Relevant bibliographies by topics / Cellules endocrines / Journal articles
To see the other types of publications on this topic, follow the link: Cellules endocrines.

Journal articles on the topic 'Cellules endocrines'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Cellules endocrines.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Pattou, F. "L’Année en… Greffe de cellules endocrines." Annales d'Endocrinologie 82, no. 5 (2021): 223. http://dx.doi.org/10.1016/j.ando.2021.07.014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Amiranoff, B. "Cellules endocrines intestinales et pancréatiques : points très communs !" médecine/sciences 13, no. 8-9 (1997): 1063. http://dx.doi.org/10.4267/10608/508.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Girard, N. "Tumeurs neuro-endocrines broncho-pulmonaires primitives : tumeurs carcinoïdes, carcinomes neuro-endocrines à grandes cellules." Revue des Maladies Respiratoires Actualités 10, no. 3 (2018): 332–39. http://dx.doi.org/10.1016/s1877-1203(18)30029-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Beauvy, J., and G. Raverot. "Rôle des oncoprotéines MafB dans les cellules endocrines antéhypophysaires." Annales d'Endocrinologie 76, no. 4 (2015): 352. http://dx.doi.org/10.1016/j.ando.2015.07.167.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Souquet, P. J., N. Girard, L. Gérinière, and D. Arpin. "Tumeurs neuro-endocrines broncho-pulmonaires primitives: tumeurs carcinoïdes et carcinomes neuro-endocrines à grandes cellules." Revue des Maladies Respiratoires Actualités 11, no. 3 (2019): 298–305. http://dx.doi.org/10.1016/s1877-1203(19)30100-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Souquet, P. J., N. Girard, L. Gérinière, and D. Arpin. "Tumeurs neuro-endocrines broncho-pulmonaires primitives : tumeurs carcinoïdes et carcinomes neuro-endocrines à grandes cellules." Revue des Maladies Respiratoires Actualités 12, no. 2 (2020): 2S132–2S140. http://dx.doi.org/10.1016/s1877-1203(20)30094-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Arbeille, Brigitte, Monique Lemesle, and Franck Fetissof. "Les cellules endocrines du tractus génital féminin: La glande Bartholin." Biology of the Cell 63, S1 (1988): 21–21. http://dx.doi.org/10.1016/0248-4900(88)90188-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Scoazec, J. Y. "Inhibiteurs de la pompe à protons et cellules endocrines de l’estomac." Annales de Pathologie 24 (November 2004): 48–51. http://dx.doi.org/10.1016/s0242-6498(04)94047-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Châari, C., S. Krichen-Makni, N. Toumi, et al. "Les carcinomes endocrines à petites cellules de la vessie: à propos d’une observation." Oncologie 11, no. 1 (2009): 53–57. http://dx.doi.org/10.1007/s10269-007-0823-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kessler, Laurence. "Différentiation et séparation de cellules pancréatiques non endocrines à l’aide du trieur COPAS en cellules à insuline chez la souris." Diabetologia Notes de lecture 1, no. 1 (2009): 13–14. http://dx.doi.org/10.1007/s13116-009-0007-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Serhane, H., B. Benkirane, H. Sajiai, A. Ait Batahar, A. Amro, and A. Alaoui Yazidi. "Les tumeurs neuro-endocrines à grandes cellules du poumon (à propos de 5 cas)." Revue des Maladies Respiratoires 32 (January 2015): A130. http://dx.doi.org/10.1016/j.rmr.2014.10.663.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Barazzutti, H., T. Capron, A. L. De Berranger, H. Berard, A. Bonnichon, and N. Paleiron. "Caractéristiques cliniques et évolutives des carcinomes pulmonaires neuro-endocrines à grandes cellules, étude multicentrique." Revue des Maladies Respiratoires 35 (January 2018): A112—A113. http://dx.doi.org/10.1016/j.rmr.2017.10.245.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Lenoir, O., C. Haumaitre, and R. Scharfmann. "PO7 Rôle des HDACs (histones désacétylases) dans le développement et la fonction des cellules endocrines." Diabetes & Metabolism 36 (March 2010): A29—A30. http://dx.doi.org/10.1016/s1262-3636(10)70113-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Faggiano, A., M. Ducreux, J. Cl Sabourin, et al. "CO30 - Les carcinomes endocrines peu différenciés à grandes cellules : modalités diagnostiques, caractéristiques cliniques et facteurs pronostiques." Annales d'Endocrinologie 65, no. 4 (2004): 272. http://dx.doi.org/10.1016/s0003-4266(04)95711-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

