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Biomedical subjects

G Fontanini

Publications and source records attributed to G Fontanini.

85 records · Page 5Linked to original sources
PubMed1990

Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts.

Here we report that the slow-transforming helper component of Friend murine leukaemia virus (Fr-MLV), which produces lymphoid leukaemias in normal mice, induces erythroleukaemia in mice given syngeneic pituitary grafts (SPG). Newborn mice were infected with Fr-MLV and, at one month of age, were transplanted with two pituitary glands under the kidney capsule. Sham-operated infected mice and uninfected transplanted mice served as controls. SPG selectively reduced the mean survival times of infected mice. Histopathology showed that, while most infected non-transplanted mice developed lymphoid leukaemias, virtually all Fr-MLF-infected mice given SPG developed erythroleukaemias. Experiments in vitro showed that Fr-MLV infection markedly depressed concanavalin A induced DNA synthesis in cells from spleen, thymus and lymph nodes. Addition of prolactin or growth hormone further suppressed lectin-induced mitogenesis of lymphoid cells from infected mice, but failed to influence the response of uninfected controls. These experiments indicate that, in mice, pituitary hormones modulate the development and the histological features of Fr-MLV induced leukaemias, and suggest that endocrine-immunological interactions play a role in retrovirus induced tumorigenesis.

Animals↗
PubMed1988

Differences in progression of BALB/cfRIII and BALB/cfC3H mammary hyperplastic alveolar nodules transplanted into the gland-free fat pads of BALB/c mice.

In BALB/cfC3H and BALB/cfRIII virgin female mice, i.e., BALB/c mice carrying milk-transmitted C3H and those carrying RIII murine mammary tumor virus infection, respectively, mammary noduligenesis and tumorigenesis are remarkably different. Focal hyperplastic alveolar changes or hyperplastic alveolar nodules were removed from BALB/cfRIII or BALB/cfC3H breeding female donors and transplanted into the gland-free mammary fat pads of syngeneic BALB/c virgin female recipients with or without hormonal supplementation. The results obtained have shown significant differences in: (a) the morphological type of outgrowths; (b) the incidence of malignant transformations; and (c) the hormonal responsiveness of the tumors arisen after pituitary transplants.

Adipose Tissue↗
PubMed1987

Lung colonization and metastasis of murine mammary tumors: relationship to various characteristics of the primary tumors.

The ability to metastasize via the bloodstream of mammary tumors occurring in Balb/cfC3H and Balb/cfRIII mice (two substrains of identical Balb/c genotype carrying milk-transmitted C3H or RIII murine mammary tumor virus (MuMTV) infection, respectively) has been compared in MuMTV-free Balb/c virgin female recipients given intravenous tumor cell suspensions or subcutaneous solid tumor transplants from mammary tumor-bearing Balb/cfC3H and Balb/cfRIII breeding female donors. Tumor cell suspensions different for MuMTV inducing variant, growth rate, tumor size, and clinical duration, injected intravenously to Balb/c virgin female recipients, have been compared with respect to the foci of lung colonization induced in recipient hosts. The results obtained indicate that MuMTV variant, growth rate and clinical duration of the primary mammary tumor, but not the size of the primary tumor, significantly influence the lung colonization. Similar results were obtained with solid subcutaneous transplants of the same mammary tumors. The significance of these results for the understanding of the general mechanisms of tumor metastases is discussed.

Animals↗
PubMed1986

Reciprocal interference between milk-transmitted mammary tumor virus and Friend leukemia viruses in mice: possible role of the interferon system.

We have previously shown that mice simultaneously infected with the murine mammary tumor virus (MuMTV) and with certain slow murine leukemia viruses (MLV) have an increased resistance to the pathological effects of both agents. Here we report that milk-transmitted MuMTV also delays the development of the acute erythroleukemia induced by Friend leukemia virus (FLV), and retards, or prevents in some cases, the development of long-term lymphomas caused by its helper component. This is confirmed by the observation that the average life span of MuMTV-carrying mice infected with FLV or its helper component is prolonged by over 30% as compared to that of MuMTV-free animals infected with the same agents and by the finding that the replication of Friend viruses is reduced in mice neonatally exposed to MuMTV. Since the antibody responses of mice to MuMTV and to FLV were not cross-reactive, we searched for antiviral activity in the tissues of mice exposed to MuMTV, FLV, or the helper component of FLV. Low levels of interferon-alpha/beta were consistently detected in spleen extracts from mice infected with all these agents but could not be demonstrated in the spleens of uninfected BALB/c mice; thus, the chronic production of endogenous interferon is likely to play a major role in the reciprocal interference in vivo between retroviruses belonging to different genera.

Animals↗
PubMed1985

Morphology and progression of preneoplastic changes in methylcholanthrene-induced mouse mammary tumorigenesis.

