL-2 treatment) and the degree of homotypic aggregation
(from 58.3% to 26.5%, 85.4% to 37.6%, 88.6% to 42.3% at 20 min, 40 min
and 60 min, respectively after high concentration of IL-2 treatment, and
25.0%, 36.4% and 42.6%, respectively after low concentration of IL-2
treatment)of HCC cells. CONCLUSIONS: IL-2 may directly alter tumor
properties associated with invasive and metastatic phenotypes of HCC
cells, and can inhibit the invasive and metastatic potentials of HCC
cells.
9
UI - 11776624
AU - Wu P; Li L; Zhang F
TI -
[The value of spiral CT in CT arterial portography and CT hepatic
arteriography]
SO - Zhonghua Zhong Liu Za Zhi 1999 Nov;21(6):450-2
AD - Cancer Center, Sun Yat-sen University of Medical Sciences, Guangzhou
510060.
OBJECTIVE: To evaluate the usefulness of spiral CT in CT arterial
portography (CTAP) and CT hepatic arteriography (CTHA). METHODS: The
CTAP and CTHA manifestations in 50 patients with small hepatocellular
carcinoma (< 3 cm in diameter) were analyzed and compared with those in
bi-phase enhanced CT. RESULTS: The detection rate of CTAP and CTHA was
92.2% and 90.1%, respectively. They could reveal tumors of 0.2 cm-0.5 cm
in diameter. Both CTAP and CTHA gave false-positive findings, such as
perfusion defects in 13.0% of CTAP and non-pathologic enhancement in
19.1% of CTHA. CONCLUSION: With the use of spiral CT technique, the
quantity of contrast material administrated in CTAP and CTHA can be
considerably reduced, and the quality of CT images significantly
improved. The detection rate of CTAP and CTHA is higher than that of
biphase enhanced CT. Simultaneous use of both procedures may help
decrease the false-positive rate, and increase the sensitivity of
diagnosis for small hepatocellular carcinoma.
10
UI - 11808941
AU - Yano Y; Yamashita F; Sumie S; Ando E; Fukumori K; Kiyama M; Oyama T;
TI -
Kuroki S; Kato O; Yamamoto H; Tanaka M; Sata M
Clinical features of hepatocellular carcinoma seronegative for both
HBsAg and anti-HCV antibody but positive for anti-HBc antibody in Japan.
SO - Am J Gastroenterol 2002 Jan;97(1):156-61
AD - Saga Social Insurance Hospital, Hyogo-minami, Saga-shi, Japan.
OBJECTIVE: We determined the prevalence of patients with hepatocellular
carcinoma (HCC) who were positive for only anti-hepatitis B core
(anti-HBc) antibody among 284 Japanese patients and compared their
clinical features to those who were hepatitis B surface antigen positive
[HBsAg(+)]. METHODS: Serum HBsAg and anti-hepatitis C virus (anti-HCV)
antibody were examined for all HCC patients. Testing for anti-HBc
antibody was performed in the HBsAg(-)/anti-HCV(-) patients. The
clinical factors and the survival rate were compared between the
HBsAg(+) patients (HCC-B) and those positive for anti-HBc alone
(HCC-PB). RESULTS: There were 19 (6.7%) HBsAg(+), 236 (83.1%)
anti-HCV(+), seven (2.5%) HBsAg(+)/anti-HCV(+), and 22 (7.7%)
HBsAg(-)/anti-HCV(-) among the 284 patients tested. Sixteen (72.7%) of
the 22 HBsAg(-)/anti-HCV(-) patients were assigned to the HCC-PB group.
The prevalence of positivity for anti-HBc alone among all 284 HCC
patients was 5.6%. Significant differences between the HCC-PB and HCC-B
groups were that age at diagnosis was higher in the HCC-PB group (72.1
yr) than in the HCC-B group (56.2 yr) (p < 0.001), the serum
alpha-fetoprotein concentrations were lower in the HCC-PB group (8.2
ng/ml) than in the HCC-B group (43 ng/ml) (p = 0.0488), and a higher
familial history of liver disease was observed in the HCC-B group (p =
0.0373). However, there was no significant difference in the cumulative
survival rate. CONCLUSIONS: Positivity for anti-HBc alone is not rare
compared to HBsAg(+), and the clinical features of positivity for
anti-HBc alone are similar to those of HBsAg(+). Some differences in the
clinical features between the two groups may be explained by differences
in the time of first exposure to hepatitis B virus. Therefore, the
natural course of acute hepatitis B may be reconsidered.
