Biomedical subjects

F Di Carlo

Publications and source records attributed to F Di Carlo.

At least 19 recordsLinked to original sources

PubMed2005

Anti-HER-2 DNA vaccine protects Syrian hamsters against squamous cell carcinomas.

This paper illustrates the efficacy of DNA vaccination through electroporation in the prevention of oral transplantable carcinoma in Syrian hamsters. At 21 and 7 days before tumour challenge, 19 hamsters were vaccinated with plasmids coding for the extracellular and transmembrane domains of rat HER-2 receptor (EC-TM plasmids), whereas 19 control hamsters were injected intramuscularly with the empty plasmid. Immediately following plasmid injection, hamsters of both groups received two square-wave 25 ms, 375 V cm(-1) electric pulses via two electrodes placed on the skin of the injection area. At day 0, all hamsters were challenged in the submucosa of the right cheek pouch with HER-2-positive HCPC I cells established in vitro from an 7,12-dimethylbenz[a]anthracene-induced oral carcinoma. This challenge gave rise to HER-2-positive buccal neoplastic lesions in 14 controls (73.37%), compared with only seven (36.8%, P<0.0027) vaccinated hamsters. In addition, the vaccinated hamsters displayed both a stronger proliferative and cytotoxic response than the controls and a significant anti-HER-2 antibody response. Most of the hamsters that rejected the challenge displayed the highest antibody titres. These findings suggest that DNA vaccination may have a future in the prevention of HER-2-positive human oral cancer.

Animals↗

PubMed2005

Animal models in oral cancer research.

Biologically and clinically relevant animal models are essential in investigation of the progression of diseases and the elaboration of diagnostic or therapeutic protocols. The several rodent models used for in vivo evaluation for oral cancer employ chemical, transplantation and genetic (knockout and transgenic) induction methods. These models are described together with their advantages and disadvantages. Their optimization and application in future research may improve the early detection and treatment of oral cancer.

Animals↗

PubMed2003

[Corrosion of titanium in presence of dental amalgams and fluorides].

AIM: The aim of this study was to evaluate the behaviour of titanium (Ti) in precipitant condition, and more precisely the resistance against corrosion of Ti in presence of fluorides and the electrochemical interaction between Ti- amalgam couples in fluorinated solution. METHODS: The experimental test was made with the use of an electrochemical cell. The following materials were tested: commercially pure Ti and 2 types of amalgams, the Persistalloy (Prs) and the IQC. Palladium (IQC.P). The free corrosion potential of Ti and the amalgams, the polarization curves of both amalgams and the corrosion current of the Ti-amalgam couples in the measurements were performed in 3 different electrolytic solutions: Ringer solution, fluorinated neutral Ringer solution and acid fluorinated solution. The three corrosive media are described. RESULTS: The results showed that Ti could be damaged by the presence of fluorides with an acid pH: Ti potential becomes more negative in acid fluorinated solution. The corrosion currents between Ti and amalgam couples were considered: the amalgams underwent anodic oxidation in neutral Ringer, but a reversal phenomenon occurred in the fluorinated acid solution: Ti was damaged and the amalgams both Prs and IQC.P became the cathodic partner of the couple. In neutral fluorinated solution the IQC.P amalgam induced a significantly higher corrosion of Ti, when compared to the Prs one. CONCLUSION: Results clearly show the dependence of the Ti corrosion behaviour on the pH and composition of the solution and that the outcome of the damage is affected by the composition of other metals.

Chemical Phenomena↗

PubMed2001

Effect of the single major proteic fractions of the liver perchloric extract UK101 on the development of oral tumours in Syrian hamsters.

Squamous cell carcinoma of the oral cavity continues to be a major clinical problem, with about 100,000 new deaths each year worldwide. There is therefore a need to search for new tools to aid oral cancer treatment. We tested the inhibitory activity on chemical carcinogenesis of the three principal protein fractions of about 50, 14, and 8.5 kDa of the mixture UK101 derived from goat liver. These are composed principally of a glycoprotein rich in mannose residues, a protein with analogy to the heat shock protein family, and ubiquitin, respectively. The animal model employed was dimethylbenzanthracene-induced hamster cheek pouch carcinoma. Number of tumours per animal, tumour mass per animal, and proliferating cell nuclear antigen (PCNA) in non-tumour mucosa were quantified: the 14-kDa fraction was the most active; this was also confirmed by testing its corresponding recombinant material. The 50-kDa fraction was inactive, while the ubiquitin showed only low inhibitory activity. It is possible that the technique described and the results obtained could lead to an interesting clinical approach to the treatment of oral cancer.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1999

Perchloric acid-soluble proteins from goat liver inhibit chemical carcinogenesis of Syrian hamster cheek-pouch carcinoma.

