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Biomedical subjects

C Lombardo

Publications and source records attributed to C Lombardo.

83 records · Page 5Linked to original sources

[Immunobiology of vesicular mole and choriocarcinoma].

Molar tissue expresses HLA antigens evidenced in the father. These antigens are present on the trophoblastic extravillous tissue, not on the syncytium and cytotrophoblast. These antigens show some characteristics of Qa murine antigens mapped in the HLA system linked to class I antigens. Antibodies anti HLA against the partner antigens and lymphocytotoxic antibodies have been evidenced in the serum of patients with vesicular mole. In vesicular mole the production of antibodies should be determined by the immunogenicity of cells that infiltrate the decidua, expressing paternal HLA antigens. It has been demonstrated that the recognition of "not self" antigens in the mother should stimulate a cellular immune response. We do not know why the tumor grows. Maybe the woman is not able to produce anti HLA antibodies although recognizes them as "not self", or the patients is not antigenically stimulated because there is immunocompatibility between the two partners. The literature shows that the development and progression of the disease are stimulated by histocompatibility, although this factors does not seem fundamental. If the two partners are histocompatible the tumor can be less immunogenic, so the mother shows a lower response and the growth of the tumor appears to be favoured.

Choriocarcinoma↗

[Abdominal-scrotal hydrocele: a report of 4 cases and a review of the literature].

The authors report on four cases of abdomino-scrotal hydroceles treated in the last 5 years. They review the literature that produces 29 cases in the pediatric age and they examine the etiopathogenesis, the diagnosis and the therapy. The clinical examination and the ultrasound are without any doubt the easier, not invasive and more adequate surveys for the diagnosis. Surgery is the treatment of choice: hydrocelectomy by inguinal approach.

Abdomen↗

Pattern of mucin gene expression in normal and neoplastic lung tissues.

This work evaluates the expression in lung cancer of the most well characterized mucin genes (MUC1, MUC2, MUC3) and of the recently described MUC4 in lung tissues, to check a correlation between the expression of any particular gene and this tumor. Hybridization with synthetic oligonucleotides obtained from a part of the sequences of MUC1, MUC2, MUC3 and MUC4, was performed on blotted RNA from 18 lung cancer tissue specimens and from 10 normal tissues samples taken, when possible, from the normal lung counterpart. By means of Northern blot analysis MUC1 revealed to be the most expressed mucin gene in lung cancer, followed by MUC4; by contrast, the expression of MUC2 and MUC3 was almost undetectable in all cancer specimens. The intensity of expression of MUC1 and MUC4 was always superior in cancer tissue than in the normal counterpart. As expected, the highest reactivity for MUC1 and MUC4 expression was observed mainly in the adenocarcinoma histotype which is mucin secreting. These findings represent a contribution to the study of mucin gene pattern in lung cancer, and, in particular, indicate that MUC4, in association with the MUC1 gene, seems to be strongly expressed in this neoplastic disease.

Base Sequence↗

Effects of steroid-free fetal serum and steroid supplementation on MUC1 gene expression in human breast cancer cell line MCF7.

MUC1 is a gene expressed by many normal epithelial tissues and aberrantly expressed by carcinomas. Studies regarding the expression of MUC1 in endometrial tissues and the constitution of its promoter region suggest a possible role for hormonal regulation of this gene. The aim of the present work was to evaluate the regulation of MUC 1 expression by 17 beta-estradiol (E2), progesterone (Pg) and by steroid-free fetal calf serum (FCS) in the hormone-sensitive cell line MCF7. MUC1 mRNA proved to be detectable by means of Northern-blot analysis in MCF7 cells, and its levels were strongly increased in cells grown with 10% steroid-free FCS. By contrast, the steady-state MUC1 mRNA levels of steroid-supplemented cells did not change compared to those of unsupplemented cells (controls). In conclusion, MUC1 expression is regulated by substances present in the steroid-stripped FCS (growth factors, e.g. Insulin-like Growth Factor). The lack of any observed MUC1 modulation by steroids could be due to: a) a low FCS concentration preventing the manifestation (permissive action) of possible gene regulation; b) an immediate stimulatory effect occuring in the first phases of the treatment, which could subsequently be lost.

Breast Neoplasms↗

Weekly epidoxorubicin therapy in hormone-refractory metastatic prostate cancer.

In a pilot trial, we treated thirty-three hormone resistant metastatic prostate cancer patients with a combination of androgen blockade plus weekly cytotoxic therapy and determined both response and toxicity in 32 of them. Their median Karnofsky performance status at the time of entry was 65. We administered Epidoxorubicin (EpiDx) intravenously, at a dose of 35 mg/m2, every week for 4 months. Initially, all patients had only hormonal therapy and chemotherapy was added once they progressed. In terms of W.H.O. criteria, 9 patients (28%) had a partial response, the disease was stable in 14 (44%), and progressive in 9 (28%); even in this last group, 6 patients with bone metastases experienced lasting relief from pain. No patients had to interrupt treatment due to leukopenia or cardiotoxicity. Other toxicities, including nausea and vomiting, mucositis and alopecia, were mild. Pretreatment prostate-specific antigen (PSA) levels decreased significantly (p < 0.05) in 26 patients (81%) after treatment. In our view, weekly EpiDx administration serves as an active regimen in hormone-refractory prostate cancer.

Adenocarcinoma↗

[Central dopaminergic D1 agonists and treatment of Parkinson disease].

Many theories about dopaminergic function in Parkinson's disease are based upon the effects of the D2 receptor. Standard treatments mostly involve dopaminergic D2 agonists. However, the recent development of dopaminergic D1 agonists should help to clarify the role of the D1 receptor in the treatment of Parkinson's disease. The authors review the physiopathological, behavioural and therapeutic data on D1 agonists administered in animal models and in patients.

Animals↗