11
UI - 11808943
AU - Nair S; Shivakumar KS; Thuluvath PJ
TI -
Mortality from hepatocellular and biliary cancers: changing
epidemiological trends.
SO - Am J Gastroenterol 2002 Jan;97(1):167-71
AD - Department of Medicine, The Johns Hopkins University School of Medicine,
Baltimore, Maryland, USA.
OBJECTIVES: The incidence of hepatocellular carcinoma may be rising in
the United States. The aim of this study was to determine the
epidemiological trends in mortality from hepatocellular carcinoma (HCC)
and biliary cancers (BCs) in Maryland during the last 3 decades.
METHODS: The number of deaths due to HCC and BCs from 1970 to 1997 were
obtained from the Maryland State Department of Health & Hygiene vital
statistics database. Malignant neoplasms of the gallbladder and
intrahepatic and extrahepatic bile ducts were grouped together as
biliary cancers. To determine the trend in mortality, the total time
period was divided into seven 4-yr periods. RESULTS: Mortality from HCC
increased from 0.94 to 1.84 per 100,000 population (rate ratio = 1.94,
CI = 1.87-2.03) and that from BCs increased from 1.28 to 1.7 per 100,000
population (rate ratio = 1.31, CI = 1.26-1.36) over the study period.
Although mortality due to HCC doubled in men (1.34 to 2.7 per 100,000)
during this period, only a modest increase was observed among women
(0.59 to 1.06 per 100,000). Because of a marked increase in the number
of deaths among white Americans, the difference in HCC-related mortality
between white Americans and African Americans decreased considerably
during this period. Mean age at death increased steadily for BCs from 67
to 73 yr, whereas there was no real trend for HCC. Among African
Americans, the death from HCC remained stable, but there was a 2-fold
increase in BC-related death. CONCLUSIONS: There was a marked increase
in deaths from HCC over the past 3 decades in Maryland. This increase
was more evident among men and white Americans. Deaths due to BCs
increased modestly during the same period of observation. The marked
rise in BC-related deaths among African Americans remains unexplained.
12
UI - 11587244
AU - Anand BS
TI -
Drug treatment of the complications of cirrhosis in the older adult.
SO - Drugs Aging 2001;18(8):575-85
AD - Baylor College of Medicine, Houston, Texas, USA. ana0@flash.net
Several age-related changes occur in the structure and functions of the
liver. The volume of the liver decreases, despite an increase in the
size of hepatocytes, suggesting loss of liver cells. There are decreases
in hepatic blood flow, the synthesis of urea and cholesterol, and the
metabolism of drugs. Moreover, the regenerative capacity of liver
becomes less efficient. Certain caveats are important when treating
older patients with liver disease. Strict dietary restrictions, such as
a low protein diet, should be avoided in the elderly (unless the patient
is encephalopathic) because these patients are often undernourished to
start with. Similarly, strict salt restriction should be enforced with
caution, since it makes food less palatable and may take away what
little desire such patients have to eat. Diuretic doses should be
adjusted carefully because of greater risks of azotaemia and electrolyte
disturbances in the elderly. Extra vigilance should be exercised in the
early detection of infections that are more likely to occur in patients
with cirrhosis. For example, spontaneous bacterial peritonitis can be
missed in the elderly because of poor systemic (fever, abdominal
tenderness) and laboratory responses (leucocytosis). In patients
presenting with acute variceal bleeding, it is better to err on the side
of underhydration than overhydration because of the risk of congestive
heart failure. Vasopressin should be avoided in the elderly, since this
drug has a high probability of precipitating an ischaemic event. Older
patients do not tolerate beta-blockers as well as younger individuals
and may require other treatment strategies for the prevention of
variceal rebleeding episodes. Hepatic encephalopathy, especially the
milder form, needs careful assessment because it can be easily confused
with senile dementia syndromes. Cirrhosis is a premalignant condition
and patients are at increased risk of developing hepatocellular
carcinoma (HCC), a tumour seen predominantly in the elderly. All
patients with cirrhosis should be maintained on a lifelong screening
programme consisting of a 6-monthly assessment of alpha-fetoprotein and
an imaging study, since early detection provides the only hope for cure
of HCC. The only definitive treatment of cirrhosis is liver
transplantation. Advanced age is not a contraindication to
transplantation, and survival in older patients (aged >60 years) is
comparable to that in younger individuals.
