Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antitumor effect of a synthetic lipid A analogue, DT-5461, was investigated using syngeneic tumor models in mice. Intravenous injection of DT-5461 into mice transplanted with solid tumors of MethA fibrosarcoma, MH134 hepatoma, MM46 mammary carcinoma, Lewis lung carcinoma (3LL), and colon adenocarcinomas 26 and 38 resulted in significant reductions in the weight of all tumors except Colon 26, with marked hemorrhagic necrosis of tumor tissues. Efficacy was almost equal to that of an Escherichia coli-type synthetic lipid A (compound 506), and also to those of some chemotherapeutics including Adriamycin, mitomycin C, fluorouracil and cisplatin. Furthermore, DT-5461 was more effective than other immunotherapeutics, including picibanil (OK-432) and lentinan. However, its antitumor effects were inferior to those of Adriamycin or OK-432 against the malignant ascites caused by intraperitoneal inoculation with MethA or with MH134 cells; life span was not prolonged by either intraperitoneal or intravenous administration. In addition, although DT-5461 showed direct inhibitory effects on the in vitro growth of MethA or MH134, these were much weaker than those of Adriamycin. These findings clearly indicated that DT-5461 with systemic administration is a highly effective antitumor agent on solid tumors, and suggest that the antitumor effect of DT-5461 with potent necrotizing activity might derive from indirect mechanisms related to the activation of host immune systems and not to the weak direct cytotoxicity.
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PMID:Significant antitumor effect of a synthetic lipid A analogue, DT-5461, on murine syngeneic tumor models. 139 35

The clinical usefulness of a I-131 anti CEA F(ab')2 MoAB and CA 19-9 F(ab')2 MoAB cocktail(IMACIS-1) for the localization of a cancer has been studied in 35 patients (Lung Ca. 10, Pancreas Ca. 7, Gastric Ca. 6, Colon Ca. 5, Hepatoma 2, Cholangio Ca. 2, Esophageal Ca. 1, Uterus Ca. 1, and, Retroperitoneal tumor 1). Of these 28 patients (80%) had an abnormal accumulation of radioactivity in the tumor sites (Lung Ca. 5, Pancreas Ca. 7, Gastric Ca. 6, Colon Ca. 5, Hepatoma 2, Esophageal Ca. 1, Uterus Ca. 1, and, Retroperitoneal tumor 1). Eighteen cases (56.3%) in 32 cases in which the primary site was known showed an abnormal radioactive accumulation and, similarly, 20 metastatic sites (71.4%) in 16 cases with 28 metastatic sites also showed an abnormal accumulation of radioimmunoscintigraphy showed no correlation with the serum CEA or CA 19-9 concentration. Further, no side effect was observed.
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PMID:[Clinical evaluation of radioimmunoscintigraphy using a I-131 anti CEA and CA 19-9 monoclonal antibodies cocktail (IMACIS-1)]. 273 74

The cancers consistently associated with ingestion of alcohol, the head and neck cancers, are also associated with tobacco use and arise from epithelia that are in direct contact with both agents. Tobacco smoking-related cancers at sites not directly in contact with alcoholic beverages, that is, lung, bladder, and perhaps pancreas, do not consistently show a relationship to alcohol consumption, although lung and pancreatic tumors are associated in some studies. Liver cancer was thought to be strongly related to alcohol consumption on epidemiological grounds and because of its relationship to cirrhosis. As knowledge of the viral etiology of some cirrhoses has evolved and as methods to detect viruses have developed, the significant association between hepatitis B virus and hepatocellular carcinoma has become clear. Alcohol and hepatitis B virus may interact in the etiology of the disease and have important separate roles as well. There are epidemiologic and experimental data showing that malnutrition (resulting from poor food choice), economic deprivation, or alcoholism contributes to the risk for head, neck, and liver cancers. Colon cancers occur about equally in men and women, are found in well-nourished populations, and are not associated with tobacco smoking. Rectal cancers show a preponderance of cases in men but are frequently found in women as well and are not thought to be associated with smoking or malnutrition. The association between colorectal cancers and alcohol consumption, when it is found, apparently occurs at even relatively low alcohol intakes and is often stronger for consumption of beer than of other beverages. Nutritional and metabolic mechanisms proposed for the influence of alcohol on carcinogenesis are supported by studies in human subjects and laboratory animals. Animal models are needed in which effects of ethanol on carcinogenesis can be consistently demonstrated and which can then be used to examine mechanisms.
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PMID:Alcohol and cancer. 303 1

