Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cooked food contains a variety of mutagenic heterocyclic amines. All the mutagenic heterocyclic amines tested were carcinogenic in rodents when given in the diet at 0.01-0.08%. Most of them induced cancer in the liver and in other organs. It is noteworthy that the most abundant heterocyclic amine in cooked food, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, produced colon and mammary carcinomas in rats and lymphomas in mice but no hepatomas in either. 2-Amino-3-methylimidazo[4,5-f]quinoline induced liver cancer in monkeys. Formation of adducts with guanine by heterocyclic amines is presumably involved in their carcinogenesis. Quantification of heterocyclic amines in cooked foods and in human urine indicated that humans are continuously exposed to low levels of them in the diet. These low levels of heterocyclic amines are probably insufficient to produce human cancers by themselves. However, a linear relationship between DNA adduct levels and a wide range of doses of a heterocyclic amine was demonstrated in animals. It suggests that even very low doses of heterocyclic amines form DNA adducts and may be implicated in the development of human cancer under conditions in which many other mutagens-carcinogens, tumor promoters, and factors stimulating cancer progression exist.
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PMID:Food-derived mutagens and carcinogens. 154 46

A therapeutic dose of labelled 5-fluorouracil (5-FU) was infused via the hepatic artery during 30 min with or without ligation of the left portal venous branch in Wistar rats with a secondary liver cancer in the left lateral lobe. After another 60 min, the incorporation of 5-FU into the acid soluble fraction (ASF), ribonucleic acid (RNA) and deoxyribonucleic acid (DNA), was determined in tumor, ligated and unligated liver lobes, small intestine, kidney, and bone marrow. The liver nucleotide profile was examined with isotachophoresis. Portal venous branch ligation (PVBL) caused the following changes, compared with the unligated control group: in the tumor, the incorporation of 5-FU into RNA and DNA decreased and the ratio RNA/acid-soluble fraction labelling decreased. The incorporation increased in intestinal and bone marrow RNA. It was unchanged in liver and kidney. The ratio of tumor to peripheral normal-tissue (small intestine, bone marrow, and kidney) labelling of RNA and DNA decreased. Liver nucleotides (F)UTP, (F)UDP-glucuronic acid, (F)UDP-N-acetylhexosamine, and NAD were lower in the ligated than in the unligated liver lobe. ATP and energy charge did not decrease significantly. In conclusion, PVBL in conjunction with hepatic arterial administration of 5-FU increased systemic drug exposure and possibly decreased hepatic tumor anabolism. It has not been examined how this interferes with the therapeutic effect.
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PMID:Incorporation of 5-fluorouracil into rat liver tumor and normal tissues and the liver nucleotide profile after administration by the hepatic artery during portal venous branch ligation. 157 Apr 10

We investigated the relationship between the growth of HCC and nutrition, especially amino acids, and reconsidered the clinical application of amino acid imbalance. At first, rat chemical hepato-carcinogenesis was performed to investigate whether Aminoleban EN stimulates or restrains the occurrence of HCC. 2-Acetyl-amino-fluorene containing diet was administered intermittently according to Epstein's method. Rats were divided into two groups; group 1 was fed on Aminoleban EN containing diet and group 2 on a basal diet. There was no significant difference between the survival rate in the two groups. The average body weight of group 1 was significantly higher than that of group 2. The rats were sacrificed at the 25th week. All 11 rats of group 1 had no liver tumor, but 2 of 17 rats of group 2 had liver tumors, including a HCC and cholangiocellular carcinoma. The incidence of the liver tumor was significantly different between the two groups. Aminoleban EN could inhibit rat liver carcinogenesis, so it is considered to be a desirable nutritional product for LC patients from the stand point of cancer prevention. Secondly, the composition of amino acid was studied on HCC and surrounding tissue. There was no significant difference of Val, Leu, Leu, Phe, Tyr, Met and Fischer ratio between HCC and surrounding tissue.
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PMID:[Nutritional treatment of hepatocellular carcinoma]. 158 Jun 35

