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Query: UMLS:C0345904 (liver cancer)
15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data on 74 pathologically confirmed cases of liver cancer among blacks and whites living in Los Angeles County, California were compared with 162 matched controls. The study was limited to only people with no hepatitis infection and to non-Asians. The risk of liver cancer for women who have used OCs for 5 years was 5.5 times higher than that for women who had never used OCs. This risk was 3 times higher for women who had ever used OCs. The data for women who were in their reproductive years when OCs 1st entered the market in the 1960s showed that the risk for 5 years of OC use increased to almost 30 times that of women who had never used OCs. Even though estrogens were presumed to be the risk factor since they induce liver cancer in animals, no significant association was found between estrogens used in estrogen replacement therapy and liver cancer. Overall, diabetics were at 3.3 times the risk for liver cancer compared with nondiabetics. People who had diabetes for at least 10 years had 4.3 times the risk and those dependent on insulin injections had 18.5 times the risk. Cigarette smokers had a 2.1 times greater risk of liver cancer than nonsmokers. Most of the women did not drink heavily which showed the independent effect of cigarette smoking. As of December 1991, these data represented the best data on OCs and cigarette smoking to date. The risk for heavy drinkers of alcohol (80g of alcohol/day=9 cans of beer, 9 glasses of wine, or 9 shots of spirits) was 4.7 times the risk of nondrinkers or light drinkers. It is concluded that alcohol and/or cigarettes caused 56% of liver cancer cases in men and that cigarettes and/or OCs caused 54% of liver cancer cases in women.
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PMID:Birth control pills, cigarettes, alcohol linked to liver cancer. 153 35

Insulin-like growth factor II is a fetal growth factor structurally and functionally related to insulin and insulin-like growth factor I. Its mRNA expression is developmentally regulated in human liver, the reexpression of insulin-like growth factor II fetal transcripts being often observed in primary liver cancer. Insulin-like growth factor II and alpha-fetoprotein mRNAs were studied in 16 human primary liver cancers, most of which were highly differentiated. Hepatitis B virus transcripts were also analyzed in the tumors from hepatitis B virus chronic carriers. alpha-Fetoprotein mRNA was detected in only four tumors and in one nontumorous cirrhotic tissue; all these samples also displayed insulin-like growth factor II fetal transcripts. Furthermore, fetal insulin-like growth factor II mRNAs were observed in five tumors and six nontumorous cirrhotic areas not expressing alpha-fetoprotein mRNA. The presence of hepatitis B virus RNA was only observed in tissues not expressing alpha-fetoprotein or fetal insulin-like growth factor II mRNA. In conclusion, fetal insulin-like growth factor II transcripts are more frequently observed than alpha-fetoprotein mRNA in highly differentiated liver cancers and in surrounding cirrhotic areas. The reexpression of fetal insulin-like growth factor II transcripts might then be a marker of early steps of liver cell transformation.
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PMID:Expression of insulin-like growth factor II, alpha-fetoprotein and hepatitis B virus transcripts in human primary liver cancer. 170 28

After hepatectomy patients with cirrhosis and liver cancer may develop progressive hepatic dysfunction and eventually hepatic failure. Insulin and glucagon are often used to treat certain kinds of hepatic dysfunction and hepatic insufficiency. We investigated the effect of glucagon on bile acid metabolism and pancreatic endocrine function. In 7 patients with severe cirrhosis and cancer of the liver, 1 mg of glucagon was injected intravenously pre- and post-operatively, and total bile acids, C-AMP, and bile acid fractions were determined. In the pre-operative glucagon tolerance test, the C-AMP level rose from a baseline of 14 +/- 0.8 PMol/ml to 362 +/- 94 PMol/ml 30 min after the injection of glucagon (p less than 0.01); and the level of total bile acids decreased from a baseline of 28 +/- 9 microMol/ml to 11 +/- 3 microMol/ml 60 min after the injection of glucagon. The post-operative C-AMP level increased from a baseline of 13 +/- 1 PMol/ml to 192 +/- 58 PMol/ml level of 30 min after the injection of glucagon (p less than 0.01), and the post-operative level of total bile acids decreased from a baseline of 64 +/- 20 microMol/ml to 26 +/- 7 microMol/ml 60 min after the injection of glucagon. There was a significant correlation between the 5-min increment ratio of C-AMP and the decrement ratio of total bile acids (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of glucagon on bile acid metabolism after resection of liver cancer in patients with cirrhosis. 196 64