Chemically induced Syrian hamster cheek-pouch squamous cell carcinoma is very similar to the corresponding human tumour. This paper describes a blind study in which inhibition of dimethylbenzanthracene-induced cheek-pouch tumours by a goat liver extract denominated UK101 was investigated. Less than 40% of animals treated with UK101 developed tumours compared with 100% of the controls. Intermediate results (80%) were noted in a positive control group treated with Calmette-Guerin bacillus. Immunocytochemical testing of cheek-pouch mucosa by Mib5 showed significantly less proliferating cells in UK101 animals than in the controls. The effect of UK101 was completely reversed when dexamethasone was added in a third control group. A significant difference in complement-mediated cytotoxicity was noted in the sera of UK101-tested and control animals. These findings suggest that an immune mechanism is responsible for the inhibition of hamster cheek-pouch carcinoma by UK101.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1998

The role of lung biopsy in children with perinatally acquired AIDS.

There is a need for a rapid and efficacious method of diagnosis of pulmonary infiltrates in perinatal HIV infection. However, controversy still exists about which method--open lung biopsy (OLB) versus bronchoscopic techniques--is the best for this population. We present our results with OLB in 24 children with HIV-related lung disease. Over a 6-year period, 27 OLBs were performed on 24 children with diagnosis of HIV infection. The procedures were performed under general anesthesia using a limited anterolateral thoracotomy. Suspicious areas were removed with the autostapler. The specimens were studied for the presence of non-infectious as well as bacterial, viral, fungal, and mycobacterial diseases. There were no operative deaths related to the procedure. Morbidity was limited to prolonged but self-resolving air leaks in two patients (8.3%). Five hospital deaths occurred between 3 and 12 weeks postoperatively and 11 late deaths between 3 months and 6.5 years. All deaths were related to AIDS. Eight patients (33.3%) are still alive 2 to 8 years postoperatively. A total of 43 pathologies were found in 27 specimens. A positive pathologic finding was obtained in all patients, with two patients having nonspecific minimal changes. This resulted in a change of therapy in all but one case. The technique of OLB in children with AIDS is safe and simple. It should be performed early in the course of the disease and, a careful selection of candidates can minimize the incidence of complications.

AIDS-Related Opportunistic Infections↗

PubMed1997

Calcyclin gene expression modulation by medroxyprogesterone acetate.

Calcyclin is a cell-cycle-related gene corresponding to a calcium-binding protein whose expression is mainly controlled by platelet-derived growth factor. This paper illustrates medroxyprogesterone acetate (MPA) inhibition of endogenous calcyclin RNA expression of both estrogen-dependent human mammary carcinoma cells and estrogen-independent hamster fibroblasts. Transfection of fragments of the calcyclin promoter driving the chloramphenicol-acetyl-transferase (CAT) gene into hamster fibroblasts was used to evaluate the hormone sensitivity of different promoter regions by considering calcyclin expression at both the RNA and protein level, as evaluated by the CAT assay. A 164 bp promoter fragment showed a good activity that was inhibited by MPA, thereby confirming the results of the observation of endogenous calcyclin gene: smaller fragments, however, required cotransfection of progestin receptor to show full activity, with MPA displaying a stimulatory effect. These findings show that progestin modulation of calcyclin gene expression may be independent of progestin receptors, and that MPA has opposite effects on different promoter regions.

Animals↗

PubMed1997

L-histidine/medroxyprogesterone acetate interaction modulates human breast cancer cell growth and progestin receptor expression in vitro.

