Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytoplasmic androgen receptor content was determined in 26 patients with benign prostatic hyperplasia using methyltrienolone (R 1881) as the radioactive ligand. Their concentrations were compared with patient age, adenoma weight, and total circulating concentrations of testosterone, 17 beta-estradiol (17 beta-E2), androstenedione (A) and dehydroepiandrosterone sulfate (DHEA-S). Statistically significant inverse correlations were noted between adenoma weight and receptor content (p less than 0.05) and significant direct correlations between DHEA-S and receptor concentration (p less than 0.05), although the levels of this androgen were similar to those observed in a 'normal' population of the same age. The possible implications of these findings relative to the pathogenesis of the disease are discussed.
 ...
PMID:Relations between circulating levels of testosterone, 17 beta-estradiol, androstenedione, dehydroepiandrosterone sulfate, and androgenic receptor content of cytosol in benign prostatic hyperplasia. 618 74

At the age of 18, our patient was diagnosed as complete androgen insensitivity syndrome(AIS) based on androgen receptor studies in cultured genital skin fibroblasts. Compatible with this diagnosis, both testosterone and LH levels in her plasma were elevated as compared to levels in normal females. Later, the patient had been uneventful until she sought medical attention for headache at the age of 38. Magnetic resonance imaging (MRI) of the brain pointed to pituitary apoplexy. Since her symptoms were not alleviated by conservative therapy, neurosurgical decompression via a transsphenoidal approach was performed. A histopathological examination of a surgical specimen revealed that the pituitary hemorrhage occurred in an LH-producing adenoma. It is likely that the adenoma developed from gonadotroph hyperplasia which could exist in the AIS pituitary. It may be worth noting that this patient has never had a chance of receiving hormonal replacement therapy with estrogen and progesterone. Considering the fact that the majority of AIS patients are treated with gonadal steroids and such a treatment reestablishes an appropriate negative feedback on enhanced LH secretion, it is possible that the lack of hormonal therapy in our patient may have served as a precipitating factor for the apoplectic episode. Although we are not aware of any documented case report of pituitary apoplexy developed in AIS, such a pituitary emergency should be born in mind in the long-term follow-up of patients with AIS. In addition, it is also suggested that the hormonal replacement therapy with gonadal steroids may be recommended for AIS patients not only to endow them with physical characteristics as a woman but also to prevent the development of gonadotroph hyperplasia and possibly also of LH-producing adenoma in the pituitary.
 ...
PMID:Pituitary apoplexy developed in a patient with androgen insensitivity syndrome. 936 55

Solitary follicular nodules of the thyroid occasionally create a diagnostic problem, especially in the differential diagnosis between adenoma and nodular hyperplasia To obtain confident histologic parameters of clonal lesions, we analyzed DNA samples prepared from paraffin-embedded archival tissue from 20 solitary follicular nodules of the thyroid for clonality with the polymerase chain reaction (PCR) method. On the base of X chromosome inactivation mosaicism, we tested restriction fragment-length polymorphism of the phosphoglycerate kinase (PGK) gene and a highly polymorphic short tandem repeat of the human androgen receptor (HUMARA) gene. Of 18 informative cases, 10 were monoclonal, 7 were polyclonal, and 1 showed microsatellite instability. All of the five completely encapsulated nodules were monoclonal. Four of the five unencapsulated nodules showed polyclonality. Of the seven partially encapsulated nodules, four were monoclonal, and the others were polyclonal. The former showed 50% or more of encapsulation degree, whereas the latter showed less than 50%. The capsule tended to be thicker in monoclonal nodules (mean, 0.33 mm) than in polyclonal nodules (mean, 0.13 mm). Other histologic features of the nodules and surrounding parenchymal changes had no significance with respect to predicting clonality. This study suggests that the degree of encapsulation and capsular thickness are morphologically important for predicting the clonality of the thyroid nodule.
 ...
PMID:Clonal analysis of a solitary follicular nodule of the thyroid with the polymerase chain reaction method. 1010 11