Six cases of primary hepatic carcinoid tumors were studied with combined immunocytochemical and electron microscopic techniques. Positive tumor immunostaining with PHE5, LK2H10, neuron-specific enolase (NSE), serotonin, gastrin, and insulin antibodies was observed. At the ultrastructural level, cytoplasmic dense granules were seen in all the cases tested. This finding supports a putative origin of these carcinoids found in the liver from a pluripotential stem cell. The clinical course and follow-up of these cases suggests that this unusual hepatic neoplasm has a more favorable prognosis than other forms of hepatic cancer.
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PMID:A clinicopathologic study of primary hepatic carcinoid tumors. 230 69

Insulin-like growth factor (IGF) I and IGF-II were measured by radioimmunoassay in the sera of seven patients with acromegaly, 36 normal control subjects, 15 patients with chronic hepatitis, 15 patients with cirrhosis, 25 patients with hepatocellular carcinomas (HCCs) who did not have hypoglycemia, 20 patients with HCCs who did have hypoglycemia, and 10 patients with metastatic liver tumors. Both IGF-I and IGF-II levels decreased as liver disease progressed from the normal control stage to chronic hepatitis and cirrhosis, and both levels reflected the severity of liver disease. Patients with HCCs who had hypoglycemia had relatively higher IGF-II levels in their sera in comparison with those who did not have hypoglycemia (272 +/- 167.5 ng/ml vs 110.4 +/- 85.9 ng/ml [mean +/- SD], p less than 0.0005), despite the fact that those with hypoglycemia had more advanced liver cancer and had lower IGF-I levels in sera (16.7 +/- 14.1 ng/ml vs 46.8 +/- 47.9 ng/ml, p less than 0.002). It is possible that a labile IGF-II material is produced by the cancer cells of patients with hypoglycemia. This factor is reactive to the IGF-II receptor and partially cross-reacts with an antibody to IGF-II; it accounted for the mildly elevated levels of serum IGF-II. Hypoglycemia may be an integral effect of relatively elevated IGF-II like material and an advanced liver cancer. Also, higher serum alpha-fetoprotein (AFP) levels were more frequently found in patients with hypoglycemia who had relatively elevated IGF-II levels and short survivals.
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PMID:Radioimmunoassay of serum IGF-I and IGF-II in patients with chronic liver diseases and hepatocellular carcinoma with or without hypoglycemia. 246 May 70

To investigate the predictive value of oral glucose tolerance test (O-GTT) and insulin secretion test (IST) on the risk of hepatectomy in liver cancer patients, we through double-blind method, compared the results of these two tests, clinical course of the patients, and the pathological findings. It was found that: 1) The positive prediction value, negative prediction value, and accuracy of O-GTT were 79.2%, 94.4%, and 85.7%, the corresponding figures of IST were 55.6%, 100%, and 61.9%, respectively. 2) Pattern of the curve of O-GTT believed to depend on roughly normal hepatic energy metabolism and islet secretion capacity suggested better tolerance for hepatectomy. 3) A part of the patients with advanced HCC had a depressed islet secretion capacity. 4) The delta IST/delta O-GTT showed an accurate negative prediction for hepatectomy when the ratio was less than 50 x 10(-9). 5) Apart from O-GTT and delta IST/delta O-GTT, the severity of the hepatitis and cirrhosis should be taken into account in the decision of carrying out hepatectomy.
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PMID:[The glucose tolerance test and insulin secretion test as risk factors in liver cancer surgery]. 256 Oct 96

In order to elucidate the response of plasma glucagon in liver cell carcinoma, a clinical study was performed in 12 patients with liver cell carcinoma in addition to 8 patients with liver cirrhosis and 8 normal subjects. Arginine infusion elicited increases in plasma insulin and glucagon in 6 patients with liver cell carcinoma as well as 8 patients with liver cirrhosis compared with the controls. However, the responses of plasma insulin and glucagon in liver cell carcinoma did not exceed those in liver cirrhosis. No glucagon secreting cell was proved in the hepatic cancer tissues from two other patients. Furthermore, no measurable glucagon was demonstrated in the tumor tissues extracted from four other patients with liver cell carcinoma. The extract of the tumors, infused into the pancreatic artery of anesthetized dogs, did not elicit any discernible changes in glucagon and insulin in the pancreatic vein. The present study demonstrates an elevated response of plasma glucagon in liver cell carcinoma. Since the morphological and biochemical studies failed to demonstrate the glucagon secreting cell or glucagon-stimulating material in the tumor tissues, the elevated plasma glucagon response might be interpreted by the increased A-cell function of the pancreas and the decreased degradation of the hormones in the liver.
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PMID:Secretion of glucagon in liver cell carcinoma. 299 19