The effect of different L-histidine concentrations on human mammary tumour cell (CG5) proliferation was studied to test the hypothesis of a role of histidine in modulating sex steroid-regulated cell proliferation. Cell growth was only possible in the 10(-5) M and 10(-2) M range, while its inhibition by medroxyprogesterone acetate was confined to the 10(-4) M and 10(-3) M range. 10(-3) M L-histidine enhanced the effect of medroxyprogesterone acetate in reducing the number of cells in the S phase. The results show also that 10(-3) M L-histidine favours progestin diffusion into cells and increases progestin receptors density. The present data are in line with previous observations of the effect of histidine on the growth of experimental animal tumours, add evidence that histidine concentration influences the control of cell proliferation by sex steroids, and suggest a possible use of histidine in association with progestational drugs in the treatment of human neoplasia.

Breast Neoplasms↗

PubMed1997

Growth inhibition of DMBA-induced rat mammary carcinomas by UK 114.

A perchloric acid-soluble protein extracted from goat liver and designated as UK 114 is known to be expressed over the cell membrane of (some) human cancer cell lines. This protein is antigenic, and specific antibodies elicit complement-dependent cytolysis of neoplastic target cells. In this study we demonstrate that administration of UK 114, either pure or as a crude extract (designated UK 101), inhibits the growth of mammary carcinomas induced in female Sprague-Dawley rats by dimethylbenzanthracene (DMBA). The mechanism of the tumour inhibitory activity of UK 114 is probably related to induction of immunosurveillance.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1997

Enhancement of calcyclin gene RNA expression in squamous cell carcinoma of the oral mucosa, but not in benign lesions.

Oral cancer is a neoplasm with some known causes. Proliferation genes are significant among its few pathogenetic and prognostic factors. Calcyclin is a cell-cycle-related gene, the function of which is still unclear. Its expression and that of Haras and histone-H3 have been investigated in an assessment of their pathogenetic role in squamous cell carcinoma. RNA extracted from the pathological and normal mucosa of patients with squamous cell carcinoma (SCC) and benign lesions was reverse transcribed and amplified by the polymerase chain reaction (PCR). The expression of all three genes in the pathological mucosa was enhanced in SCC only. This suggests that they may be involved in its pathogenesis and provides another parameter for the differentiation of malignant and benign lesions.

Adult↗

PubMed1993

Regulation of uterine estrogen receptors (ER) by beta-adrenergic stimulation in immature rats.

The effects of a 3-day intramuscular (i.m.) administration of clenbuterol (25 micrograms/Kg), propranolol (12 mg/kg), clenbuterol (25 micrograms/kg) plus propranolol (12 mg/Kg) and estradiol (0.5 microgram) upon the female reproductive system were investigated in immature Sprague-Dawley rats. Clenbuterol and estradiol treatments induced a significant increase in uterus weight and in relative uterus weight, whereas in the groups treated with propranolol and clenbuterol plus propranolol no differences were detected versus controls. The uterine estrogen receptor levels were significantly increased by clenbuterol administration. In the rats dosed with propranolol and clenbuterol plus propranolol, no modifications occurred in estrogen receptor concentrations when compared with control values. Uterine progesterone receptors were never significantly affected by any of the considered treatments. Data obtained indicate that clenbuterol treatment induces an increase in uterus weight and in estrogen receptor levels and that these effects are regulated by acute beta-adrenergic stimulation, as the contemporaneous administration of high doses of a beta-blocker inhibit such effects.

Animals↗

PubMed1993

Effects of long-term administration of clenbuterol in mature female rats.

Female Sprague-Dawley rats were treated IM with 0, 2.5, 25, and 50 micrograms of clenbuterol HCl/kg of body weight/d for 21 days. In all treated rats, significant increase in body weight gain (P < 0.05) and improvement in feed conversion ratio (P < 0.05) were recorded. Hydrometra was observed in the uterus of treated rats, and histologically, it was possible to see dilatation of luminal glands and ovarian alterations. Clenbuterol treatment induced significant (P < 0.05) increase in uterine estrogen receptor concentration of rats treated with the 2 higher doses. Treatment apparently failed to enhance the rate of oxidative and conjugative biotransformations, except for glucuronidation of p-nitrophenol (P < 0.05). On the basis of the data obtained, we could affirm that high doses of clenbuterol affect the female reproductive system of rats inducing, almost in part, estrogen-like modifications, but probably by a different mechanism of action correlated to intense adrenergic stimulation.

