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G Della Porta

Publications and source records attributed to G Della Porta.

At least 91 records · Page 5Linked to original sources
PubMed1986

Detection of two TaqI polymorphisms in the VTR region of the human HRAS1 oncogene.

Restriction enzyme analysis of the variable tandem repetition (VTR) region of the human HRAS1 oncogene revealed two TaqI polymorphisms. The first polymorphism overlaps that detected with MspI/HpaII restriction enzymes and is due to a variable number of repeat units which form the VTR region at the 3' end of the oncogene. The second polymorphism appears to be due to two new TaqI restriction sites created within the VTR region itself. This novel polymorphism was detected in 26 of 145 human DNA samples and was found to segregate in a Mendelian fashion.

Chromosome Mapping↗
PubMed1986

Expression of retroviral sequences and oncogenes in murine hepatocellular tumors.

The expression of endogenous retroviral sequences and of three cellular oncogenes was examined in three hepatocellular adenomas and in four carcinomas induced in male C57BL/6JDp X C3Hf/Dp F1 (hereafter called B6C3F1) mice by a single dose of nitrosodiethylamine, in five carcinomas that arose spontaneously in male C3Hf mice, and in the livers of normal age-matched control mice. In all of these adenomas and carcinomas, there was increased expression of Moloney murine leukemia virus- and intracisternal A particle-related sequences. The retrovirus-like VL30 sequence was expressed at significant levels in the normal liver of these mice and increased expression of this sequence was found in only 4 of the 12 tumors examined. Expression of endogenous mouse mammary tumor virus-related sequences was not detected in the normal livers or in any of the liver tumors. With respect to cellular oncogenes, increased expression of c-myc was seen in all of the B6C3F1 tumors. Two of five normal liver samples and all of the tumors of the C3Hf mice displayed significant expression of c-myc. There was a slight increase in expression of c-Ha-ras in some of the tumors. Increased expression of c-fos was found in only 1 of the 12 tumors. Taken together, these studies indicate that both carcinogen-induced and spontaneous liver tumor formation in mice is associated with abnormalities in the expression of endogenous retrovirus-related DNA sequences and also specific cellular oncogenes.

Animals↗
PubMed1985

Kinetics of sister-chromatid exchange induction by different carcinogens in C57BL/6J and DBA/2 mice.

Sister-chromatid exchange (SCE) levels were determined in bone marrow cells of DBA/2 and C57BL/6J mice at 18, 24, 30 and 48 h after treatment with 10 mg/kg cyclophosphamide (CP), 300 mg/kg urethane or 25 mg/kg N-nitroso-N-methylurea (NMU). DBA/2 mice showed higher SCE frequencies than C57BL/6J mice at all time points examined after CP and urethane treatment, whereas NMU administration resulted in similar SCE levels in both strains. After CP and urethane treatments, SCE values reached the highest level at 18 h, were similarly high at 24 and 30 h, and returned to base-line level at 48 h. In NMU-treated mice, the SCE values had the same level at 18, 24 and 30 h and returned to normal at 48 h. The results are interpreted as indicating that different metabolic capabilities are responsible for the difference in SCE response in the two strains.

Animals↗
PubMed1985

Promoting effects of 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene in mouse hepatocarcinogenesis.

The effects of phenobarbital (PB) and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) on liver hyperplasia, induction of microsomal enzyme activities, and two-stage hepatocarcinogenesis were evaluated in B6C3F1 female mice. For 4 weeks four groups of mice received PB (500 p.p.m. in the drinking water), TCPOBOP (3 mg/kg i.p. once every week), PB together with TCPOBOP or corn oil vehicle i.p. TCPOBOP induced liver hyperplasia and hypertrophy and increased p-nitroanisole-O-demethylase and aminopyrine-N-demethylase more than PB. Neither chemical changed UDPG-transferase activity. The association of PB and TCPOBOP gave the same effects as TCPOBOP alone. Other four groups of mice were treated with N-nitroso-N-diethylamine at 7 days of age and then, starting from 8 weeks of age, received the above specified weekly treatments for 20 weeks and were then sacrificed. Hepatocellular nodules greater than 150 microns were found in all animals of all groups. Due to increased size of the liver compared to controls, the number of nodules/cm3 decreased after PB and TCPOBOP treatments given alone or together; however the mean volume of nodules and the percentage of liver volume occupied by nodules increased after TCPOBOP but not after BP treatment, and the association of PB and TCPOBOP was even more effective than TCPOBOP alone. Hepatocellular adenomas greater than 2.4 mm in diameter were observed in 5 of 10 TCPOBOP-treated mice (total of 11 nodules) and in 5 of 11 mice that received PB plus TCPOBOP (total of 15 nodules). Hepatocellular carcinomas were seen in one mouse treated with PB and in three mice given PB and TCPOBOP.

