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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nested case-control study of HCC based on a cohort of 18,244 middle-aged men in Shanghai, China, who had been followed for an average of 5.3 years, was conducted. Our hypothesis dealt with the possible role of testosterone in the etiology of HCC, which shows a minimum of a 2- to 3-fold male excess in all populations world-wide. Seventy-six incident cases of HCC and 410 control subjects drawn from the cohort and individually matched to the cases by age (within 1 year), time of blood sample collection (within 1 month) and neighborhood of residence were assessed for serum HBsAg, anti-HBc, anti-HBs, anti-HCV and testosterone. Among controls, serum testosterone levels were similar between those who had no markers of HBV infection, those who were positive for anti-HBs only and those who were positive for anti-HBc but negative for HBsAg. However, the geometric mean level of testosterone in HBsAg-positive controls was 21% higher relative to HBsAg-negative controls and the difference was statistically significant (2-sided p = 0.0006). Relative to controls, HCC cases had a significantly higher mean level of testosterone at the time of recruitment (570 vs. 485 ng/dl, 2-sided p = 0.0005), but the difference was explicable on the basis of a higher proportion of HBsAg-positive individuals among cases than controls (p = 0.42 after adjustment for HBsAg status).
Int J Cancer 1995 Nov 15
PMID:A cohort study of serum testosterone and hepatocellular carcinoma in Shanghai, China. 759 Dec 55

Colorectal cancer is the second leading cause of death from malignancies in Western Countries. In spite of advances in treatment, little change in survival has been accomplished in last decades and this mandates greater importance to prevention and early detection. Although dietary factors have received primary attention familial clustering suggests that susceptibility to KCR is inherited. Hereditary colorectal cancer can arise on Familial Adenomatous Polyposis (HCC) or not on polyposis (HNPCC) and members of these families are at high risk of such neoplasias. Anyway, even in "sporadic" forms of KCR first-degree relatives have a 2 to 3-fold increased risk of the same cancer. The most desirable screening protocol would be a simple procedure involving only a blood test to identify gene defect by molecular biology techniques. Unfortunately, this is not practically possible, for lack of specific genetic alterations, out of FAP, and only the study of family history can enable targeted surveillance and cost-effective management strategies.
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PMID:[Heredity and colorectal cancer]. 765 49

In order to clarify the factors contributing to the signal intensities (SIs) of HCC on T1-weighted images, the amount of water, lipid, copper (Cu), iron (Fe), and manganese (Mn) was determined in HCC and surrounding hepatic parenchyma of 13 patients. The relationships among these findings, the histopathologic findings, and the SIs of T1-weighted images were evaluated. Among the 13 HCC, 3 had a high SI, 5 were isointense, and 5 had a low SI on T1-weighted images compared to the surrounding hepatic parenchyma. The paramagnetic ions which contributed to the SI patterns were assumed to be Cu in HCC (38.0 +/- 62.4 micrograms/g ww), and Fe in the liver (61.1 +/- 42.4 micrograms/g ww) and HCC (40.0 +/- 34.3 micrograms/g ww). In 8 HCC with high- or isointensity, 2 were grades I, 5 were grade II, and one was grade III according to the Edmondson-Steiner's histopathologic classification. It is concluded that the SI patterns alone can not be a sign of low grade malignancy because of the existence of Fe in livers and HCC.
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PMID:MR imaging of hepatocellular carcinoma. Correlation of metal content and signal intensity. 771 Jul 97

Chronic liver diseases, in particular chronic HBV and HCV infections, frequently progress to liver cirrhosis and HCC. The molecular events underlying hepatocarcinogenesis are not yet well defined. It appears likely, however, that HCCs result from a stepwise carcinogenesis: due to chronic liver disease there is liver cell necrosis, inflammation and regeneration with a high mitotic rate of liver cells. In this setting, chromosomal DNA rearrangements occur which may result in the activation of cellular oncogenes or inactivation of tumor suppressor genes. Viral genes or gene products as well as cofactors, such as alcohol or aflatoxins, may make a specific contribution to these molecular events. Apart from the molecular aspects of hepatocarcinogenesis, for clinical practice the implementation of measures to prevent or treat chronic liver diseases should reduce the incidence of HCCs, one the most frequent malignancies in some areas of the world.
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PMID:[Hepatocellular carcinoma: molecular biology aspects]. 784 55

Preneoplastic and neoplastic liver cell lesions, induced by EHEN (N-ethyl-N-hydroxyethylnitrosamine) in rats, were investigated to establish the numbers of simultaneously expressed altered enzyme phenotypes within the lesion cells. The lesions were divided into 5 classes on the basis of altered expression in one or more of the following 5 enzymes: glutathione S-transferase placental form, glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, adenosine triphosphatase, and gamma-glutamyl transpeptidase. Class 1 lesions contained cells expressing one altered enzyme. Similarly, class 2, 3, 4 and 5 lesions had cells simultaneously expressing 2, 3, 4, and 5 enzyme alterations, respectively. Four histopathological categories of lesions, ACF (altered cell foci) (274 lesions), HN (hyperplastic nodules) (47 lesions), HCC (hepatocellular carcinomas) (99 lesions) and THC (transplanted hepatocellular carcinomas) (5 lesions) were studied. Proliferation potential was assessed in terms of 5-bromo-2'-deoxyuridine (BrdU) incorporation. The distribution profiles of classes 1 to 5 showed a clear reciprocal change from low class (1 to 2 enzymes) predominance in ACF to high class (4 to 5 enzymes) predominance in HN. Increase of BrdU labeling indices was clearly correlated with progression from HN to HCC. Only a small population of class 5 ACF showed a high BrdU labeling index, indicating particular potential for further development. Thus, the stages of EHEN-induced neoplasia were found to be characterized by gradual increase in the number of altered enzyme phenotypes, with acquisition of proliferative potential being associated with further progression towards malignant conversion.
Jpn J Cancer Res 1993 Dec
PMID:Number of simultaneously expressed enzyme alterations correlates with progression of N-ethyl-N-hydroxyethylnitrosamine-induced hepatocarcinogenesis in rats. 790 86