7-Alkoxycoumarin O-Dealkylase↗

PubMed1992

Effects of a beta 2-agonist (clenbuterol) on cultured human (CG-5) breast cancer cells.

In order to gain further knowledge about the possible oestrogen-like activities of clenbuterol (a beta 2-adrenergic drug illegally used as partitioning agent in food producing animals), we treated a hormone dependent human breast cancer cell line (CG-5) with different concentrations of the drug (10(-3) M to 10(-8) M). The effects of clenbuterol and oestradiol on cell proliferation were compared. Both oestradiol and clenbuterol, at low concentrations (10(-7) M and 10(-8) M) stimulated cell proliferation, but the effects of clenbuterol were less marked and significant. Probably clenbuterol elicited cell proliferation through a different mechanism, since it did not affect the cellular oestrogen receptor concentration. Clenbuterol failed in binding to the high affinity oestrogen receptors present in the CG-5 cells. As the beta-adrenergic receptors and the susceptibility to their stimulation have been recently demonstrated in vivo and in vitro in many tumour and normal cells, it is reasonable to suppose that clenbuterol may induce cell proliferation through beta-adrenergic stimulation.

Breast Neoplasms↗

PubMed1991

Potentiation of medroxyprogesterone acetate antineoplastic activity by histidine in rat mammary tumours.

The antitumour activity of arginine, histidine and medroxyprogesterone acetate (MPA) was studied in female rats with dimethylbenzanthracene (DMBA)-induced mammary adenocarcinomas. After 15 days of treatment, regression was observed in 4 of 19 (21%), 3 of 18 (16.7%) and 22 of 59 (37.3%) tumours taken from rats given arginine, histidine or MPA, respectively. A total of 17 rats with tumours that had been non-responsive to MPA were then treated with MPA plus histidine for 15 more days; the growth of 3 lesions (17.6%) was arrested, and 5 tumours (29.4%) regressed markedly. The antineoplastic activity of MPA was found to be related to the oestrogen-(ER) and progesterone-receptor (PgR) concentrations measured in the tumours before the start of treatment, whereas that of arginine and histidine appeared to be independent of receptor status. A significant reduction in serum prolactin (PRL) levels occurred in rats that were responsive to MPA alone or to MPA plus histidine. In tumours taken from the same rats, the PRL receptor content was also significantly increased in comparison with that in non-responsive tumours. In contrast, serum PRL levels increased significantly in rats with tumours that were non-responsive to MPA, whereas no change in serum PRL or PRL receptor levels was observed in rats treated with arginine or histidine. Histidine showed the ability to increase the number of ERs and PgRs in responsive tumours; this could have been responsible for the unexpected potentiation of MPA antineoplastic activity. In contrast, the levels of ER and PgR in uteri taken from the same rats were not modified. Furthermore, the addition in vitro of histidine to cytosols obtained from tumours of control animals did not influence ER and PgR concentrations. These results suggest that the effect of histidine on ER and PgR levels is probably specific for tumour tissue and is not due to a direct activity.

Animals↗

PubMed1988

High tumour prolactin receptor content and lack of increase in serum prolactin levels as predictors of good response to endocrine therapy in rat mammary cancer.

Correlations between anti-neoplastic activity of medroxyprogesterone acetate (MPA), on the one hand, and serum prolactin (PRL) levels as well as tumour PRL and insulin receptor content, on the other, were investigated in female rats bearing dimethylbenzanthracene (DMBA)-induced mammary tumours. Changes in liver PRL receptor concentrations were also studied. MPA was injected for 15 days. Regression was observed in 16 out of 50 (32%) tumours from rats treated with MPA. Twenty-seven out of 50 (54%) continued to grow regardless of treatment. Stasis was seen in the remaining 7 tumours (14%). Serum PRL levels increased significantly in rats with tumours which were non-responsive to MPA. Concentration of PRL receptors in the liver of all animals was reduced by MPA treatment. A remarkable increase occurred only in those mammary tumours which responded to therapy. The concentrations of PRL receptors in the tumours non-responsive to MPA were similar to those detected in control tumours. Unlike PRL receptors, tumour insulin receptor levels were not modified by MPA treatment. Five out of 14 tumours (35.7%), previously growing in spite of MPA administration, regressed when bromocriptine was added to MPA. A significant reduction in serum PRL levels occurred in all rats undergoing the latter treatment. No difference was observed between responsive and non-responsive animals; on the contrary, the PRL receptor content of responsive tumours increased significantly in comparison with that of non-responsive tumours.

