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Endocrine markers

Zembowicz and colleagues have described another primary cutaneous carcinoma with histologic features that are entirely dissimilar from PCNC namely, endocrine mucin-producing sweat gland carcinoma. That lesion histologically resembled mucinous carcinoma of the skin and was immunoreactive for estrogen and progesterone receptor proteins in addition to endocrine markers. [Pg.472]

DAs are typically negative for pancreatic enzymes such as trypsin, chymotrypsin, and lipase °76 unless there is a mixed acinar component, which is uncommon. They also fail to label with endocrine markers however, in 30% of DAs there are scattered, possibly non-neoplastic, endocrine cells in close association with the neoplastic cells, which can be highlighted with immunostains for chromogranin A, synaptophysin, and NSE.2 2 77-79 latter two markers can occasionally show more diffuse expression, which should not be regarded as evidence of neuroendocrine differentiation if the tumor is an otherwise conventional adenocarcinoma. [Pg.545]

The endocrine component shows immunoreactivity for chromogranin or synaptophysin > ° and, rarely, peptide hormones such as glucagon or somatostatin are expressed. In some cases of ACC, even the most typical acinar areas may show positivity with endocrine markers. Markers typically present in solid-pseudopapillary neoplasms (vimentin, CD56, and progesterone receptors) are negative. [Pg.554]

Pancreatic endocrine neoplasm versus ACC Scattered endocrine cells or a focal endocrine component are common in ACC however, diffuse and strong reactivity for the endocrine markers (chromogranin and synaptophysin) throughout the tumor is characteristic of PENs. Additionally, PENS do not show immunoreactivity for acinar markers. [Pg.554]

Nonspecific endocrine markers synaptophysin, CD56, and NSE are consistently positive in SPNs however, the most specific endocrine marker, chromogranin, is consistently negative in SPNs. [Pg.556]

Abrahamsson PA, Falkmer S, Fait K, Grimelius L. The course of neuroendocrine differentiation in prostatic carcinomas. An immunohistochemical study testing chromogranin A as an endocrine marker. Pathol Res Pract. 1989 185 373. [Pg.652]

Schulte-Oehlmann, U., Tilhnann, M., and Marker , B. et al. (2000). Effects of endocrine disrupters on prosobranch snails (Mollusca gastropoda) in the laboratory. Part II Triphenyltin as a xeno-androgen. Ecotoxicology 9, 399 12. [Pg.367]

WANGEN K E, DUNCAN A M, MERZ-DEMLOW B E, XU X, MARCUS R, PHIPPS W R, KURZER M S (2000) Effects of soy isoflavones on markers of bone turnover in premenopausal and postmenopausal women. J Clin Endocrin Metab 85(9), 3043-8. [Pg.106]

There is a recent clinical report by Emil Coeearo and colleagues that I think might be relevant to the kind of thing you have done in rats. They have been looking at endocrine responses to fenfluramine in humans as a marker of central serotonergic function. And they have observed an increase in serum prolactin concentration, which is felt to be due to serotonin release. They reported that, in subjects who received a seeond dose of fenfluramine within 12 days after the first dose, that there was a blunted response to serum prolactin. [Pg.155]

Patients must be monitored to assess their response to treatment and to detect recurrent diseases. PSA as a specific marker for prostate cancer is most useful in monitoring patients who have been treated with radical prostatectomy, radiation therapy, or endocrine therapy. The concentration of PSA falls to undetectable levels following a radical prostatectomy because all prostate tissue has been removed. Generally, PSA is measured at periodic intervals. In studies, the extent of disease at the time of surgery correlated well with the postoperative PSA concentration. A significant measurable PSA concentration after prostatectomy indicates that residual tumor may be present. PSA concentrations decline gradually after radiation therapy (36). [Pg.188]

Rotchell JM, Ostrander GK (2003) Molecular markers of endocrine disruption in aquatic organisms. J Toxicol Environ Flealth B Crit Rev 6(5) 453 196... [Pg.294]

Bieche, I., Parfait, B., Doussal, V. L., Olivi, M., Rio, M.-C., Lidereau, R., and Viduad, M. 2001. Identification of CGA as a novel estrogen receptor-responsive gene in breast cancer An outstanding candidate marker to predict the response to endocrine therapy. Cancer Res. 61 1652-1658. [Pg.308]

The most useful markers for a successful outcome of assisted reproduction are those that can be assessed before the treatment begins. The following tests are therefore less useful from a clinical point of view. However, sometimes a stimulation or challenge test can give more detailed information about the functioning of the endocrine system of a subject, or can predict pregnancy more precisely than baseline tests. [Pg.306]

A.F. Gazdar et al.. Expression of neuroendocrine cell markers L-dopa decarboxylase, chromogranin A, and dense core granules in human tumors of endocrine and nonendocrine origin. Cancer Res. 48 (1988)4078-4082. [Pg.236]

Monoamines share the acid environment of the storage granule matrix with ATP, peptides, and proteins, the most well known of which are the chromogranins. The chro-mogranins are ubiquitous components of secretory vesicles and their widespread presence among endocrine tissue has led to their measurement in plasma as useful albeit relatively nonspecific markers of neuroendocrine tumors, including pheochromocytomas and carcinoid tumors. [Pg.1035]

Metabolic bone diseases result from a partial uncoupling or imbalance between bone resorption and formation. Decreased bone mass, or osteopenia, is more common than abnormal increases of bone mass. The most prevalent metabolic bone diseases are osteoporosis, osteomalacia and rickets, and renal osteodystrophy. Osteoporosis, the most prevalent metabolic bone disease in developed countries, is characterized by loss of bone mass, microarchitectural deterioration of bone tissue, and increased risk of fracture. Rickets and osteomalacia, which are more common in the less-developed countries, are characterized by defective mineralization of bone matrix. Renal osteodystrophy is a complex condition that develops in response to abnormalities of the endocrine and excretory functions of the kidneys. These three metabolic bone diseases and Paget s disease, a localized bone disease, are discussed below followed by laboratory markers of bone metabolism. [Pg.1932]


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