13
UI - 11813698
AU - Wartenberg D; Siegel Scott C
TI -
Carcinogenicity of trichloroethylene.
SO - Environ Health Perspect 2002 Jan;110(1):A13-4
14
UI - 11740693
AU - Kardorff R; Fuchs J; Peuster M; Rodeck B
TI -
[Infantile hemangioendothelioma of the liver--sonographic diagnosis and
follow-up]
SO - Ultraschall Med 2001 Dec;22(6):258-64
AD - Marien-Hospital Wesel, Klinik fur Kinder- und Jugendmedizin, Germany.
ruediger.kardorff@marien-hospital-wesel.de
OBJECTIVE: Hepatic haemangioendothelioma is the most frequently observed
hepatic tumour of early infancy. Lesions may cause life-threatening
disease due to av-shunt-related cardiac failure, Kasabach-Merritt
syndrome or encroachment on surrounding tissue. In this paper, the value
of ultrasonography at initial work-up as well as during follow-up under
various management strategies is discussed. METHOD: Retrospective
analysis of sonographic and clinical data as well as outcome of 14
patients. RESULTS: The tumours may present initially with a typical
sonographic pattern of a roundish solitary lesion consisting
predominantly of massively perfused, tortuous cavities. In these cases,
histological verification of the diagnosis is not mandatory, provided
serological tumour markers are negative. Multifocal
haemangioendotheliomata with a solid appearance, however, cannot be
reliably distinguished from other entities sonographically. Tumour
development - with or without therapy - can be followed up precisely
using repeated ultrasound evaluations of tumour volume and
sono-morphology as well as Doppler examination of tumour perfusion.
CONCLUSIONS: Guidelines for the management of these patients are
discussed, based on our experience and a review of the literature.
Sonography proves to be of outstanding importance.
15
UI - 11690710
AU - Kanetaka K; Sakamoto M; Yamamoto Y; Yamasaki S; Lanza F; Kanematsu T;
TI -
Hirohashi S
Overexpression of tetraspanin CO-029 in hepatocellular carcinoma.
SO - J Hepatol 2001 Nov;35(5):637-42
AD - Pathology Division, National Cancer Center Research Institute, 5-1-1
Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
BACKGROUND/AIMS: The molecules involved in the progression of
hepatocellular carcinoma (HCC) are not fully understood. The aim of this
study was to elucidate the crucial genes involved in cancer progression
and metastasis. METHODS: Selectively expressed genes were screened using
differential display analysis, and then further analyzed by real-time
quantitative reverse-transcription polymerase chain reaction (RT-PCR)
and immunohistochemistry. RESULTS: Tetraspanin CO-029 was found to be
frequently and significantly overexpressed in HCC. Real-time
quantitative RT-PCR showed that the CO-029 mRNA level was 1.7 times
higher (P=0.030) in cancerous tissues than in non-cancerous tissues.
mRNA expression of the other tetraspanins, CD9 and CD82, was
downregulated in HCC, especially in tumors with intrahepatic spreading
(portal vein invasion and/or intrahepatic metastasis). In contrast, mRNA
expression of CO-029 tended to be increased in cancerous tissue showing
intrahepatic spreading compared with tumors without such spreading.
Immunohistochemical analysis revealed that CO-029 was overexpressed in
poorly differentiated HCCs compared with well to moderately
differentiated tumors (P<0.001), and in HCCs showing intrahepatic
spreading compared with those without spreading (P=0.019). CONCLUSIONS:
Our findings suggest that CO-029 has some roles in the promotion of
metastasis of HCC.
16
UI - 11775832
AU - Liu J; Zhou R; Zhang N; Rui J; Jin C
TI -
Biological function of a novel gene overexpressed in human
hepatocellular carcinoma.