FK973, a new, substituted dihydrobenzoxazine (11-acetyl-8-carbamoyloxymethyl-4-formyl-14-oxa-1,11- diazatetracyclo[7.4.1.0.0]tetra-deca-2,4,6-trien-6,9-diyl diacetate), was obtained by chemical modification of a novel antibiotic which was isolated from the fermentation products of Streptomyces sandaensis No. 6897. FK973 had cytotoxic effects against in vitro cultured human and murine tumor cells. FK973 in doses of 0.032-5.6 mg/kg (i.p.) had stronger antitumor activities and higher chemotherapeutic ratio than mitomycin C against such murine ascitic tumors as P388 and L1210 leukemia, B16 melanoma, M5076 reticulum cell sarcoma of ovarian origin, Colon 26 carcinoma, Ehrlich carcinoma, and MH134 hepatoma. In tests against murine and human solid tumors implanted s.c. in normal mice and nude mice, respectively, FK973 (i.v.) inhibited growth of murine tumors (M5076 sarcoma, Colon 38 carcinoma, B16 melanoma, and Lewis lung carcinoma) by 66-100% and human tumors (LX-1 lung, MX-1 mammary, and SC-6 stomach carcinoma) by 84-99%. In studies with drug-resistant P388 leukemia, FK973 was also effective against vincristine-resistant P388, moderately effective against mitomycin C (MMC)- and adriamycin-resistant P388, and partially effective against cyclophosphamide-resistant P388 cells in mice. Leukopenic effects of FK973 and MMC in mice were comparable at doses which gave antitumor activity almost equally. FK973 had no effect on the numbers of platelets and red blood cells, whereas MMC markedly decreased both. FK973 decreased the numbers of colony forming units in spleen and in culture and the effect was less than that of MMC. Therefore, FK973 may give weaker myelosuppression than MMC. The results suggest that FK973 will be a beneficial drug for the treatment of cancer.
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PMID:Antitumor activity and hematotoxicity of a new, substituted dihydrobenzoxazine, FK973, in mice. 334 97

The antitumor activity of recombinant human tumor necrosis factor (rTNF-alpha) was examined on murine tumors in mice and in cultured cells in vitro. Mice were implanted intradermally with Meth A fibrosarcoma (Meth A) on day 0. rTNF-alpha caused tumor necrosis and inhibited the tumor growth when given i.v. on day 7 or 10, but not when given on day 3. When rTNF-alpha was given i.v. in doses of 0.1-3.2 micrograms/mouse twice a week for 3 weeks beginning on day 7 or 11, the growth of solid Meth A, Colon 26 adenocarcinoma, Colon 38 carcinoma, Sarcoma-180, and M5076 reticulum cell sarcoma tumors implanted s.c. or intradermally was markedly inhibited, and the life of the mice bearing these tumors, except M5076 reticulum cell sarcoma, was prolonged. The growth of Meth A implanted i.m. was also markedly inhibited by rTNF-alpha given i.v. However, the life of mice bearing i.p. Colon 26 adenocarcinoma, MH134 hepatoma, Sarcoma-180, and Ehrlich carcinoma was not prolonged by rTNF-alpha given i.p. nine times (days 1-9) in doses up to 1.0 or 3.2 micrograms/mouse. Only in the case of mice bearing i.p. Meth A, the life was slightly prolonged by i.p. treatment with rTNF-alpha but not by i.v. treatment. In experiments against in vitro cultured cells, rTNF-alpha did not show any direct cytotoxicity against mouse tumor cells: Meth A, Colon 26 adenocarcinoma, Colon 38 carcinoma, and Sarcoma-180, but had a cytotoxic effect against L929 mouse fibroblast. The results suggest that rTNF-alpha is a unique antitumor drug with potent necrotizing activity against solid tumors in mice, and that this activity may derive from indirect mechanisms related to the growth of tumors and not to the direct cytotoxicity of the drug.
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PMID:Recombinant human tumor necrosis factor-alpha: evidence of an indirect mode of antitumor activity. 359 35

The antiproliferative activity of flavone acetic acid (LM 975) was investigated on human adenocarcinoma cell lines (HCC-P2998, HCC-M1544, HCC-M1410, HT 29, LoVo), on a murine colon adenocarcinoma cell line (Colon 26), on murine pancreatic adenocarcinoma cells growing in primary culture (Pan 03) and on human normal fibroblasts (N1). No cytotoxic effects were found against human normal fibroblasts. LM 975 was active against murine adenocarcinoma Pan 03 and Colon 26, known to be sensitive in vivo too and, to variable extents, on human adenocarcinoma cell lines. LM 975 in vitro cytotoxic potency was relatively low. The high concentrations (1.0-1.4 mM) required to obtain a cytotoxic effect are, however, pharmacologically reasonable since they are comparable with drug plasma levels in mice or in patients treated with tolerable doses. After a relatively short LM 975 treatment (2 h) DNA, RNA and protein synthesis were inhibited in different proportions. In more sensitive cells LM 975 appeared to inhibit RNA synthesis more than DNA and protein synthesis. Inhibition of macromolecule synthesis after 2 h exposure was completely reversed in 24 h recovery. After 2 h treatment no detectable DNA breakage was found by the alkaline elution method, thus corroborating the idea that this compound does not act by causing DNA damage.
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PMID:Antiproliferative properties of flavone acetic acid (NSC 347512) (LM 975), a new anticancer agent. 367 16