We reported a case of metastatic liver cancer from rectal carcinoma, which was successfully treated by systemic continuous 5-Fluorouracil and intermittent Mitomycin C chemotherapy. A 70-year-old male with rectosigmoid carcinoma was admitted to our hospital. Abdominal CT and echography revealed solid mass in the liver. He underwent low anterior resection and infuse-a-port was inserted because of arterial infusion chemotherapy for metastatic liver cancer. 5-FU (250 mg per day) was infused continuously and MMC at the dose of 8 mg for one time in a week was administered. Two months later, hepatic tumor disappeared and the serum CEA level also normalized. At this writing, the patient is alive and well and complete remission has been obtained for more than 10 months.
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PMID:[A case report of complete remission of liver metastasis from rectal carcinoma treated with intra-arterial infusion chemotherapy]. 158 Jun 47

After cis-diamminedichloroplatinum ethylcellulose microcapsules (CDDPmc) and unencapsulated CDDP were infused into the hepatic arteries of New Zealand rabbits, both CDDP concentrations in the circulating blood and in hepatic tissue were measured at different time intervals. In the rabbits infused with CDDPmc, the CDDP concentration was maintained at a high level for a significantly longer time in the hepatic tissue and the maximum CDDP level in the circulating blood was greatly reduced, as compared with those in the rabbits infused with unencapsulated CDDP. The tumoricidal effects of arterial infusion of CDDPmc were also evaluated in a model of liver tumor in rats. The therapeutic effects on rat liver tumor of CDDPmc were superior to those of unencapsulated CDDP and blank ethylcellulose microcapsules. The rats treated with CDDPmc showed a significantly lower tumor growth ratio, more extensive tumor necrosis and longer survival time. The results of this study indicate that CDDPmc is a more potential dosage from than conventional CDDP for hepatic arterial infusion in the treatment of liver cancer.
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PMID:Hepatic arterial chemoembolization with CDDP microcapsules. Experimental studies. 159 70

The caudate lobe is the only real and constant hepatic lobe of mammals and it requires a better delimitation in a modern conception of human liver segmentation. Owing to its dorsal, central and low anatomical situation, this lobe is connected to many segments of the liver and its inflow and outflow vessels are complex and variable. The authors, who studied 242 human livers, describe the typical pattern of these vessels and their anatomical and numerical variants. By its portal branches the lobe seems to depend upon the left lobe of the liver and its arterial and portal inflow as well as its hepatic vein system are better than these of other segments of the liver; moreover this segment can be compared to a quadrangular pyramid which presents an external part, superficial with easy surgical access, and an internal part, deeper and very difficult to resect. It is possible to remove segment I of the liver without any other hepatic resections but, usually, a partial resection of the lobe is performed or a left lateral segmentectomy is required. In liver cancer, the invasion of the lobe generally means widespread tumor dissemination and its resection is not justified; on the contrary, the caudate lobe should be resected for radical operation in hilar cholangiocarcinoma. The tendency of the caudate lobe to overlap with the other 2 liver lobes and its very good inflow and outflow systems explain its ability to avoid postoperative hepatic failure because it can support the hepatic vein drainage and it has a considerable disposition to regenerate.
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PMID:[Anatomy of the caudate lobe of the liver. New aspects and surgical applications]. 161 84

Cell proliferation has long been recognized as having an important role in chemically induced carcinogenesis. Based on findings that certain nongenotoxic chemical carcinogens induced cell proliferation in the same organ that had an increased incidence of tumors, it has been hypothesized that a chemically induced response of enhanced DNA synthesis and cellular division causes cancer by increasing the rate of spontaneous mutations. It was further suggested that there would be no increased human risk of cancer by non-DNA-reactive compounds at doses that do not cause a proliferative response. An evaluation of the literature on the relationship between chemically induced cell proliferation and liver carcinogenesis reveals that very few systematic cell proliferation studies have been conducted over periods of extended exposure, and in many cases the exposure concentrations were not similar to those used in the cancer studies. The proliferative response resulting from exposure to many nongenotoxic carcinogens is not well sustained, whereas the carcinogenic response by these chemicals often requires prolonged exposure. The available literature leads to the conclusion that quantitative correspondences between cellular proliferation and carcinogenic responses have not been demonstrated and do not support the hypothesis that chemically induced cell proliferation is the primary mechanism by which nongenotoxic chemicals cause liver cancer. Studies of liver carcinogenesis in two-stage models point out the need to better understand chemical effects on cell loss as well as on cell replication, and demonstrate that measurements of cell proliferation alone are not sufficient to elucidate mechanisms of tumor development.
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PMID:Does chemically induced hepatocyte proliferation predict liver carcinogenesis? 161 94