SO - Chin Med J (Engl) 2000 Oct;113(10):881-5
AD - Department of Cell Biology, Beijing Medical University, Beijing 100083,
China.
OBJECTIVE: To clone the full-length of a differentially expressed cDNA
fragment, LC27, and study its biological function tentatively. METHODS:
Northern blot was used to analyze the expression pattern of LC27 in
hepatocellular carcinoma, matched nontumor liver tissues, fetal liver
and normal adult liver tissues, as well as BEL-7402 hepatocellular
carcinoma cell line ESTs splicing and 5' rapid amplification of cDNA
ends (5' RACE) were used to clone the full-length of LC27 cDNA. An
antisense oligodeoxynucleotide approach was used to investigate the
biological role of the gene in the proliferation of BEL-7402 cells.
RESULTS: A 2186 bp novel cDNA with an open reading frame encoding a 283
amino acid protein was cloned. Analysis of the deduced amino acid
sequence indicated that it is 38% (88/229) identical to human Golgi
4-transmembrane spanning transporter MTP. The gene and the encoded
protein was termed hepatocellular carcinoma overexpressed transmembrane
protein (hotp) and HOTP, respectively. Hotp mRNA was almost undetectable
in normal adult liver and fetal liver tissues. However, it was
significantly up-regulated in hepatocellular carcinoma and some matched
nontumor liver tissues, as well as BEL-7402 cells. The proliferation of
BEL-7402 cells was suppressed by an antisense oligodeoxynucleotide
against hotp mRNA at a concentration of 50 micrograms/ml. CONCLUSION:
HOTP may be an integral membrane transporter protein. The overexpression
of the gene in hepatocellular carcinoma may play an important role in
hepatocarcinogenesis and disease progression.
17
UI - 11775834
AU - Huang J; Shen W; Li B; Luo Y; Liao S; Zhang W; Cheng N
TI -
Molecular and immunohistochemical study of the inactivation of the p16
gene in primary hepatocellular carcinoma.
SO - Chin Med J (Engl) 2000 Oct;113(10):889-93
AD - Department of General Surgery, First Affiliated Hospital, Third Military
Medical University, Chongqing 400038, China.
OBJECTIVE: To determine whether p16 gene is involved in the genesis of
primary hepatocellular carcinoma (HCC). METHODS: Twenty-five HCC tumor
samples with corresponding non-tumor liver tissue specimens were
examined for p16 gene alterations. The identification of deletion of
exon 1 and exon 2 in p16 gene was performed using comparative multiplex
polymerase chain reaction (PCR) analysis. The point mutation of exon 2
in p16 gene was investigated by single strand conformational
polymorphism (SSCP) analysis, and the status of p16 gene methylation was
screened using a PCR based methylation analysis. 35 parafin-embedded
specimens of HCC with corresponding non-tumor liver tissues, including
the 25 cases described above for screening p16 gene alterations, were
investigated for p16 protein expression using immunohistochemical
analysis. RESULTS: Among 25 cases, 2 homozygous deletions and 1
hemizygous deletion were found in HCC samples. No point mutation was
identified in the remaining 22 tumor samples without p16 gene deletions.
Hypermethylation was detected in 24% (6/25) of tumor samples. However,
the corresponding non-tumor liver tissue specimens were always
unmethylated at the p16 locus. Loss of p16 protein expression occurred
in 16 of 35 (45.7%) tumor samples, and all the non-tumor liver tissue
specimens showed positive p16 staining. For the 25 cases examined for
p16 gene alterations, the loss of p16 protein expression was observed in
all tumors with p16 gene alterations and also in 3 tumors without p16
gene alterations. CONCLUSION: Inactivation of the p16 gene may play an
important role in the genesis of primary hepatocellular carcinoma.
18
UI - 11801910
AU - Park MS; Kim KW; Yu JS; Kim MJ; Yoon SW; Chung KW; Lee JT; Yoo HS
TI -
Radiologic findings of gastrointestinal tract involvement in
hepatocellular carcinoma.
SO - J Comput Assist Tomogr 2002 Jan-Feb;26(1):95-101
AD - Department of Diagnostic Radiology and Research Institute of
Radiological Science, Yonsei University College of Medicine, Seoul,
South Korea.