At the National Cancer Institute of Milan, 118 patients underwent surgical resection and 35 had liver transplants for HCC (hepatocarcinoma). Postoperative mortality was 14% and 17% after resection and transplantation respectively. The five-year survival was 35% for resected patients and 83% at 30 months for transplanted patients. Analysis of the literature shows that patients receiving a liver transplant for HCC stage I-II survive longer than those resected at the same stage.
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PMID:[The surgical treatment of hepatocarcinoma]. 802 74

The western HCC registry comprised data from 322 patients who underwent hepatic resection for HCC over a 50-year period. The majority of patients had lesions > 4 cm and were symptomatic at presentation. Lesions were mostly unicentric. Cirrhosis was not a prevalent problem, unlike the East. In the most recent decade, 1980-1989, we noted a significant decrease in operative mortality from 19% to 10% overall, and 15% to 4% in the noncirrhotic group. We identified four variables that resulted in poorer postresectional outcome: cirrhosis, regional nodal disease, multicentric disease, and tumor-free resectional margin < 1 cm. Although these factors are associated with a poorer outcome after resection, whether they should serve as contraindications to surgery should be determined by individual surgeons, taking into account the patient's overall status, concomitant risk factors, and treatment objectives.
Cancer Treat Res 1994
PMID:Hepatoma registry of the Western world. Repeat Hepatic Resection Registry. 803 52

For the majority patients with HCC, the prognosis is poor. Only a fraction of patients will be resectable at the time of their diagnosis. For the oncologic surgeon caring for such patients, the challenges are multifaceted. First, he or she must have a familiarity with current imaging techniques and reliable support from a radiologist to determine whether a given patient can be technically resectable. We rely most heavily upon the initial diagnostic CT scan followed by the staging CTAP in order to define the resectable patient as clearly as possible. Additionally, the risk of postoperative hepatic failure must be assessed. Careful physical exam, blood chemistries, and volumetric analysis of CT scans demand much judgment on the part of the surgeon. While some patients are clearly capable of undergoing a resection, and others are clearly inoperable due to poor hepatic function, a large group of patients exist in a "gray area" where resection can be entertained but the risk of hepatic failure looms large. In this group the use of the ICG retention test or the 14C-aminopyrine breath test are occasionally useful. Further research into better assessment of hepatic reserve is clearly needed. Once a laparotomy is undertaken, IOUS is a key component of intraoperative staging and the final determinant of resectability. Resection itself must be performed with three goals: Resection of all disease with negative surgical margins, retention of as much hepatic parenchyma as possible in keeping with oncologic principles, and maintenance of hemodynamic stability with minimal transfusion requirements in an effort to minimize the stress of surgery. The combination of vascular control and the porta hepatis (and IVC where necessary), segmental hepatic resection where appropriate, and ultrasonic dissection can accomplish these goals. Intrahepatic recurrence, despite adequate resection, can be expected in many patients, and few will be candidates for a second resection. For this reason, and because most patients are unresectable at presentation, the oncologic surgeon must be familiar with palliative options available for his patients, as well as the surgical management of operable tumors. Close collaboration with one's colleagues in medical oncology, invasive radiology, and gastroenterology are critical to the optimal care of this difficult patient population.
Cancer Treat Res 1994
PMID:Surgical management of hepatoma. 803 57

The expression of intercellular adhesion molecule-1 (ICAM-1) was investigated in frozen sections obtained from 40 resected liver specimens of patients with hepatocellular carcinoma using immunoperoxidase techniques and immunoelectron microscopy. ICAM-1 was expressed in 80% of the HCC specimens on the membrane of cancer cells. In noncancerous regions characterized by cirrhosis in 28 cases and chronic hepatitis in 12 cases, ICAM-1 was rarely expressed on hepatocytes but was expressed mainly on the endothelium of portal vessels and sinusoidal lining cells. These results suggest that expression of ICAM-1 in hepatocellular carcinoma may be induced by malignant transformation of hepatocytes.
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PMID:Expression of intercellular adhesion molecule-1 in hepatocellular carcinoma. 810 90

Color Doppler sonographic images of five patients with a total of six lesions of FNH were reviewed. All cases were confirmed pathologically. All six lesions showed increased intralesional flow in comparison to surrounding liver parenchyma on color Doppler sonography. Four of the six lesions showed significant peripheral flow; two of the six lesions showed central flow radiating peripherally from a central vessel. We conclude that increased color Doppler flow may be a characteristic feature of FNH. Increased internal flow has also been reported in HCC and hepatic metastatic disease. Considerable overlap is seen in color Doppler flow patterns. However, in patients clinically at low risk for malignancy, detection of a liver mass with increased color Doppler flow should suggest the diagnosis of FNH.
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PMID:Hepatic focal nodular hyperplasia: findings with color Doppler sonography. 810 87


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