Susceptible BALB/c virgin female mice were treated with 3-methylcholanthrene in almond oil (0.5%) by skin painting and killed at monthly intervals. The mammary glands were prepared as whole mounts for stereoscopic study of the glandular tree with removal of any focal change for histology. The results showed a marked disarrangement in the architecture of the glandular tree, a prevalent ductal tree, and an overcrowding of ducts. Focal hyperplastic changes were frequently observed, including hyperplastic alveolar nodules, hyperplastic ductal nodules, noduloids and intraductal epithelial growths, and their respective rates of malignant transformation observed at histology were 22%, 15%, 7% and 50%. Data suggest a different weight of these preneoplastic changes as sources of malignant transformation and a prevalent ductal origin of the methylcholanthrene-induced neoplasms.

Animals↗
PubMed1984

Factors that affect metastasis in virus-induced mouse mammary tumors.

Two hundred and forty-one mammary tumor-bearing breeding female mice of the BALB/cf C3H and BALB/ cfRIII strains, carrying milk-transmitted murine mammary tumor virus (MuMTV) of C3H and RIII origin, respectively, were studied to evaluate the factors that affect tumor metastasis. Only lung metastases were considered and the following factors taken in account: MuMTV inducing variant (C3H, RIII), number of deliveries, tumor histotype , number of tumors per mouse, clinical duration of tumors, tumor size, and tumor growth rate. Only the number of deliveries, the tumor size and the number of tumors per mouse were found to significantly influence the rate of metastasis. The tumor growth rate affects concurrently with tumor size the metastatic process. In fact, the larger the tumor the higher the tumor growth rate. This direct relationship is significant (P less than 0.01) and, in case of lung metastases at autopsy, there was a prevalence of large tumors (greater than 2 cm) and high growth rate (greater than 0.3 mm/day). The discordance of these data with those concerning mammary tumor metastasis in virgin females of the same two strains, the enhancing effect of pregnancies on metastatic spread of tumors, and the significance of results for the understanding of the general mechanisms of tumor metastasis are discussed.

Animals↗
PubMedDate not supplied

Modulation of neoangiogenesis in bronchial preneoplastic lesions.

We have previously demonstrated that vascular count significantly increases in the preneoplastic lesions of the bronchial tree, starting from very low levels in the normal epithelium to a significantly higher number of microvessels in moderate dysplastic lesions and in situ carcinomas. Vascular endothelial growth factor (VEGF) protein expression has shown to be strictly associated with neovascularization both in human cancer and in various type of preinvasive lesions. A number of studies have demonstrated that mutant p53 is involved in the regulation of angiogenesis, and immunohistochemical detection of the p53 protein is associated with p53 gene mutations. In this study we looked for possible correlation between p53 protein detection, VEGF expression and vascular count in a series of preneoplastic and neoplastic lesions of the bronchial tree in order to investigate the angiogenic pattern and its genetic control in the early steps of bronchial cancer development. Twenty-four retrospective bronchial lesions with different grades of dysplasia and a case of normal bronchial epithelium were analysed. Surgical specimens removed from patients either confirmed, or suspect for lung carcinoma were stained immunohistochemically for CD34, VEGF, and p53. There were significant increases in microvascular density (MVD), VEGF, and p53 expression from normal bronchial epithelium through moderate dysplasia to in situ carcinoma to invasive cancer and these factors were significantly associated with moderate dysplastic lesions. A statistically significant difference was observed in MVD between hyperplastic-metaplastic, moderate dysplastic lesions and in situ carcinoma. A similar pattern was also observed for VEGF and p53 protein expression but no significant difference was observed between moderate dysplastic lesions and in situ carcinoma with regard to VEGF protein expression. The association between MVD, VEGF expression, p53 mutations and preinvasive lesions of the bronchial tree suggests that neoangiogenesis is early in non-small cell lung cancer (NSCLC) development and that p53 may have an important role in promoting angiogenesis in this human model of carcinogenesis.

Bronchi↗
PubMedDate not supplied

Neoangiogenesis in colon cancer: correlation between vascular density, vascular endothelial growth factor (VEGF) and p53 protein expression.

Angiogenesis is an essential requirement for the development, progression and metastasis of malignant tumors. Vascular endothelial growth factor (VEGF) plays an essential role in the development of angiogenesis of numerous solid malignancies, including colon cancer. The tumor suppressor gene p53 is a potent transcriptional regulator of genes which are involved in many cellular activities, including cell-cycle arrest, apoptosis and angiogenesis. In order to better understand the relation among p53 status, VEGF expression and microvessels count (MVC) in colon cancer, we evaluated immunoreactivity for CD34 endothelium-associated antigen, VEGF and p53 proteins in 43 cases of colon adenocarcinoma. Our results demonstrated an association between VEGF expression, p53 status and angiogenesis, suggesting that mutant p53 plays a central role in promoting angiogenesis in colon cancer progression.

Aged↗
PubMedDate not supplied

Inclusion body myopathy associated with motor neuron syndrome: three case reports.