The lipotropes (choline, methionine, folate, and vitamin B12) have a rich history, with many fluctuations in scientific effort and popularity, covering the past 6 decades. A thin thread of common interest in 1-carbon metabolism and a small band of dedicated individuals have kept this area of biology alive. Today, the lipotropes are enjoying a resurgence of interest and effort with promise for significant contributions to some of our most serious chronic diseases. Between 1920, when Banting and Best initiated a work that led to the discovery of insulin, and 1982-83, when investigators working in 3 laboratories announced that lipotrope deficiency alone could result in liver cancer in rodents, many have used this model to study nutritional problems and, more recently, carcinogenesis. Lipotropes are important to lipid metabolism and to synthesis and maintenance of cellular membranes. When weanling rats were fed a diet low in lipotropes, within a few days the liver accumulated lipid, first in the centrilobular zone and later throughout the entire lobule and lobe. If the diet was continued for a longer period, the liver underwent fibrosis and cirrhosis with some rats ultimately developing hepatocellular carcinoma. Although lipotrope deficiency can result in liver cancer, all hepatocarcinogens tested thus far were enhanced in their activity by diets low in lipotropes. Important changes associated with lipotrope deficiency included membrane damage, decreased serum very low density lipoprotein and drug metabolizing enzymes, decreases in S-adenosylmethionine and in methylation of cytosine, increases in cellular peroxidation products and free radicals, decreased immunocompetence, and a markedly shortened lag time for chemical induction of liver cancer in animals. The overall effect of lipotrope deficiency is an increase in the susceptibility to cancer in animals; the exact mechanisms are unclear.
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PMID:Lipotropic factors and oncogenesis. 303 98

The study was prompted by the apparent detection of insulin antibodies in a black patient with HCC and recurrent hypoglycemia who had never received insulin. It consisted of two parts. Initially the sera of 30 individuals (six normoglycemic HCC patients, three with HCC and recurrent hypoglycemia, 11 patients with noncancerous liver diseases, and 10 healthy black controls) were analyzed for the presence of insulin (and glucagon) antibodies by precipitating the bound, labeled hormone with ethanol and also by the technique of radioimmunoelectrophoresis. In the nine HCC patients, binding of 125I-insulin averaged 13% by ethanol separation and 0.018 mU/ml with radioimmunoelectrophoresis, levels that were similar to those of patients with noncancerous liver disease and significantly higher than those of the healthy controls. Mean binding of 125I-glucagon was 11% in HCC sera. Serum binding of labeled hormones correlated significantly with IgG concentrations in the patients. The second part of the study attempted to define the nature of insulin binding in HCC and other forms of liver disease. After confirmation of the increased serum binding of labeled insulin by another method of precipitation, PEG, an attempt was made to compete with the labeled insulin for its serum binding sites by adding a large amount of unlabeled insulin. This binding was not displaceable, however, and was therefore considered nonspecific. When the same procedures were repeated using normal serum to which increasing amounts of gamma globulin were added, the nonspecific binding of insulin increased in a linear fashion. Furthermore, a similar degree of high nonspecific insulin binding occurred in six patients with multiple myeloma and raised serum IgG concentrations. We therefore conclude that in the many clinical situations where hypergammaglobulinemia exists, false positive tests for the detection of antibodies against insulin (and probably other peptide hormones) will emerge unless appropriate methods are used to check for nonspecific peptide binding.
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PMID:Nonspecific blinding of insulin to gamma globulin in the serum of black patients with hepatocellular carcinoma and other forms of liver disease. 618 Jan 12

A transient hypoglycemia was found 4 hrs after injection of 25-hydroxycholecalciferol (25-HCC) in mice. This was not associated with any significant alteration in the serum insulin concentration, suggesting that the hypoglycemic response is due to extrapancreatic factors. Pretreatment with 25-HCC did not affect the development of alloxan diabetes.
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PMID:Transient hypoglycemia following 25-hydroxycholecalciferol administraton to mice. 700 May 8


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