Adenoma↗
PubMed1984

Spontaneous and urethan-induced tumor incidence in B6C3F1 versus B6CF1 mice.

The incidences of spontaneous tumors of the murine hybrids (C57BL/6J X C3Hf)F1 (B6C3F1) and (C57BL/6J X BALB/c)F1 (B6CF1) were compared in untreated mice kept until 110 weeks of age. Male B6C3F1 and B6CF1 mice had respectively 16% and 20% incidence of lymphomas, 26% and 4% of liver tumors and 12% and 22% of lung tumors. Among B6C3F1 and B6CF1 females, a 36% and 12% incidence of lymphomas, a 6% and zero incidence of liver tumors, and a 4% and 16% of lung tumors were observed. A few other tumors were seen in both hybrids. Groups of male and female mice of the 2 hybrids received 5 i.p. injections of 1000 mg/kg urethan once every other day starting at 10 days of age, and were kept under observation until 65-80 weeks of age. Treated B6C3F1 mice had an earlier mortality than B6CF1 mice due to tumor development. The statistical analysis, allowing for survival, showed a significantly higher lymphoma incidence in male and female B6C3F1 than B6CF1 mice, which had instead a higher incidence of lung tumors. Hepatocellular tumors were seen in both sexes of the 2 hybrids, with a higher frequency in B6C3F1 mice. Male mice of both hybrids had a higher incidence of liver tumors than females.

Animals↗
PubMed1984

Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient.

A single genetic alteration, a guanine-to-cytosine transversion, is responsible for the acquisition of malignant properties by K-ras genes of two human tumor cell lines established from carcinomas of the bladder (A1698) and lung (A2182). As a consequence, arginine instead of the normal glycine is incorporated into the K-ras-coded p21 proteins at amino acid position 12. This mutation creates a restriction enzyme polymorphism that can be used to screen human cells for transforming K-ras genes. This approach was used to identify the mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man; this point mutation was not present in either the normal bronchial or parenchymal tissue or in the blood lymphocytes. Hence, malignant activation of a ras oncogene appears to be specifically associated with the development of a human neoplasm.

Base Sequence↗
PubMed1984

Carcinogenic activity in mice of diftalone, an anti-inflammatory agent.

The anti-inflammatory agent diftalone was administered in the diet to male and female BALB/c mice at 300-, 600-, and 1200-ppm dose levels for 80 weeks, starting at 8 weeks of age. The animals were kept under observation until 126-128 weeks of age, when the experiment was terminated. Diftalone treatment at the highest dose was hepatotoxic and induced hepatocellular tumors in females, angiomas of the liver in males, and angiosarcomas of the liver in male and female mice. The 300- and 600-ppm dose levels were not carcinogenic. The compound was not mutagenic for Salmonella typhimurium.

Animals↗
PubMed1983

Carcinogenicity study in mice on pildralazine, a hydralazinelike antihypertensive compound.

Pildralazine, a hydralazinelike antihypertensive vasodilator containing a free hydrazine group, was administered in the drinking water to male and female B6C3F1 and to female BALB/c mice at 100, 200, and 400 ppm dose levels for 80 weeks. The animals were kept under observation until 130-133 weeks of age, when the experiment was terminated. A transplacental-infantile bioassay was also carried out with pildralazine administered in the drinking water at 200 and 400 ppm dose levels to female C57BL/6J mice for 1 week before mating with C3Hf males and during mating and pregnancy. The progeny received the same doses for 10 weeks after birth and were kept under observation until 80-85 weeks of age, when the experiment was terminated. In both long-term and transplacental-infantile assays, control and treated groups developed the pattern of tumors usually observed in the strains used and no tumor type at any site appeared to be related to treatment.

Animals↗
PubMed1983

Comparison of urethane-induced sister-chromatid exchanges in various murine strains, and the effect of enzyme inducers.