PURPOSE: The purpose of this work was to evaluate the radiologic
findings of gastrointestinal (GI) tract involvement in hepatocellular
carcinoma (HCC) and to discuss mechanisms of spread. METHOD: Eighteen
patients with histologically proven GI tract metastasis in HCC for 4.5
years underwent CT and five also underwent upper GI (UGI) series. The
cases were classified according to the mode of spread, based on the
radiologic findings. RESULTS: The involved portion of the GI tract was
the stomach (n = 11), duodenum (n = 4), and colon (n = 4). The mode of
spread was direct invasion from a contiguous primary tumor (n = 12),
hematogenous metastasis (n = 3), peritoneal seeding (n = 1), and
undetermined (n = 2). In cases of direct invasion from contiguous
primary tumors, CT revealed GI tract invasion directly from bulky
hepatic masses (n = 9) or daughter masses at the portion of the bowel
wall contiguous to the hepatic masses (n = 3). In cases of hematogenous
spread, CT revealed an intramural mass in the stomach and duodenum (n =
2) or a diffuse thickening of the wall of the stomach (n = 1). In the
case of peritoneal seeding, CT revealed multiple small nodules in the
right paracolic gutter, omentum, and mesentery with invasion to the
colon. CONCLUSION: GI tract involvement in HCC shows various radiologic
findings according to the mode of spread, but the most common finding is
direct invasion of the stomach, duodenum, or colon from contiguous
primary tumor.
19
UI - 11813174
AU - von Schweinitz D; Kraus JA; Albrecht S; Koch A; Fuchs J; Pietsch T
TI -
Prognostic impact of molecular genetic alterations in hepatoblastoma.
SO - Med Pediatr Oncol 2002 Feb;38(2):104-8
AD - Department of Pediatric Surgery, University of Basle Childrens'
Hospital, Basle, Switzerland. Dietrich.vonSchweinitz@unibas.ch
BACKGROUND: During recent years, we identified characteristic genetic
alterations in sporadic hepatoblastoma (HB). These include loss of
heterozygosity (LOH) at the chromosomal region 11p15.5, LOH on
chromosome arms 1p and 1q, activating mutations in exon 3 of the
beta-catenin gene, as well as overexpression of the c-met oncogene,
which encodes the hepatocyte growth factor receptor. We now wanted to
evaluate the prognostic relevance of these abnormalities concerning the
outcome in a large group of patients. PROCEDURE: All but 7 of 56
patients with HB were treated either with primary resection for small
tumors, or neo-adjuvant chemotherapy with ifosfamide, cisplatin and
doxorubicin (IPA) before delayed surgery in case of extended disease and
additional adjuvant IPA therapy in all cases. Seven tumors were
primarily resected and adjuvantly treated with different cytotoxic
drugs. LOH 11p15.5, LOH 1p, and LOH 1q were detected in tumor tissue in
comparison to normal liver and/or peripheral blood leukocytes by PCR
based microsatellite analysis. Beta-catenin mutations were analysed with
SSCP, deletion screening and direct sequencing. RT-PCR was used for
identification of c-met mRNA overexpression. The results were correlated
with the tumors' stage, histological type and epithelial
differentiation, as well as with the patients' outcome. RESULTS: Overall
disease-free survival after median follow-up of 5 years was 43/56
patients (77%). LOH 11p15.5 was found in 15/56, LOH1p in 11/53, LOH1q in
7/53 and beta-catenin mutations in 25/55 HB. 13/23 HB had a c-met
overexpression. LOH 11p15.5 and LOH 1p were significantly more often
found in embryonal HB, while there was no correlation of other genetic
alterations with histological type or differentiation. Furthermore,
statistical analysis revealed no correlation of any of these disorders
with initial tumor stage, nor with the patients' outcome. CONCLUSION:
None of the investigated molecular genetic alterations are suited to
serve as a prognostic indicator in HB. Further investigations,
especially genetic screening of tumor tissue may reveal prognostic
markers for this neoplasm. Copyright 2002 Wiley-Liss, Inc.
