Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlorozotocin, 2-(3-(2-chloroethyl)-3-nitrosoureido)-D-glucopyranose, is a newly synthesized, water-soluble nitrosourea antitumor agent that is active against L1210 leukemia in mice. A 701% and a 401% increase in life-span were attained with a dose that was lethal to 10% of the animals (15 to 20 mg/kg, i.p.) in mice treated on Day 2 or Day 6 of L1210 tumor growth, respectivley. Sixity % of Day 2-treated mice and 30% of Day 6-treated mice survived for 90 days. At the maximally effective dose against L1210, chlorozotocin produced no significant depression in normal bone marrow DNA synthesis nor in peripheral neutrophil count, in contrast to a sustained greater than 90% inhibition in L1210 ascites cell DNA synthesis. If the antitumor activity and reduced bone marrow toxicity of chlorozotocin are confirmed in man the use of this compound would facilitate treatment of patients with neoplastic disease who have preexisting abnormal bone marrow function or would allow for the more effective use of a nitrosourea agent in combination with anticancer agents possessing more potent myelosuppressive properties.
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PMID:Chlorozotocin, 2-(3-(2-chloroethyl)-3-nitrosoureido)-D-glucopyranose, an antitumor agent with modified bone marrow toxicity. 12 70

1-(2-Chloroethyl)-3-(beta-D-glucopyranosyl)-1-nitrosourea (GANU), a water-soluble nitrosourea, differs from 2-[3-(2-chloroethyl)-3-nitrosoureido]-D-glucopyranose (chlorozotocin) by the placement of the cytotoxic group on C-1 of glucose. Its biological and biochemical properties are compared with those of chlorozotocin. At a 10% lethal dose (10 mg/kg i.p.), GANU demonstrates minimal myelosuppression. This dose failed to depress normal bone marrow DNA synthesis, in contrast to a 96% inhibition in L1210 DNA synthesis. In L1210 cell suspension, equimolar doses of GANU and chlorozotocin produced equivalent degrees of inhibition in DNA synthesis. GANU has significant L1210 activity in BALB/c X DBA/2 F1 mice treated on Day 2 of tumor growth. A 117% increased life-span and 15% 45-day survivors are atained with 15 mg/kg i.p., a 50% lethal dose. However, in concurrent studies using randomly selected littermate groups of mice, GANU proved less active than chlorozotocin which produced a 306% increased life-span (15 mg/kg i.p.). GANU and chlorozotocin have similar in vitro alkylating activity but the in vitro carbamoylating activity of GANU is sevenfold that of chlorozotocin. On a molar basis, the lethal toxicity of GANU is twice that of chlorozotocin. The significant carbamoylating activity of GANU may contribute to its greater toxicity and therefore limit the mumoles of alkylating agent that can be administered to the tumor. These structure-activity studies further confirm that the addition of a glucose carrier to a cytotoxic nitrosourea moiety can selectively reduce bone marrow toxicity while retaining antitumor activity.
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PMID:Biological and biochemical properties of 1-(2-chloroethyl)-3-(beta-D-glucopyranosyl)-1-nitrosourea (NSC D 254157), a nitrosourea with reduced bone marrow toxicity. 13 78

Relaxation time(s) (T1), growth rates, and the water content of six Morris hepatomas, several murine tumors, and a selection of normal tissues indicated that malignant tumors did not always exhibit longer T1 values than any normal tissue, as previously suspected. This overlap raised the possibility of confusion between normal and malignant tissues studied by this method. Tissue T1 values depended primarily on the hydration of the tissue and correlated well with water content determinations. A rough correlation of T1 and water content with tumor growth rate was also observed.
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PMID:Nuclear magnetic resonance studies of cancer. VI. Relationship among spin-lattice relaxation times, growth rate, and water content of Morris hepatomas. 16 93

During carcinogenesis, induced by diethylnitrosamine in rats Wistar (in doses of 2.5 mg per Kg of weight daily with drinking water), the hexokinase (HK) activity in blood serum was observed with the appearance of the first morphological symptoms of tumor growth. It is observed mainly starting from the first months. At the end of the experimental period (8-9th month), when hepatomas develop in the liver, the HK activity in blood serum was noted almost in all cases. No serum HK activity was found in control rats.
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PMID:[Hexokinase activity in blood serum during carcinogenesis]. 19 94

Intraperitoneal injection of trace amounts of corn oil prior to and following the injection of 40-50 mg of tissue from hepatoma 7777 or 7800 into the thigh of adult male Buffalo rats resulted in a marked decrease in the growth rate of both tumors. Exhaustive extraction of the corn oil with water indicated that the active component was not water soluble. Similar injections of safflower oil or isotonic saline had no effect on tumor growth rate. Analysis of the tissue phospholipid fatty acids revealed that the injected corn oil caused no change in the esterified fatty acids in this lipid fraction.
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PMID:Inhibition of growth of Morris hepatomas 7777 and 7800 by corn oil. 19 60