We examined 40 cases of primary liver cancer with color doppler flow imaging and duplex doppler. In 20 cases, there was arterial flow in the tumor. In 17 cases, there was arterial and portal venous flow in the tumor. In 22 cases, there was arterial flow entering the tumor from its surroundings. In 28 cases, the right or left hepatic artery was dilated. We compared the results of digital subtraction angiography with the doppler ultrasound in 28 cases and found the difference was not significant (chi 2 = 1.05, P greater than 0.05). Therefore, we believe that the doppler ultrasonography is the method of choice in the diagnosis of primary liver cancer.
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PMID:[Color Doppler flow imaging and duplex Doppler in the examination of primary liver cancer]. 161 84

It has been reported that hepatoma (HCC) cells produce abnormal proteins such as erytropietin, fibrinogen, prothrombin, and, recently, antithrombin III (AT III). In a preliminary report, we reported increased AT III levels in patients bearing HCC independent of their clinical liver status. The present study was performed to assess antithrombin III levels and other serological data present in patients with cirrhosis and in patients with cirrhosis and clinical findings of neoplastic disease. In 70 well-matched patients (47 with cirrhosis and 23 with cirrhosis and proven HCC) serum total cholesterol, albumin, prothrombin, alkaline phosphatase, AFP, aminotransferases, and AT III were determined. Together with AFP and alkaline phosphatase, patients with HCC had higher values of AT III (88 +/- 7%) and total cholesterol (184 +/- 17 mg/100 ml), as compared with cirrhotic patients (AT III 56 +/- 3.6%; total cholesterol 113 +/- 5 mg/100 ml) (P less than 0.001). No difference was observed between these two groups for albumin, prothrombin, and aminotransferases. In HCC patients, AT III levels were related to the total cholesterol level (R2 = 0.317), whereas in the cirrhotic patients it correlated with the prothrombin level (R2 = 0.274). These data suggest that in HCC patients a greater rate of synthesis of AT III occurs, whereas in cirrhotic patients lower levels of AT III occur due to impaired synthesis or increased catabolism of the protein. The serial determination of AT III in cirrhotic patients as a means of detecting neoplastic transformation is suggested.
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PMID:Hepatocarcinoma in cirrhosis. Is antithrombin III a neoplastic marker? 164 42

Eighty-three patients with primary liver cancer (PLC) having survived over 5 years were investigated. 50.6% (42/83) of them were in Stage I and 49.4% (41/83) were in Stage II. Resection was performed in 94.0% (78/83), and hepatic artery ligation and/or cannulation was done in 6.0% (5/83). By the end of March 1990, 66.3% (55/83), were cancer-free, 4.8% (4/83) were living with the cancer, 20.5% (17/83) died from recurrence or metastasis of cancer, 7.2% (6/83) died from liver failure, and 1.2% (1/83) lost followup. 29 cases survived over 10 years after resection of PLC. A comparison with 811 patients having less than 5 years during the same period demonstrates that early discovery, lower gamma glutamyl transpeptidase (gamma-GT) and alanine aminotransferase (ALT), tumor less than or equal to 5 cm, single nodule, well-encapsulated tumor, radical resection, and alpha fetoprotein (AFP) normalization after resection may contribute to prolonged survival. It is concluded that early detection and early radical resection are essential to improve the therapeutic effects.
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PMID:[Analysis of follow-up data in 83 cases of primary liver cancer]. 165 Jun 34


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