20
UI - 11595469
AU - Lotz G; Kiss A; Novak PK; Sobel G; Schaff Z
TI -
Hepatitis viruses and hepatocarcinogenesis.
SO - J Physiol Paris 2001 Jan-Dec;95(1-6):417-22
AD - Second Department of Pathology, Semmelweis University of Budapest, Ulloi
street 93, H-1091 Budapest, Hungary.
Hepatocellular carcinoma (HCC) is among the most frequent malignancies
worldwide. Hepatitis viruses, such as the hepatitis B virus (HBV) and
hepatitis C virus (HCV) are undoubtedly listed in the etiology of HCC.
Studies show that, in the near future, viral hepatitis will carry
increasing weight in the etiology of HCC. This review briefly discusses
the known carcinogenic effects of HBV and HCV in the light of
experimental and human studies. The data show that viral proteins may
directly interfere with gene products responsible for cell proliferation
and cell growth. Many other signal transduction cascades may be affected
as well. Direct integration of HBV viral sequences into the host genome
increases the genomic instability. The genomic imbalance allows the
development and survival of malignant clones bearing defected genomic
information. HBV and HCV infection induces indirect and direct
mechanisms through cellular damage, increased regeneration and cell
proliferation, therefore enhancing the development of HCC.
21
UI - 11780561
AU - Polakow J; Ladny JR; Janica J; Serwatka W; Walecki J; Puchalski Z
TI -
Three-dimensional sonography in the diagnosis of hepatic hemangiomas.
SO - Rocz Akad Med Bialymst 2001;46():182-8
AD - Department of Radiology, Medical Academy of Bialystok, Bialystok,
Poland.
The purpose of the study was to compare power 3-D with conventional 2-D
sonography with color and power Doppler in assessment of tumor
vascularity in small hepatic hemangiomas. The study group comprised 12
patients (7 males and 5 females) aged 28-60, (mean 44) with diagnosed
hemangiomas. In all the patients 2-D and 3-D sonography was performed
and their results were compared. Both color and power Doppler 2-D
sonography failed to detect blood flow in the tumors. Blood flow signals
were detected in 3-D power Doppler sonography. 3-D power Doppler is
superior to 2-D color and power Doppler imaging in the detection of
blood flow signal in hemangiomas.
22
UI - 11572758
AU - Takeda Y; Nakao K; Nakata K; Kawakami A; Ida H; Ichikawa T; Shigeno M;
TI -
Kajiya Y; Hamasaki K; Kato Y; Eguchi K
Geranylgeraniol, an intermediate product in mevalonate pathway, induces
apoptotic cell death in human hepatoma cells: death receptor-independent
activation of caspase-8 with down-regulation of Bcl-xL expression.
SO - Jpn J Cancer Res 2001 Sep;92(9):918-25
AD - The First Department of Internal Medicine, Nagasaki University School of
Medicine, Nagasaki University, Nagasaki 852-8501, Japan.
f1231@cc.nagasaki-u.ac.jp
Geranylgeraniol (GGOH), an intermediate of mevalonate metabolism, is
known to induce apoptosis in various lines of cancer cells. The present
study was undertaken to clarify the signaling pathways of apoptosis
induced by GGOH in human hepatoma cells. HuH-7 human hepatoma cells were
incubated in the absence or presence of GGOH. Activation of caspase-8
/-9 /-3 in HuH-7 cells was found after 8 h treatment with GGOH, at which
time DNA fragmentation and loss of mitochondrial transmembrane potential
(Deltaphim) occurred. HuH-7 cells do not express Bcl-2; however,
down-regulation of Bcl-xL expression preceded activation of the caspase
cascade in GGOH-treated HuH-7 cells, while Bax expression was not
changed by GGOH treatment. Addition of caspase inhibitors restored the
decreased cell viability of HuH-7 cells by GGOH, including Deltaphim, to
the baseline level, which indicated that caspase triggers
mitochondria-dependent apoptotic pathways in GGOH-treated HuH-7 cells.
