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

Fifty woman patients with adenoma or fibroadenoma, cystic, simple or complex dysplasias were treated with tamoxifen in daily doses of 20 mg. (2 tbs.) for 10 or 20 days during one or two menstrual cycles (in most cases 2 successive treatments) and uninterrupted for 30 or 90 days in menopaused women. A response was recorded in the main and associated lesions as well as in several similar lesions in the same case, and therefore, the results are analysed according to the lesion surface reduction in percentage. The different responses recorded can explain why the classification into responders and non-responders is difficult to make sometimes. 64% of the cases responded to the treatment. The results are most relevant if lesions are summed up and considered by type of lesion. Subjective symptoms disappeared or improved in 97% for mastodynia and 100% for dysmenorrhoea with a general decrease in menstrual bleeding. Short-term treatment of two tamoxifen cycles can be a means to select the responsive cases. They may be a preliminary stage before further endocrine treatment or before further surgery. This medicating pattern can solve some cases otherwise fit for surgery only.
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PMID:Short-term tamoxifen treatment in benign breast diseases. 404 17

In order to avoid secondary induction of estrogens caused by tamoxifen treatment, tamoxifen was associated with the progestative lynestrenol in 48 menstrual women with benign breast disease (adenoma or fibroadenoma, cystic, simple or complex dysplasia). In one variant tamoxifen dosage was 20 mg (2 tablets) daily taken orally from day 5 to day 25 of the menstrual cycle, associated with 10 mg (2 tablets) of lynestrenol daily, only during the last 15 days. In another variant the above mentioned drugs were given concomitantly from day 10 to 15 of the cycle (according to cycle length) for 10 days. The average duration of the treatment was 4 cycles. The results are analysed according to surface percentage reduction of the main and associated lesions within the same case. In all cases of simple dysplasia, in 78% of the cases with complex dysplasia and in 54% of the adenomas, the lesions decreased to less than half their initial size, and in some instances the lesions disappeared altogether and the breasts became normally soft. Breast pain was improved or disappeared altogether in 96% of the cases. Despite its positive results the associated treatment used should be applied only in certain cases, especially those diagnozed as complex dysplasia and only in those medical units that have adequate diagnosis and treatment follow-up facilities.
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PMID:Combined tamoxifen-lynestrenol treatment in benign breast disease. 408 4

We describe a 54-year-old woman presenting with mastalgia and a 6 mm breast lesion on imaging. Core biopsy revealed a lesion characterised by a predominant epithelioid and a minor spindle cell component. Our differential diagnosis included intraduct papilloma/adenoma and adenomyoepithelioma. However, initial immunohistochemistry did not support these diagnoses and further immunohistochemistry raised the possibility of a synovial sarcoma. This was confirmed with the finding, using fluorescence in-situ hybridisation, of the characteristic translocation t(x; 18) (p11.2; q11.2). Establishing a diagnosis of synovial sarcoma at unusual sites may be difficult, especially when limited tissue is available, for example, within a core biopsy. In this case, immunohistochemistry was useful, but cytogenetics was the key additional investigation. It is important to consider the possibility of rare tumours when the morphological and immunohistochemical features of a lesion initially appear conflicting or inconclusive.
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PMID:An unusual breast mass: primary synovial sarcoma. 2378 72

Primary bilateral macronodular adrenocortical hyperplasia (PBMAH) is an uncommon cause of adrenal Cushing syndrome (CS) in which cortisol and occasionally other steroid hormones can be secreted under the influence of aberrantly expressed G-protein coupled receptors (GPCRs) in the adrenal cortex. We describe the unique case of a 64-year-old postmenopausal female with PBMAH whose adrenal lesions expressed luteinizing hormone receptors (LHr). She presented initially with CS and underwent right adrenalectomy; a few years later she presented with macromastia and mastodynia, possibly due to estrogen excess from her remaining left adrenocortical masses. Testing before and after treatment with quarterly leuprolide acetate therapy and immunohistochemistry on tissue and targeted sequencing of the genes of interest were performed. Tissue from the patient's right adrenal was tested for P450 aromatase (CYP19A1) and LHr expression; both were expressed throughout the hyperplastic cortex, although expression was more intense in the adenomatous areas. Targeted sequencing revealed a pathogenic PDE11A mutation, as well as variants in the ARMC5 and INHA genes. PDE11A expression was decreased in the adenoma but there was no loss of heterozygosity for the PDE11A locus. Because of the clinical presentation and LHr expression, quarterly leuprolide acetate therapy was started. Shortly after initiation of therapy, the patient reported decreased breast size and pain; she remains well controlled to date, after 10 years of treatment. This is the first description of a patient with PBMAH presenting with severe macromastia and mastodynia from what appears to be excess estrogen production from her adrenal tumor. The patient had a long-lasting response to chronic leuprolide acetate treatment, showing that drug therapy exploiting the aberrant receptor expression in PBMAH is possible even in the absence of cortisol overproduction.
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PMID:Successful Treatment of Estrogen Excess in Primary Bilateral Macronodular Adrenocortical Hyperplasia with Leuprolide Acetate. 2918 89