The population of eels in the Elbe estuary showed a high rate of affliction with epidermal papillomas. Distinct seasonal fluctuations were observed in the frequency of occurrence and tumor size. In spring and autumn, the frequency was low, and the tumors were relatively small. In summer, the tumors reached a maximum in both frequency and size. A distinct influence of water temperature on tumor growth was demonstrated experimentally. Summer temperatures of 15--22 degrees C caused very rapid growth. In the field and in the laboratory, the tumors exhibited a fourfold increase in average volume within 3 months. These fast-growing neoplasms had certain relatively uniform histologic features. The tumor cells were separated by wide intercellular spaces. The basal layer was composed of tall columnar cells, while the surface layer was composed of slightly flattened cells. Winter water temperatures (5--10 degrees C) inhibited tumor growth and even caused tumor regression. In 3 months, the papillomas shrank to half of their initial size. Histologic and ultrastructural examinations revealed signs of tissue degeneration: necrobiotic processes in the epidermal region, cellular and nuclear polymorphisms, dissolution of membranes, loss of cell integrity, and loosening and reduction in size of the basal cell layer.
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PMID:Temperature-dependent growth and regression of epidermal tumors in the european eel (Anguilla anguilla L.). 28 Jan 83

Indomethacin was continuously administered in the drinking water of inbred C3H mice given grafts of syngeneic 3-methylcholanthrene-induced fibrosarcomas. A minor proportion of these animals died at the same time as the untreated controls, and others completely rejected their tumors; however, in most cases, the tumor growth rate was significantly slowed, and growth recommenced rapidly after drug withdrawal. This was the pattern for tumors either in their 10th to 14th transplant generation or only their third in vivo passage. Indomethacin exerted little prophylactic effect, in that it neither increased the minimal cell number required to initiate tumor growth nor significantly decreased the proportion of tumors established in drug-treated animals recieving tumor grafts. The injection of killed Corynebacterium parvum organisms into small, growing McC3-I tumors [intratumor (IT) route] caused the regression of most of these. In contrast, IT injection of BCG, ip injection of C. parvum, or IT injection of C. parvum into larger tumors had no effect. Oral administration of indomethacin enhanced BCG treatment and augmented the activity of C. parvum injected either systemically into animals with small tumors or IT into those with substantial tumor burdens. The duration of these effects was, however, often dependent on the continued administration of the drug.
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PMID:Tumor growth inhibition and potentiation of immunotherapy by indomethacin in mice. 28 66

In vivo MSB tumor growth and cell-mediated cytotoxicity (CMC) to MSB tumor cells in vitro were studied in male C57BL/6 mice exposed to 0, 3, 30, or 300 ppm Cd as CdCl2 in their drinking water for 21 weeks prior to and during tumor growth. CMC was assessed on days 5, 12, and 19 post injection with the use of both a 51Cr release assay and a 51Cr post-label assay. Cd exposure significantly inhibited the growth of MSB tumors in vivo and enhanced the levels of CMC in the tumor-bearing hosts. Peak levels of CMC on day 12 post tumor injection were significantly increased in Cd-exposed animals. However, whereas the inhibition of tumor growth was directly dependent on the dose of Cd, the enhancement of CMC was inversely related to dosage. These data suggested that other mechanisms in addition to increased CMC were involved in tumor growth inhibition. Possible factors such as direct inhibition of tumor growth by Cd and decreased serum blocking levels in Cd-exposed animals are discussed.
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PMID:Effect of cadmium exposure on primary tumor growth and cell-mediated cytotoxicity in mice bearing MSB sarcomas. 28 37

The joint administration of 2 ppm of arsenic as arsenite and of 2 ppm of selenium as selenite in the drinking water of inbred female C3H/St mice increases the incidence of spontaneous mammary adenocarcinoma significantly over the simultaneous controls and animals receiving 2 ppm As as arsenite or 2 ppm Se as selenite alone, indicating that arsenic abolishes the anticarcinogenic effect of selenium. Arsenite caused a significant increase of the tumor growth rates and raised the incidence of multiple tumors. The tumor growth rates in the As-Se group were also increased, but the incidence of multiple tumors was lower than in the 2 ppm As group.
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PMID:Arsenic and cancer: effects of joint administration of arsenite and selenite on the genesis of mammary adenocarcinoma in inbred female C3H/St mice. 69 83

The essential trace element selenium retards the growth of certain chemically induced tumors in animals. The addition of subtoxic amounts of this element in form of selenite to the supply water lowers the incidence of spontaneous mammary tumors in female C3H mice significantly without affecting the health and life-span of the animals. Arsenic, a selenium antagonist, administered in form of arsenite in the supply water, also lowers the tumor incidence at dosage levels of 10 ppm, but those animals which develop spontaneous mammary tumors under these conditions demonstrate dramatically enhanced tumor growth rates. The results of initial epidemiological studies suggest that the human cancer mortality is lower in areas providing an adequate dietary intake of selenium as estimated from the selenium content in grains and forage crops in various regions of the United States, or the dietary selenium intakes as calculated from food consumption data in various countries.
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PMID:Selenium and cancer: a review. 76 40


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