Similarly, GGOH-mediated apoptosis of HuH-7 cells was clearly prevented
by coadministration of ursodeoxycholic acid (UDCA), which led to
restoration of the level of Bcl-xL expression. Activation of caspase-8
/-9 /-3, as well as Deltaphim, by GGOH treatment was suppressed by
addition of UDCA. Our results indicate that activation of the caspase
cascade initiating from caspase-8, which could be accelerated by
down-regulation of Bcl-xL expression, plays a key role in an apoptotic
process induced by GGOH in human hepatoma cells.
23
UI - 11705869
AU - Parasole R; Izzo F; Perrone F; Pignata S; Galati MG; Leonardi E;
TI -
Castiglione F; Orlando R; Castello G; Esposito G; Gallo C; Daniele B
Prognostic value of serum biological markers in patients with
hepatocellular carcinoma.
SO - Clin Cancer Res 2001 Nov;7(11):3504-9
AD - Division of Clinical Immunology, National Cancer Institute, Via M.
Semmola, 80131 Naples, Italy.
PURPOSE: Prognosis of patients with hepatocellular carcinoma (HCC) is
assessed by using indexes based on clinical and instrumental parameters.
The Cancer of the Liver Italian Program (CLIP) staging system combines
the Child-Pugh classification with tumor size, portal invasion, and
alpha-fetoprotein and predicts the outcome of HCC patients more
precisely than the Okuda staging system. Serum levels of a number of
biological variables have been found to be increased in patients with
HCC and are associated with different outcomes. Our aims in this study
were to test the prognostic role of the serum levels of soluble
intercellular adhesion molecule-1 (sICAM-1), soluble interleukin-2
receptor (sIL-2R), interleukin 6 (IL-6), and anti-p53 and to assess
whether the addition of any of the above serum markers could further
improve the predictive ability of the CLIP score. EXPERIMENTAL DESIGN:
Serum levels of sICAM-1, sIL-2R, IL-6, and anti-p53 were assayed in 80
patients with HCC and correlated with their outcomes. Nonparametric
procedures were applied to test correlations between serum sICAM-1,
sIL-2R, IL-6, anti-p53, and other prognostic factors. For survival
analyses, the product-limit method, log-rank test, and Cox proportional
hazards model were applied. RESULTS: Only serum levels of sIL-2R
correlated with survival, which was longer for patients with lower
values (< or =950 units/ml). However, with multivariate analysis sIL-2R
did not confirm its predictive role when tested with the CLIP score as a
covariate, with a hazard of death of 1.51 (95% confidence interval,
0.76-3.01). CONCLUSIONS: Serum levels of sICAM-1, sIL-2R, IL-6, and
anti-p53 are not useful as prognostic factors for HCC in clinical
practice. They do not improve the predictive ability of the CLIP score.
24
UI - 11780342
AU - Cheng J; Leng X; Cai S; Cao Z; Cao G; Peng J; Wang S; Du R
TI -
bcl 10 gene mutation in hepatocellular carcinoma.
SO - Chin Med J (Engl) 2001 Jul;114(7):747-51
AD - Department of Surgery, Peking University People's Hospital, Beijing
100044, China.
OBJECTIVE: To detect the mutation frequency of the bcl 10 gene in the
early and advanced stages of hepatocellular carcinoma (HCC). METHODS:
Genome DNA samples were extracted from 46 cases of fresh HCC tumor
tissues and their non-tumor adjacent tissues. Polymerase chain
reaction-single strand conformation polymorphism method was used to
detect point mutations of the three exons of the bcl 10 gene. For each
individual exon, six random samples from those showing abnormal DNA
bands were sequenced to verify those mutations. The relationship between
serum alpha-fetoprotein (AFP) level and bcl 10 mutation, between the
tumor size and bcl 10 mutation was also analyzed. RESULTS: Among the 46
samples, 26 cases (56.5%) were found to have mutations in exon 1, 5 out
of the 6 cases were shown to have 5744 C-->G mutation by sequencing; 25
cases (54.3%) were found to have mutations in exon 2, 4 out of the 6
cases were shown to have 11,311 T deletion mutation by sequencing.
Twenty-one cases (45.7%) were found to have mutations in exon 3, all of
the 6 cases selected for sequencing were shown to have 14,116 C-->T
mutation. Statistical analysis showed that neither serum
alpha-fetoprotein level nor the size of hepatocellular carcinoma has a
significant relationship with bcl 10 mutation. CONCLUSION: The bcl 10
gene has a high mutation frequency in liver cancer.
