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Biomedical subjects

R Covello

Publications and source records attributed to R Covello.

10 recordsLinked to original sources
PubMed2002

[Benign metastasizing pulmonary leiomyoma: description of a case and review of the literature].

We report the case of a 48-year-old woman with multiple benign metastasizing leiomyomas in both lungs and a single retroperitoneal leiomyoma. The patient underwent surgical resection of the lesions 15 years after total hysterectomy for uterine myomas. Immunohistochemical studies performed on the retroperitoneal and pulmonary neoplasms showed them to be of mesenchymal derivation with smooth muscle differentiation; the samples were negative for HMB-45. Some histogenetic hypotheses for the multiple leiomyomas are presented.

Antigens, Neoplasm↗
PubMed1998

Uterine diffuse adenomatoid tumor. Does it represent a different biological entity?

Adenomatoid tumor represents a type of mesothelioma apparently confined to the genital tract and characterized by its benign behavior. Its morphological aspects are well known and, until now, it has been described as a nodular mass except for a case diffusely infiltrating the entire myometrium in an immunosuppressed patient. We report a case of benign mesothelial tumor characterized by histological, immunophenotypical and ultrastructural features of an otherwise typical adenomatoid tumor but diffusely growing below uterine serosal surface into the myometrium without discernible borders. The existence of a diffuse type of adenomatoid tumor might reflect a different nature of this neoplasm leading to the hypothesis that this variant of benign mesothelioma represents a distinct biological entity.

Adenomatoid Tumor↗
PubMed1997

Langerhans cell histiocytosis of vulva and cervix in a 19-year-old woman.

Langerhans cell histiocytosis of the female genital tract is a rare disease. A clinical diagnosis is impossible to establish because no typical lesions are found. Immunohistochemistry of bioptic samples is the easier technique to obtain the correct diagnosis. We present a case of a 19-year-old woman with Langerhans cell histiocytosis of mandible and maxilla with subsequent cervical and vulvar histiocytosis.

Adult↗
PubMed1997

[A case of cellular neurothecoma].

The Authors report a case of cellular neurothecoma, a rare benign tumor of possible nerve sheath origin. Differential diagnosis with classic neurothecoma and malignant melanoma is discussed.

Adolescent↗
PubMed1995

Mutations of the growth hormone receptor in children with idiopathic short stature. The Growth Hormone Insensitivity Study Group.

BACKGROUND: Short stature in children who are not deficient in growth hormone (GH) is probably caused by a variety of defects. Some children with idiopathic short stature have low serum concentrations of GH-binding protein, which is derived from the GH receptor. The possibility that low serum concentrations of GH-binding protein might indicate partial insensitivity to GH led us to investigate possible defects in the gene for the GH receptor in children with idiopathic short stature and low serum concentrations of GH-binding protein. METHODS: We studied 14 children with idiopathic short stature who were selected on the basis of normal GH secretion and low serum concentrations of GH-binding protein. Analysis of single-strand conformation polymorphisms and DNA sequencing were both used to identify mutations in the GH-receptor gene. RESULTS: Mutations in the region of the GH-receptor gene that codes for the extracellular domain of the receptor were found in 4 of the 14 children, but in none of 24 normal subjects. One of the four children with mutations was a compound heterozygote, with one mutation that reduced the affinity of the receptor for GH and a second mutation that may affect a function other than ligand binding. The remaining three children had single mutations in one allele of the gene. One mutation introduced a premature termination codon, and two caused substitutions of single amino acids in a structurally conserved domain of the receptor. CONCLUSIONS: Some children with idiopathic short stature may have partial insensitivity to GH due to mutations in the GH-receptor gene.

Adolescent↗
PubMed1994

Localization of inhibin and activin binding sites in the testis during development by in situ ligand binding.

