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Three possible models of cell proliferation, which are slow turnover with linear increase first-order kinetics in BrdU labeled cells, a heterogeneous model with a proliferating compartment that reached a plateau second-order kinetics , and a rapid growth model where all cells had incorporated BrdU third-order kinetics Fig.

Similar analysis of the proliferation in lactotrophs of the anterior pituitary Fig. Comparison of the predicted a priori models of proliferation Fig.

Cell type and a priori model: slow turnover model, first-order kinetics; heterogeneous model, second-order kinetics; and rapid growth model, third-order kinetics.

P value for observed data being significantly different from a priori model. We further analyzed proliferation in the pancreatic islets and anterior pituitaries, because these glands are heterogeneous in being composed of different endocrine cells that each give rise to distinct NETs.

We hypothesized that differences in the proliferation of these cell types may help to partly explain the predominant development of some tumors, e.

Thus, to investigate the dynamics of pancreatic and pituitary tumorigenesis in terms of size and time required for development, we designed a mathematical model Fig.

Using just the observed growth rate Fig. Similar analysis of the pituitary using the observed growth rates Fig. These results indicate that mutations of both Men1 alleles are required for pancreatic and pituitary NET development and are consistent with the reported findings in human and mouse MEN1 tumors and with the Knudson two-hit hypothesis 13 , 28 — These results, which indicate that the predicted model best approximates to the observed situation when the effects of tumor microenvironment are minimal i.

This predicted the development of an insulinoma i. Thus, application of the refined mathematical model to anterior pituitary cell types lactotrophs, somatotrophs, and corticotrophs predicted development of NETs i.

However, development of corticotrophinomas was predicted by Mathematical modeling of pancreatic and anterior pituitary NET growth. Time course of observed A pancreatic islet and B anterior pituitary NET growth rate proliferation rate minus apoptotic rate for constituent cell types, determined by BrdU labeling and TUNEL assays Figs.

In addition, these advances help to provide further insights about NET development as well as a method that could be used for assessing the effects of treatments for these NETs.

Thus, our study has helped to establish a valid method for labeling proliferating cells in vivo and thereby measuring the proliferation rates of endocrine neoplasias, which have not been previously reported in mouse or man.

These findings will help future studies that are aimed at assessing the antiproliferative effects of emerging new treatments, such as inhibitors of tyrosine kinase receptors 35 , the mammalian target of rapamycin pathway 36 , fibroblast growth factor, and vascular endothelial growth factor-A 37 , for these endocrine neoplasias.

Our studies may partly help to explain the more frequent occurrence of some tumor types in endocrine glands that have multiple cell types, e.

For example, insulinomas occur more frequently in MEN1 patients below the age of 40 yr, whereas glucagonomas and somatostatinomas rarely occur in MEN1 patients 4 , 38 — Furthermore, our mathematical modeling analysis Figs.

Simply put, it seems that the life expectancy of the mice allows expression of only the most rapidly growing tumor types.

The situation for the development of anterior pituitary tumors is similar, in which PRLomas are the most commonly occurring tumor in MEN1 patients, who occasionally develop somatotrophinomas and rarely corticotrophinomas.

The observed higher proliferation rates of lactotrophs and the mathematical modeling analysis Figs.

Thus, the mathematical modeling of anterior pituitary NET growth has provided insights into the variety of pituitary NET types that are found and suggests that pituitary lactotrophs and somatotrophs are most susceptible to tumorigenesis from loss of the wild-type Men1 allele Fig.

However, the higher proportion of lactotrophs and somatotrophs in the anterior pituitary, when compared with corticotrophs, gonadotrophs, and thyrotrophs, may also contribute to the higher prevalence of lactotrophinomas and somatotrophinomas.

These in silico predictions correlate with observations in MEN1 patients and Men1 mouse models in which insulinomas and lactotrophinomas frequently arise as the pancreatic and pituitary NETs, respectively 13 , However, it is important to note the limitations of the mathematical modeling, which does not consider the occurrence of additional mutations in genes other than MEN1 that may suddenly increase the proliferation rates and conferment of invasive and malignant potential, and the changes in tumor hormonal expression during growth that may render a nonsecreting tumor into a secreting tumor, or vice versa.

The mathematical model Fig. Our mathematical modeling, which demonstrates the importance of the occurrence of mutations in both Men1 alleles Fig.

