Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Report is made of a mature retroperitoneal teratoma in a 32-year-old man. Investigation of the tumor revealed cells immunoreactive for ACTH, Met-enkephalin, beta-LPH, serotonin, FSH, BPP, S100, Neuron-specific-enolase. These cells were mainly present in the glandular epithelium, lining the cysts of the tumor. Ultrastructurally, neuro-secretory granules were demonstrated in the cytoplasm of the tumoral endocrine cells. At no time did the patient display endocrine symptoms.
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PMID:Immunocytochemical and ultrastructural findings in a mature retroperitoneal teratoma. 283 Jun 4

A 24-year-old woman with severe Cushing's syndrome was found to have corticotroph cell pituitary adenoma arising within a benign cystic ovarian teratoma. The patient manifested sustained hypercortisolemia and lack of suppression of either adrenocorticotropin (ACTH) or cortisol production. There was no evidence of a pituitary mass or secretion of other hormones. After careful clinical evaluation, no other tumor masses were found. Resection of the ovarian tumor led to normalization of ACTH and cortisol levels. Densely granulated corticotroph tumor cells with prominent Type I microfilaments and intracytoplasmic ACTH immunoreactivity characterized the neoplasm as a pituitary corticotroph cell adenoma. This is, to our knowledge, the first case reported of a functioning pituitary adenoma arising within a benign cystic teratoma.
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PMID:Corticotroph cell pituitary adenoma within an ovarian teratoma. A new cause of Cushing's syndrome. 354 46

A 22-year-old black woman presented with symptoms suggestive of Cushing's syndrome three years after chemotherapy for a presumed teratoma with cervical lymphadenopathy. Initially, the absence of clinical signs and the demonstration of two normal 24 h urinary free cortisols appeared to exclude the diagnosis, but an ectopic adrenocorticotropin-producing thymic carcinoid was subsequently removed surgically. Cushing's syndrome due to ectopic adrenocorticotropin production can be difficult to diagnose, particularly if there is periodic hormonogenesis.
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PMID:Diagnostic difficulties in periodic Cushing's syndrome. 933 31

Several different in vivo and in vitro bioassays are used to evaluate melanosome transfer efficacy from melanocytes to keratinocytes. However, these methods are complicated and time consuming. Here, we report on a simple, rapid, direct, and reliable in vitro method for observing the process of melanosome transfer from melanocytes to keratinocytes. First, we selected and tested a melanoma cell line RPMI-7951 that can normally synthesize melanin and transfer from mature melanosomes to keratinocytes in vitro. We cocultured these cells with a human ovarian teratoma transformed epidermal carcinoma cell line, which is also capable of accepting melanosomes transferred from melanocytes, as in normal keratinocytes. The cells were cocultured for 24-72 h and double labeled with FITC-conjugated antibody against the melanosome-associated protein TRP-1, and with Cy5-conjugated antibody against the keratinocyte-specific marker keratin 14. The cells were examined by fluorescence microscope and flow cytometry. Melanosome transfer from melanocytes to keratinocytes increased in a time-dependent manner. To verify the accessibility of this method, the melanosome transfer inhibitor, a serine protease inhibitor, 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, and a melanosome transfer stimulator, alpha-melanocyte-stimulating hormone, were added. The serine protease inhibitor decreased melanosome transfer, and alpha-melanocyte-stimulating hormone increased melanosome transfer, in a dose-dependent manner. In conclusion, this is a simple, rapid, and effective model system to quantify the melanosome transfer efficacy from melanocytes to keratinocytes in vitro.
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PMID:A method for quantifying melanosome transfer efficacy from melanocytes to keratinocytes in vitro. 1870 35

A 46-year-old woman with Cushing's syndrome secondary to ectopic adrenocorticotropic hormone (ACTH) secretion caused by primary ovarian mature teratoma with carcinoid components was presented in our case. The patient manifested sustained hypercortisolemia without circadian rhythm and a lack of suppression of either low-dose dexamethasone suppression test (LDDST) or high-dose dexamethasone suppression test (HDDST). There was no evidence of a pituitary mass or secretion of other hormones. After careful clinical evaluation, no other tumor masses were found. Resection of the ovarian tumors led to sharp reduction of serum ACTH and cortisol concentrations. Immunohistochemistry showed positivity in CgA, Syn, CK, NSE. To the best of our knowledge, there are rare reports of an ACTH-secreting carcinoid components located in an ovarian mature teratoma, and bilateral ovarian mature teratoma makes it rarer.
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PMID:Cushing's syndrome secondary to ectopic ACTH secretion from carcinoid tumor within an ovarian mature teratoma: a case report and review of the literature. 2439 95

An immature ovarian teratoma containing adenohypophyseal tissue with a central arteriole and interpositioned in mature neural tissue is reported in an asymptomatic 31 -year-old woman. The tumor was a grade 2 immature teratoma according to the modified ThurlbeckScully histological grading system. Immunocytochemistry showed positive staining for growth hormone, prolactin, adrenocorticotropin, and alpha-subunit human chorionic gonodotropin and negative staining for thyroid-stimulating, follicle-stimulating, and luteinizing hormones in the adenohypophysis. The absence of staining for growth-hormonereleasing and corticotropin-releasing hormones, somatostatin, vasopressin, and neurophysin in adjacent tissue is consistent with the view that adenohypophyseal development is independent of the influence of these peptides.
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PMID:Adenohypophyseal tissue in an immature teratoma of the human ovary. 3213 49