BACKGROUND: Hereditary inclusion body myopathy (h-IBM) is an autosomal-recessive or autosomal-dominant hereditary disease characterized by peculiar findings in muscle biopsies which resemble those occurring in inclusion body myositis (IBM). The absence of an inflammatory infiltrate in myofibers in h-IBM is a relevant differential criterion between the two pathologies. Motor neuron diseases (MND) represent a group of disorders involving both upper and lower motor neurons, characterized by fasciculations, progressive muscle weakness, and muscle atrophy. The most common form and prototype of MND is the amyotrophic lateral sclerosis (ALS) or Charcot's Disease, a progressive and fatal neurodegenerative disorder occurring in late adulthood. The pathogenesis of ALS remains still unknown, a variety of hypotheses having been proposed to account for the disease. The association of both pathologies is not common and offers new hypotheses about the pathogenic mechanisms in skeletal muscle and nervous system degeneration. PATIENTS AND METHODS: Described are three case reports in which we observed the clinical, laboratory and histopathological association of IBM and MND. In one case, dementia was also present. Muscle data was obtained by muscle biopsies and immunohistochemistry, while diagnosis of MND was supported by common neurophysiological techniques. RESULTS: The accumulation ofphosphorylated neurofilaments with a hereditary IBM-like pattern in skeletal muscle fibers without accumulation of amyloid-beta protein was observed. CONCLUSIONS: A better knowledge of the mechanisms in cellular death cascade could explain the pathogenesis of these different degenerative disorders.

Aged↗
PubMedDate not supplied

[A case of tuberous sclerosis: anatomo-pathologic description].

The authors describe the simultaneous presence of renal and pulmonary hamartomas occurring in a young man affected by tuberous sclerosis. The clinical diagnosis was based on the characteristic symptoms of epilepsy, adenoma sebaceum and mental retardation. These symptoms began at the age of four and were mostly characterized by epilepsy and adenoma sebaceum. The mental retardation was slight. The anatomopathological findings at death refer the presence of encephalic, renal and pulmonary lesions; the later are very rare.

Adult↗
PubMedDate not supplied

p53 expression in non small cell lung cancer: clinical and biological correlations.

p53 is a tumor suppressor gene, located in the short arm of chromosome 17, which encodes for a nuclear protein involved in the control of cellular growth. Mutations in p53 gene are the most common genetic alterations in a several human cancers, including Non Small Cell Lung Cancer (NSCLC). However, up to now, the role of p53 in the tumour's behaviour and its progression has not been completely clear. We performed immunohistochemical staining for mutated p53 using two monoclonal antibodies, PAb1801 and PAb240, in fresh tumour specimens from 103 consecutive patients who underwent surgery for resectable NSCLC. PAb1801 detects both the normal and mutant form of p53, while PAb240 is specific only for the mutant form and recognizes a denaturation-resistant epitope located between aminoacids 156-335. Both antibodies showed a mainly nuclear staining in neoplastic cells but not in surrounding uninvolved lung tissues. 68 out of 100 (68%) and 37 out of 103 (35.9%) of the cases were positive with PAb1801 and with PAb240, respectively. Tumours from patients with hilar-mediastinal lymph node involvement showed a higher p53 expression, detected by PAb1801, than those without nodal metastases (p = 0.04). Moreover, tumours expressing more than 60% of positive cells with both antibodies showed a significant increase of nodal involvement (p = 0.1; p = 0.03). Furthermore, p53 expression was significantly related to post-surgical stage (p Tumor Stage) (p = 0.04). In addition, we did not find any correlation between p53 expression and proliferating activity evaluated by PCNA, Ki-67 and DNA flow cytometric cell cycle. In conclusion, the evaluation of p53 oncogene expression may identify individuals whose resectable NSCLCs have a more aggressive tumour behaviour.

Antigens, Neoplasm↗
PubMedDate not supplied

Determination of angiogenesis in human neoplasms: current prognostic and therapeutic implications.

The growth of solid tumours beyond a certain mass is strictly dependent on the formation of a vascular bed from a pre-existing host vasculature. This process has been termed OangiogenesisO and its importance in the process of tumour growth and metastasis has recently gained wide acceptance. Studies have been reported in several kinds of human cancers in which the number of microvessels in the most intense areas of neo-vascularisation (Ohot spotsO) have been shown to be strictly related to the development and progression of the tumour. In the majority of these studies highly vascularised tumours showed a poor prognosis and the influence of tumour angiogenesis proved to be independent of conventional prognostic indicators. The evaluation of tumour angiogenesis by quantitative pathology may represent an important prognostic indicator in human cancers and will be increasingly important in the investigation of new therapies directed to inhibiting angiogenesis or targeting tumour vasculature. This review will briefly summarise the current knowledge on the prognostic impact of tumour angiogenesis in human cancers with a final reference to angiogenesis inhibitors which are currently used in phase I/II and III clinical trials.

Antineoplastic Agents↗