A case of polyposis coli preceded by hepatocellular carcinoma and epidermoid cysts is described. Only one other documented case of hepatoma in association with polyposis coli has been reported in the literature. This patient is not only the youngest to develop an extracolonic malignancy, but has also been fortunate to survive a disease often considered fatal. The possibility of a polyposis-linked resistance to extracolonic malignancies is discussed.
Dis Colon Rectum
PMID:Polyposis coli preceded by hepatocellular carcinoma: report of a case. 626 63

A case is reported of a 33-year-old man with hepatocellular carcinoma associated with familial polyposis of the colon. During subtotal colectomy for diffuse colonic polyposis, a small tumor was excised from the right lobe of the liver. Histologic examination revealed hepatocellular carcinoma. The association of primary hepatoma in familial polyposis of the colon is very rare. However, it is well known that familial polyposis of the colon has a potent oncogenicity not only in the colon but also in the extracolonic organs. The hepatoma may also be one of the extracolonic malignant manifestations in this inherited disease.
Dis Colon Rectum 1983 Jul
PMID:Hepatocellular carcinoma associated with familial polyposis of the colon. Report of case. 630 3

Zinostatin stimalamer (ZSS) is a new anticancer agent derived from neocarzinostatin (NCS), which is synthesized by conjugation of one molecule of NCS and two molecules of poly(styrene-co-maleic acid). ZSS exhibited potent in vitro and in vivo antitumor activity in preclinical experiments, and a clinical trial of the intra-arterial administration of ZSS with iodized oil on hepatocellular carcinoma showed potent antitumor activity. We investigated the effect of ZSS and NCS on antitumor resistance and found that pretreatment with either drug suppressed the growth of MethA tumors in Balb/c mice and induced tumor eradication when given separately by single administration at therapeutic doses between 1 day and 4 weeks before tumor transplantation. The findings that the cytocidal activity of these drugs was not detected in vivo at the time of tumor transplantation and that tumor regression was preceded by a period of transient growth suggested that tumor regression was due to host-mediated antitumor activity induced by these drugs. Pretreatment with ZSS or NCS also suppressed the growth of Colon 26 carcinoma and Sarcoma 180. The finding that NCS showed the same effect as ZSS suggests that poly(styrene-comaleic acid) is not essential for the induction of host-mediated antitumor activity. Furthermore, apo-ZSS, which lacks cytocidal activity, did not induce antitumor activity. From this, it is suggested that the cytocidal effect of ZSS involves the induction of host-mediated antitumor resistance. In athymic Balb/c nu/nu mice, pretreatment with ZSS or NCS did not induce tumor eradication, suggesting that mature T lymphocytes play an important role in tumor eradication. Challenging MethA was rejected without transient growth in mice that had been cured of MethA, but challenging Colon 26 was not, showing that anti-MethA resistance was augmented selectively in the MethA-eradicated mice. Splenocytes from MethA-bearing mice pretreated with the drug showed tumor-neutralizing activity beginning 14 days after tumor transplantation. Tumor-neutralizing activity was only induced after MethA transplantation. The effector cells of this tumor-neutralizing activity were Thy1.2+ T lymphocytes that had been passed through a nylon-wool column, but no significant augmentation of cell-mediated cytotoxic activity of splenocytes from MethA-eradicated mice was observed in vitro.
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PMID:Antitumor resistance induced by zinostatin stimalamer (ZSS), a polymer-conjugated neocarzinostatin (NCS) derivative. I. Meth A tumor eradication and tumor-neutralizing activity in mice pretreated with ZSS or NCS. 760 May 66

PSK (Krestin) is a protein-bound polysaccharide with antitumor and immunomodulatory activity. In this study, the effects of the oral administration of PSK were investigated on the natural killer (NK) activity of liver-associated lymphocytes and their subfractions separated by density gradient centrifugation, in WKAH rats with liver metastasis of KDA hepatoma. PSK was administered orally, at a dose of 500 mg/kg once a day for 3 weeks. The NK activity of nonparenchymal liver cells (NPLC) and their subfractions, including large granular lymphocytes (LGL), was markedly augmented by this treatment. The effects of oral PSK were also examined in CDF1 mice with liver metastases of Colon 26 adenocarcinoma; the survival of tumor-bearing mice was prolonged and both metastatic foci and liver weight were decreased. These results suggest that PSK may be effective for the suppression of liver metastasis through activation of liver-associated NK cells.
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PMID:Suppression of hepatic natural killer activity by liver metastasis of cancer and restoration of killer activity by oral administration of a Basidomycetes-derived polysaccharide, PSK. 786 94


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