Inhibin and activin are related proteins thought to be potential paracrine regulators of testicular development and maintenance of spermatogenesis. Messenger RNA and proteins immunologically related to both factors have been identified in the adult testis. However, the role(s) of these factors in paracrine regulation of testicular function is poorly understood. To identify potential targets for inhibin and activin in immature and adult testis, we used in situ binding of [125I]-labeled ligands to localize and describe the distribution of binding sites for inhibin and activin in testes of 15-, 18-, 21-, 30-, 45-, and 60-day-old rats. Nonspecific binding was defined as that occurring in the presence of a 1000-fold excess of unlabeled recombinant human (rh) inhibin or activin. [125I]-Inhibin was found to bind to interstitial cells throughout development. Inhibin binding was shown to co-localize with cells that showed positive staining for 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). Competition studies demonstrated that this binding was indeed specific for inhibin. In contrast, [125I]-activin showed two distinct patterns of binding. First, [125I]-activin was shown to bind in a non-stage-dependent manner to cells located in the basal compartment of the seminiferous tubules in testis obtained from animals of all ages studied. Binding of [125I]-activin in the periphery of the tubule could be inhibited entirely by coincubation with excess unlabeled activin and partially with excess unlabeled inhibin. The ability of inhibin to compete with activin for binding appeared to be more pronounced in younger animals. In 45- and 60-day-old animals, a second stage-dependent component of [125I]-activin binding was also apparent. This binding was localized to spermatids found in stage VII-VIII tubules and was inhibited by the presence of excess activin, but not inhibin. These results indicate that inhibin can bind specifically to testicular interstitial cells throughout development and may be an important regulator of Leydig cell testosterone production or interstitial cell function. In contrast, activin appears to bind in a specific and stage-dependent manner to receptors or high-affinity binding proteins on spermatids as well as to sites on the periphery of all seminiferous tubules. These results support the hypothesis that both activin and inhibin may act at several levels to regulate proliferation or differentiation of germ and Sertoli cell function as well as to modulate interstitial cell activity.

3-Hydroxysteroid Dehydrogenases↗
PubMed1993

Pharmacokinetic profile of recombinant human (rh) inhibin A and activin A in the immature rat. II. Tissue distribution of [125I]rh-inhibin A and [125I]rh-activin A in immature female and male rats.

The tissue distribution of recombinant human inhibin A (rh-inhibin A) and rh-activin A was determined in immature female Sprague Dawley-derived rats after iv administration of radiolabeled proteins. [125I]rh-Inhibin A and [125I]rh-activin A diverge in their distribution to tissues of the immature female rat as examined histologically (whole body autoradiography and thin section analysis) and by computing the percent dose and tissue to blood ratios for individual tissues. [125I]rh-inhibin A accumulated in the spleen, adrenal, bone marrow, and ovary after iv injection. Iodinated rh-inhibin A was also found in the anterior and posterior pituitary. [125I]rh-activin A was found in the ovary and pituitary after iv injection. Little specific binding was found in the spleen or adrenal. The bone marrow accumulated some [125I]rh-activin A which was competed by rh-activin A. The primary route of excretion for radioactivity was the kidney, with the label appearing in the bladder by 10 min after iv injection. Not only do rh-inhibin A and rh-activin A have different pharmacokinetics, but fewer tissues accumulate radioactive rh-activin A than rh-inhibin A.

Activins↗
PubMedDate not supplied

[Clinical guidelines for the management of gastrointestinal stromal tumors].

Treatment of gastrointestinal stromal tumors (GIST) has been revolutioned by the recently discovered molecular mechanism responsible for the oncogenesis of this disease. In addition, due to the rapid progress at molecular and clinical level observed in the last few years, there is a need to review the current state of the art in order to delineate appropriate guidelines for the optimal management of these tumors. A panel of experts from several specialities, including medical oncology, surgery, pathology, molecular biology and imaging, were invited to participate in a meeting to present and discuss a number of pre-selected questions, and to achieve a consensus according to the categories of the National Comprehensive Cancer Network (NCCN) and the Standard Options Recommandations (SOR) of the French Federation of Cancer Centers. Generally, consensus points were from categories 2A of the NCCN and B2 of the SOR. Conventional histologic examination with immunohistochemistry for CD117, CD34, SMA, S-100 and desmin is considered standard. Molecular analysis for the identification of KIT and PDGFRA mutation may be indicated in CD117-negative GIST. Complete tumor resection with negative margins is the optimal surgical treatment. Adjuvant imatinib should be considered an experimental approach. Neoadjuvant imatinib is also experimental, although its use may be justified in unresectable or marginally resectable GIST. Imatinib should be started in metastatic or recurrent disease, and should be continued until progressive disease or drug intolerance. In these cases, sunitinib can be used. The optimal criteria for the assessment and monitoring of GIST undergoing imatinib therapy are not well known, but they should include reduction in tumor size and disease stabilization, as well as reduction of tumor density on CT scan and metabolic activity on PET scan.

Antineoplastic Agents↗