Gestational and lactational exposure to di(n-butyl) phthalate (DBP) at >/=250 mg/kg/day disrupts male rat reproductive development and function. Although this indicates an antiandrogenic mechanism, DBP and its biologically active metabolite do not interact with the androgen receptor (AR) in vitro. In the present study, we compared the effects of DBP and the antiandrogen flutamide using a shorter exposure during the prenatal period of male sexual differentiation in rats. Pregnant CD rats received DBP at 0, 100, 250, or 500 mg/kg/day po (n = 10) or flutamide at 100 mg/kg/day po (n = 5) from Gestation Days 12 to 21. In F1 males, DBP (500 mg/kg/day) and flutamide caused hypospadias; cryptorchidism; agenesis of the prostate, epididymis, and vas deferens; degeneration of the seminiferous epithelium; and interstitial cell hyperplasia of the testis. Flutamide and DBP (250 and 500 mg/kg/day) also produced retained thoracic nipples and decreased anogenital distance. Interstitial cell adenoma occurred at 500 mg DBP/kg/day in two males. The only effect seen at 100 mg DBP/kg/day was delayed preputial separation. In contrast to flutamide, DBP caused a low incidence of prostate agenesis and hypospadias with no vaginal pouch. The low incidence of DBP-induced intraabdominal testes contrasted with the high incidence of inguinal testes seen with flutamide. Thus prenatal male sexual differentiation is a sensitive period for the reproductive toxicity of DBP. A no observed adverse effect level was not established and the lowest observed (adverse) effect level was 100 mg/kg/day. Flutamide and DBP disrupted the androgen signaling necessary for male sexual differentiation but with a different pattern of antiandrogenic effects. DBP is an example of an environmental antiandrogen that disrupts androgen-regulated male sexual differentiation without interacting directly with the AR, as does flutamide.
 ...
PMID:Disruption of androgen-regulated male reproductive development by di(n-butyl) phthalate during late gestation in rats is different from flutamide. 1103 75

Although androgen receptors have been identified in normal gonadotroph and somatotroph cells of the pituitary, immunohistochemical studies have failed to reveal these receptors in pituitary adenomas so far. Using a monoclonal antibody to androgen receptor in our series of 60 adenomas of the gonadotroph cell complex (20 FSH/LH cell adenomas, 20 null cell adenomas, 20 oncocytic adenomas), only one null cell adenoma showed strong nuclear immunostaining. All the other antibodies were completely negative. The significance of this finding in correlation with clinical data is still unclear, although it may be associated with more rapid tumor growth. In paraadenomous tissue, some normal gonadotrophs expressed the androgen receptor.
 ...
PMID:Androgen receptor in pituitary adenomas of the gonadotroph cell complex. 1118 73

The pituitary contains estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR). In accordance with immunocytochemistry, it is agreed that sex hormone receptors reside into the nucleus. All three receptors are found predominantly in gonadotrophs and lactotrophs, and less frequently in other cell types. ER plays a major role in prolactin (PRL) production and lactotroph proliferation, and protracted estrogen administration induces lactotroph hyperplasia and adenoma in rodents. Most research on PR and AR is focused on their role in the fine-tuning of gonadotropin secretion during estrous cycle. Contrary to the effect in nontumorous pituitary, estrogens can inhibit the proliferation of transplantable rat pituitary tumors and of cell lines derived from them. In humans, despite the presence of ER in all types of adenohypophysial tumors, the role of estrogen in tumor cell proliferation is still unclear. Few results indicate that tumor growth is stimulated by estrogen, and inhibited by progesterone and androgen. Novel data reveal that steroid hormones can act directly on plasma membrane or via other receptors, and interact with growth factors, oncogenes, and other transcription factors. The mechanisms by which steroid hormones control cell proliferation remain a major challenge for future research.
 ...
PMID:Pituitary Sex Steroid Receptors: Localization and Function. 1211 30

Benign conditions of the parathyroid gland have been classified as adenomas and hyperplasias. These entities however are difficult to distinguish when only a single gland is enlarged. Adenomas are defined as neoplastic clonal growths whereas hyperplasias are considered to be reactive processes of polyclonal origin. In order to analyze the clonal pattern of these lesions, we have studied hyperplasias and adenomas of parathyroid glands from women by the human androgen receptor (HUMARA) assay, a recently reliable and highly-lnformative technique based on the X-chromosome inactivation pattern in females. Samples consisted of formalin-fixed as well as frozen tissues. Informativeness with HUMARA marker was 87% (13/15 cases). All hyperplasias (5/5) and 6/8 adenomas yielded polyclonal results, since two alleles of similar intensity appeared when the lesion was HpaIl-digested. Two parathyroid adenomas had a loss of one X-alIeIe for the HUMARA gene and they were interpreted as monoclonal. These results show that parathyroid hyperplasias and adenomas, considered as multigland or monogland involvement diseases respectively, may be both polyclonal in origin, and that only a small subset of adenomas is found to be clonal. Consequently, clonality analysis cannot allow a clear distinction between these two entities as classically diagnosed. A different approach should be considering hyperplasia or adenoma when a polyclonal or monoclonal result has been obtained by clonality analysis.
 ...
PMID:Clonality Analysis of Benign Parathyroid Lesions by Human Androgen Receptor (HUMARA) Gene Assay. 1211 77