Adenocarcinoma↗

PubMed1988

Effects of medroxyprogesterone acetate on serum prolactin levels and liver prolactin binding capacity in the rat.

Modifications in liver prolactin (PRL) receptor levels and serum PRL concentration induced by administration of medroxyprogesterone acetate (MPA) were investigated in rats of both sexes. MPA induced a reduction both of the levels of PRL in the serum and of liver PRL receptors in the female rat. The reduction of the number of PRL receptors caused by MPA was rapid and almost complete after 10 days of treatment and appeared earlier than that of serum PRL levels. Furthermore the MPA-induced decrease in PRL receptors was specific, since insulin binding to the same liver membranes was not affected. MPA given simultaneously with oestradiol (which increases both the number of liver PRL receptors and the serum PRL levels in the male rats) was able to counteract the increase in PRL binding induced by oestradiol. On the contrary, the oestrogen-induced increase in serum PRL was not affected by MPA treatment. Similar results were obtained using tamoxifen, a well known antioestrogenic drug. In conclusion, our results show that the reduction of PRL receptor levels induced by MPA in rat liver is specific, not correlated to serum PRL concentration, and seems to depend on the antioestrogenic activity of the drug.

Animals↗

PubMed1985

Estrogen and progesterone receptors in the human vagina.

Estrogen (E) and progesterone (Pg) receptor (R) levels were determined in the human vagina in relation to menopausal status, day of ovarian cycle and pregnancy. The results obtained confirmed that the human vagina contains ER and, in addition, demonstrated for the first time the presence of PgR in this organ in humans. In cycling women, ER and PgR did not vary significantly during the ovarian cycle; however low (less than or equal to 10 fmoles/mg cytosol protein) concentrations of PgR were more frequently (6 out of 8 cases) detected during the secretory phase. No substantial difference was seen in ER and PgR values between anterior and posterior wall of the vagina. In postmenopausal patients the levels of ER (range: 10-83 fmoles/mg) were similar to those found in premenopause (range: 12-78 fmoles/mg). As regards PgR, the majority (14 out of 20) of vaginae were devoid of PgR, 4 had a very low (less than or equal to 6 fmoles/mg) PgR content and only 2 cases had a PgR level higher than 10 fmol/mg cytosol protein. In pregnant patients (6th to 8th week) ER were found in all vaginae, while PgR were present only in some cases (3 out of 8). It was concluded that the behavior of ER in the human vagina seems different from that in the human endometrium, since ER levels do not vary in relation to changes in the concentrations of sexual hormones in the circulation. On the contrary, PgR levels appear to depend on blood estradiol and progesterone concentration, as in other target tissues.

Adult↗

PubMed1985

Effects of medroxyprogesterone acetate on DMBA-induced mammary tumors.

Rats with DMBA-induced mammary tumors were treated for 30 days i.m. with medroxyprogesterone acetate (MPA) at doses of 7.5, 15 or 75 mg/kg. Complete regression (disappearance of tumor) was observed in 60% and 20% of tumors from rats treated with 75 or 15 mg/kg MPA respectively. Partial regression (50% decrease in tumor area) was found in the remaining 20% of tumors from rats treated with 15 mg/kg MPA. The dose of 7.5 mg/kg MPA resulted in being devoid of effectiveness. Estrogen receptor (ER) levels were significantly reduced at all doses of MPA injected both in responsive and non-responsive tumors. However, only tumors with ER levels above 15 fmol/mg before therapy resulted in being responsive to MPA treatment. Progesterone receptors were so reduced at the end of the experiment as to not be detectable in all treated groups. It was concluded that MPA is effective as an antitumoral drug also in DMBA-induced mammary tumors and that this effect is at least in part related to ER levels before treatment.

9,10-Dimethyl-1,2-benzanthracene↗