25
UI - 11756708
AU - Pauleit D; Textor J; Bachmann R; Conrad R; Flacke S; Layer G; Kreft B;
TI -
Schild H
Hepatocellular carcinoma: detection with gadolinium- and
ferumoxides-enhanced MR imaging of the liver.
SO - Radiology 2002 Jan;222(1):73-80
AD - Department of Radiology, University of Bonn, Germany. pauleit@web.de
PURPOSE: To test the hypothesis that the accuracy of gadolinium- and
ferumoxides-enhanced magnetic resonance (MR) imaging is different in
small (< or =1.5-cm) and large (>1.5-cm) hepatocellular carcinomas
(HCCs). MATERIALS AND METHODS: Forty-three consecutive patients with
chronic liver disease were enrolled in this study. The imaging protocol
included unenhanced breath-hold T1-weighted fast field-echo sequences,
unenhanced respiratory-triggered T2-weighted turbo spin-echo (SE)
sequences, dynamic gadolinium-enhanced T1-weighted three-dimensional
turbo field-echo sequences, and ferumoxides-enhanced T2-weighted turbo
SE sequences. Images of each sequence and two sets of sequences
(ferumoxides set and gadolinium set) were reviewed by four observers.
The ferumoxides set included unenhanced T1- and T2-weighted images and
ferumoxides-enhanced T2-weighted turbo SE MR images. The gadolinium set
included unenhanced T1- and T2-weighted images and dynamic
gadolinium-enhanced three-dimensional turbo field-echo MR images. In
receiver operating characteristic (ROC) curve analysis, the sensitivity
and accuracy of the sequences were compared in regard to the detection
of all, small, and large HCCs. RESULTS: Imaging performance was
different with gadolinium- and ferumoxides-enhanced images in the
detection of small and large HCCs. For detection of small HCCs, the
sensitivity and accuracy with unenhanced and gadolinium-enhanced imaging
(gadolinium set) were significantly (P =.017) superior to those with
unenhanced and ferumoxides-enhanced imaging (ferumoxides set). The area
under the composite ROC curves, or A(z), for the gadolinium set and the
ferumoxides set was 0.97 and 0.81, respectively. For large HCC, the
ferumoxides set was superior compared with the gadolinium set, but this
difference was not statistically significant. Analysis of all HCCs
demonstrated no significant differences for gadolinium- and
ferumoxides-enhanced imaging. CONCLUSION: For the detection of early
HCC, gadolinium-enhanced MR imaging is preferred to ferumoxides-enhanced
MR imaging because the former demonstrated significantly greater
accuracy in the detection of small HCCs.
26
UI - 11756710
AU - Brancatelli G; Federle MP; Grazioli L; Carr BI
TI -
Hepatocellular carcinoma in noncirrhotic liver: CT, clinical, and
pathologic findings in 39 U.S. residents.
SO - Radiology 2002 Jan;222(1):89-94
AD - Department of Radiology, University of Pittsburgh Medical Center, 200
Lothrop St, Pittsburgh, PA 15213, USA.
PURPOSE: To review clinical, pathologic, and computed tomographic (CT)
findings in patients with hepatocellular carcinoma (HCC) in noncirrhotic
liver. MATERIALS AND METHODS: Clinical, pathologic, and imaging findings
were retrospectively evaluated in 39 patients with HCC in noncirrhotic
liver. Helical multiphasic CT scans obtained with 125 mL of contrast
medium at a rate of 4 or 5 mL/sec were reviewed for morphologic features
such as tumor size, margins, and hemorrhage and degree of enhancement.
RESULTS: All patients (25 men, 14 women; mean age, 61 years) were U.S.
residents; none had an Asian surname. Twenty-four patients (62%) had no
identifiable risk factors; 34 (87%) were symptomatic. HCC was proved and
cirrhosis excluded with biopsy in all cases. HCC was moderately (n = 32)
or well (n = 6) differentiated in 97% of cases and poorly differentiated
in one. Serum alpha-fetoprotein level was elevated in 26 patients. Large
tumors (mean diameter, 12.4 cm) were depicted at C
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