Malignant pituitary tumours are rare and their pathogenesis is not fully understood. We have performed genetic analyses on tissues arising from a pituitary carcinoma that initially presented as a silent corticotroph adenoma but which failed to respond to repeated, aggressive surgical and medical therapy. Loss of heterozygosity (LOH) of known or putative tumour suppressor genes (TSG) was assessed by microsatellite analysis of microdissected tumour and matched patient blood DNA. Clonality of the pituitary tumour samples was analysed by two PCR-based techniques; one employing the highly polymorphic short tandem repeat (STR) within the human androgen receptor allele (HUMARA), another based on a restriction fragment length polymorphism of the X chromosome phosphoglycerokinase (PGK-1) gene. Screening with 9 microsatellite markers demonstrated allelic loss at 3 sites (D1S190, D3S1283 and D10S297) in all tumour samples except the presenting pituitary tumour. X chromosome inactivation analysis demonstrated polyclonality in the original presenting tumour and a metastatic deposit but monoclonality in tissue samples from a second and third transsphenoidal resection. In these cases of tumour recurrence both LOH and X chromosome inactivation suggest that monoclonality arose from preferential clonal growth from the original polyclonal tumour. Polyclonality of the metastatic deposit suggests that this was derived from the presenting tumour, although the LOH pattern indicates that a single clone dominates. The data are consistent with increasing allelic loss associated with tumour dedifferentiation and malignant transformation.
 ...
PMID:Corticotroph carcinoma presenting as a silent corticotroph adenoma. 1467 23

An invasive micropapillary component has been described in tumors of several organs and is nearly always associated with aggressive biologic behavior. We present 14 cases of salivary duct carcinoma (SDC) with an invasive micropapillary component (invasive micropapillary SDC) and compare the clinicopathologic findings of these cases with those of cases of conventional SDC. The mean age of the 14 patients (10 men, 4 women) was 65.8 years (range, 26-80 years). The mean size of the tumors was 2.4 cm (range, 1.3-5 cm). The parotid gland was involved in 12 patients and the submandibular gland in 2. Histologically, all tumors had an invasive micropapillary architecture admixed with features typical for SDC. Invasive micropapillary carcinoma was characterized by morula-like small cell clusters without fibrovascular cores, surrounded by a clear space. Tumor cells exhibited moderate- to high-grade nuclear features, conspicuous nucleoli, and eosinophilic cytoplasm. This component was distributed diffusely in 9 tumors and focally in 5. Angiolymphatic and perineural invasion was seen in all tumors. A residual pleomorphic adenoma was detected in four tumors. Of the 12 tumors examined, all were diffusely positive for cytokeratin 7 and epithelial membrane antigen (with a distinctive "inside-out" pattern) but negative for cytokeratin 20. Tumors were frequently immunoreactive for BRST-2 (gross cystic disease fluid protein-15) and androgen receptor protein. Aberrant expression of HER-2/neu or p53 was detected in seven tumors each. The mean Ki-67 labeling index was 33.1% (range, 6.3%-61.6%). All 14 patients with invasive micropapillary SDC had cervical or periglandular lymph node metastasis, and this value was significantly higher than for conventional SDCs. Local recurrence developed in 4 patients and distant metastatic disease in 9. Clinical follow-up (mean, 25.5 months) was available for 13 patients: 9 died of disease within 24 months after the diagnosis (mean, 17.6 months), 1 was alive with metastatic disease at 19 months, and 3 were free of disease. Overall survival of these patients with invasive micropapillary SDC was significantly shorter than that of patients with conventional SDC (n = 49) in our series (P = 0.031). Our results suggest that invasive micropapillary SDC is a distinct, aggressive variant of SDC, with a propensity for extensive lymph node metastasis and rapid disease progression.
 ...
PMID:Invasive micropapillary salivary duct carcinoma: a distinct histologic variant with biologic significance. 1510 94

Primary salivary gland tumors resembling giant cell tumor of bone are very rare and have unsettled histogenesis. Both mesenchymal and epithelial origins have been suggested. We review 14 cases in the English-language literature and report another case, the first of which to be studied by microdissection-based microsatellite analysis. One-half of the tumors have been associated with a carcinoma, usually salivary duct carcinoma and carcinoma ex pleomorphic adenoma. Significant differences between this tumor and giant cell tumor of bone were observed. Unlike giant cell tumor of bone, in which the nuclei of the mononuclear and giant cells are similar, those of salivary gland show obvious differences between the nuclei of mononuclear cells and osteoclastic giant cells. In addition and in contrast to giant cell tumor of bone, the mononuclear cells of giant cell tumor of salivary gland express epithelial markers (epithelial membrane antigen, EMA; carcinoembryonic antigen, CEA) and androgen receptor. Genotypically, the microsatellite pattern of the giant cell component is more akin to the carcinomatous component and does not resemble giant cell tumor of bone. Biologically, giant cell tumor of salivary gland tends to be more aggressive than giant cell tumor of bone. We conclude that giant cell tumor of salivary gland is an unusual carcinoma that is not related to giant cell tumor of bone.
 ...
PMID:Osteoclast-type giant cell neoplasm of salivary gland. A microdissection-based comparative genotyping assay and literature review: extraskeletal "giant cell tumor of bone" or osteoclast-type giant cell "carcinoma"? 1522 68


1 2 3 Next >>