This prediction could be tested by breeding conditional Men1 knockout mice with appropriate transgenic mice expressing Cre under the control of a tissue-specific promoter Thus, development of glucagonomas may be related to the occurrence of the Men1 mutations, and use of other tissue-specific conditional Men1 knockout mice may help to further assess the validity of the mathematical modeling and the development of other NETs in the pancreas and pituitary.

The apoptotic response was found to differ in the endocrine tumors. Thus, apoptosis was increased in the gonadal tumors Fig. These findings are difficult to reconcile with a unifying explanation.

Menin has been reported, by in vitro studies, to promote the transcription of caspase 8 and stimulate the extrinsic apoptotic pathway 12 , 49 , However, the findings of increased apoptosis in the gonadal tumors and no change in the pancreatic NETs, pituitary NETs, and parathyroid tumors are at variance with the in vitro effects of menin, and it may be that menin interacts with proteins that inhibit apoptosis in these tissues or that menin does not have a significant in vivo role in apoptosis in these glands and their tumors.

Further investigation of apoptotic pathways in this model may therefore elucidate the different in vivo mechanisms involved. Finally, use of long-term BrdU to label proliferating cells in vivo and thereby assess proliferation rates may help in evaluating the effectiveness of novel treatments aimed at reducing NET growth, such as monoclonal antibodies, gene therapy, and other genetic modifying agents.

This work was supported by the United Kingdom Medical Research Council Grants G, and G, to G. Thakker RV Multiple endocrine neoplasia type 1 MEN1.

Best Pract Res Clin Endocrinol Metab 24 : — Google Scholar. Newey PJ , Thakker RV Role of multiple endocrine neoplasia type 1 mutational analysis in clinical practice.

Endocr Pract 17 Suppl 3 : 8 — Calender A , Giraud S , Cougard P , Chanson P , Lenoir G , Murat A , Hamon P , Proye C Multiple endocrine neoplasia type 1 in France: clinical and genetic studies.

J Intern Med : — Trump D , Farren B , Wooding C , Pang JT , Besser GM , Buchanan KD , Edwards CR , Heath DA , Jackson CE , Jansen S , Lips K , Monson JP , O'Halloran D , Sampson J , Shalet SM , Wheeler MH , Zink A , Thakker RV Clinical studies of multiple endocrine neoplasia type 1 MEN1.

QJM 89 : — Lemmens I , Van de Ven WJ , Kas K , Zhang CX , Giraud S , Wautot V , Buisson N , De Witte K , Salandre J , Lenoir G , Pugeat M , Calender A , Parente F , Quincey D , Gaudray P , De Wit MJ , Lips CJ , Höppener JW , Khodaei S , Grant AL , Weber G , Kytölä S , Teh BT , Farnebo F , Thakker RV Identification of the multiple endocrine neoplasia type 1 MEN1 gene.

The European consortium on MEN1.

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Ähnliche Pornos. Whether your pheno hunting or breeding, the Planted Evidence team has you covered! Nature : 85 — Kidd MModlin IM Small intestinal neuroendocrine cell Sexwideos 'carcinoid' tumors. Svejda BKidd MGiovinazzo FEltawil KGustafsson BIPfragner Dralle OmasModlin IM The 5-HT 2B receptor plays a key regulatory role in both neuroendocrine tumor cell proliferation and the modulation of the fibroblast component of the neoplastic microenvironment. Furthermore, our mathematical modeling analysis Figs. In "open source" we trust MEN1 missense mutations impair sensitization to apoptosis Dralle Omas by wild-type menin in endocrine pancreatic tumor cells. Proc Natl Acad Sci USA 80 : — Very unique variety and fast delivery. Article Navigation. Curr Opin Oncol 23 : 45 — Ähnliche Deutsche Hausfrauen Sex Videos. Ältere Beiträge. However, it is important to note the limitations of the mathematical modeling, which does not consider the occurrence of additional mutations in genes other than MEN1 that may suddenly increase the proliferation rates and conferment of invasive and malignant potential, and the changes in tumor hormonal expression during growth that may render a nonsecreting tumor into a secreting tumor, or vice versa. Bitte anmelden, um TV-Erinnerung zu aktivieren arrow.
Dralle Omas
Dralle Omas

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