The induction of sister-chromatid exchanges (SCEs) by urethane, 150 and 300 mg/kg administered i.p., was examined in bone-marrow cells of AKR, BALB/c, C3Hf, C57BL/6J and DBA/2 male mice. In all strains, the base-line level of SCE/cell was similar, ranging from 4.3 to 8.7, and the response increased with the dose of urethane. DBA/2 mice were the most susceptible to urethane at both dose levels, with 30.6 SCE/cell after treatment with 300 mg/kg, whereas the response of the other strains was from 17.4 to 21.5 SCE/cell at the same urethane dose. Pretreatment of C57BL/6J and DBA/2 mice with phenobarbital decreased the SCE frequencies induced by urethane, 300 mg/kg, to 70%, whereas a prior administration of beta-naphthoflavone reduced SCE levels in C57BL/6J but not in DBA/2 mice.

Animals↗
PubMed1983

Effect of enzymatic induction and inhibition on cyclophosphamide-induced sister chromatid exchange in vivo.

The influence of the enzymatic inducer beta-naphthoflavone (BNF) and of the inhibitors alpha-naphthoflavone (ANF) and 2-diethylaminoethyl-2,2-diphenylvalerate HCl (SKF 525-A) on the frequency of sister chromatid exchanges (SCE) induced by cyclophosphamide (CPA) was studied in vivo in C57BL/6J male mice. Neither inducer nor inhibitors substantially modified the SCE level induced by 5 or 10 mg/kg CPA. The enzymatic induction by BNF was effective as treated animals showed a reduced paralysis time by zoxazolamine whereas ANF appeared to be ineffective. The enzymatic inhibition by SKF 525-A was confirmed by a longer sleeping time in pentobarbital-treated mice and also by a longer paralysis in zoxazolamine-treated mice. The lower susceptibility to CPA-induced SCEs of C57BL/6J mice relative to DBA/2 strain observed in a previous work seems not to be simply related to Ah locus mediated metabolism.

Animals↗
PubMed1981

Lack of carcinogenicity in mice of 4,4-'diaminobenzanilide and 4,4'-diaminoazobenzene, two intermediates used in the manufacture of azo dyes.

4,4'-Diaminobenzanilide and 4,4'-diaminoazobenzene were administered in the diet to BALB/c mice at 100, 300 and 600 ppm dose levels for 60 weeks. The animals were kept under observation until 140 weeks of age when the experiment was terminated. Control and treated groups developed the pattern of tumours usually observed in BALB/c mice. No tumour type at any site was related to treatment.

Anilides↗
PubMed1980

Carcinogenicity study of 3-(5-nitro-2-furyl)-imidazo(1,2-alpha) pyridine in mice and rats.

3-(5-nitro-2-furyl)-imidazo(1,2-alpha) pyridine was tested for carcinogenicity by long-term administration in the diet to CTM mice at 0.1, 0.2 and 0.4% dose levels and to Wistar rats at 0.2 and 0.4% dose levels, and by short-term intraperitoneal injections to suckling BALB/c mice. The compound was a strong carcinogen. In CTM mice it induced carcinomas of the esophagus and forestomach at all dose levels and thymic lymphosarcomas at the two highest doses. In male and female rats, esophagus and forestomach papillomas were observed at all dose levels, whereas esophagus and forestomach carcinomas and kidney tumors were observed only at the high dose. In female rats, an increased incidence of mammary tumors was seen at the high dose. The treatment of BALB/c suckling mice by intraperitoneal injections did not induce a clear carcinogenic response.

Age Factors↗
PubMed1980

Comparison of the natural humoral antitumor reactivity of different strains of mice.

Normal serum from C3Hf mice showed a complement-dependent cytotoxic reactivity against EL4 lymphoma cells, starting from 2 to 3 months of age, whereas normal serum from BALB/c and C57BL/6J mice became reactive only at a later age. The cytotoxins of normal sera of the 3 strains, as well as of a C57BL antiembryo antiserum studied in parallel, belong to the IgM class. When absorption were performed, using a variety of absorbing cells, marked differences were found among the sera, which according to their behavior could be divided in two groups: one group comprises the BALB/c and the C57BL sera, the other group the C3Hf serum from both young and old mice and the antiembryo antiserum. The reactivity of the 3 latter sera seems to be directed against specifities related to an ecotropic N-tropic virus, which on the contrary did not seem to be involved in the reactivity of BALB/c and C57BL sera. The C57BL antiembryo antiserum obtained by immunization with C3Hf embryos behaved differently from the C57BL normal serum and similarly to the C3Hf normal serum.

Animals↗