Marhfour, I., J. Marchandise, A. Lefèvre, J. Rahier, C. Sempoux, and Y. Guiot. "P62 Que devient la sous-unité Kir6.2 dans les cellules endocrines du pancréas de souris déficientes en SUR1 ?" Diabetes & Metabolism 34 (March 2008): H60. http://dx.doi.org/10.1016/s1262-3636(08)72974-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

Castaldo, L., G. Andreozzi, R. Antonucci, P. de Girolamo, and G. Gargiulo et C. Lucini. "Etude Immuno-Histochimique et Ultrastructurale des Cellules Endocrines de la Région Pylorique chez la Taupe Européenne (Talpa europaea)*." Anatomia, Histologia, Embryologia 20, no. 3 (1991): 215–24. http://dx.doi.org/10.1111/j.1439-0264.1991.tb00298.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Joly, A., A. Lambert, F. Leulier, and F. De Vadder. "La malnutrition protéique et le probiotique Lactiplantibacillus plantarumWJL modulent la quantité de cellules entéro-endocrines de l’intestin grêle." Annales d'Endocrinologie 82, no. 5 (2021): 253. http://dx.doi.org/10.1016/j.ando.2021.08.007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

Keramidas, M., C. Faudot, A. Cibiel, J. J. Feige, and M. Thomas. "P196 - Expression d’EG-VEGF, de BV8 et de leurs récepteurs dans les cellules endocrines et endothéliales du cortex surrénal bovin." Annales d'Endocrinologie 66, no. 5 (2005): 480. http://dx.doi.org/10.1016/s0003-4266(05)82037-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
19

Renon, M., W. Bazzi, C. Vercherat, A. Calender, J. Y. Scoazec, and M. Cordier-Bussat. "Analyse des conséquences fonctionnelles des variations de l’expression de la protéine suppresseur de tumeur menin dans des cellules endocrines digestives." Gastroentérologie Clinique et Biologique 30, no. 5 (2006): 712. http://dx.doi.org/10.1016/s0399-8320(06)73289-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Bazzi, W., M. Renon, C. Vercherat, et al. "P1-122 - Analyses des conséquences fonctionnelles de modifications du niveau d’expression de la protéine suppresseur de tumeur « menin » dans les cellules endocrines digestives." Annales d'Endocrinologie 67, no. 5 (2006): 448–49. http://dx.doi.org/10.1016/s0003-4266(06)72775-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Villaume, K., G. Gouysse, T. Walter, C. Lombard-Bohas, C. Roche, and J. Y. Scoazec. "P.237 Effets des analogues de la somatostatine et de la rapamycine sur la sécrétion du VEGF par les cellules endocrines tumorales digestives." Gastroentérologie Clinique et Biologique 33, no. 3 (2009): A167. http://dx.doi.org/10.1016/s0399-8320(09)72928-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Couderc, C., G. Poncet, T. Walter, et al. "P.238 Inhibition de la voie de signalisation PI3K/mTOR dans les cellules endocrines tumorales STC-1 : étude in vitro et in vivo." Gastroentérologie Clinique et Biologique 33, no. 3 (2009): A167. http://dx.doi.org/10.1016/s0399-8320(09)72929-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
23

Kobiita, A., F. Moreau, F. Zobairi, Laurence Kessler, and Florence Toti. "PO19 - Réponse au stress des cellules exocrines humaines mutées CFPAC-1 et effets de leurs microparticules sur les cellules endocrines RIN-m5F. Incidence de la mutation CFTR F508 et de la concentration en glucose." Diabetes & Metabolism 37, no. 1 (2011): A28. http://dx.doi.org/10.1016/s1262-3636(11)70597-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
24

Doga, Mauro, Stefania Bonadonna, and Andrea Giustina. "Glucocorticoids and bone: cellular, metabolic and endocrine effects." HORMONES 3, no. 3 (2004): 184–90. http://dx.doi.org/10.14310/horm.2002.11125.

Full text
APA, Harvard, Vancouver, ISO, and other styles
25

Salzet, Michel, and Robert Day. "Marqueurs endocriniens dans les cellules immunitaires : Notion de phénotype endocrinien." Journal de la Société de Biologie 197, no. 2 (2003): 97–101. http://dx.doi.org/10.1051/jbio/2003197020097.

Full text
APA, Harvard, Vancouver, ISO, and other styles
26

Josso, N., and R. Rey. "La cellule de Sertoli, une cellule endocrine." médecine/sciences 11, no. 4 (1995): 537. http://dx.doi.org/10.4267/10608/2243.

Full text
APA, Harvard, Vancouver, ISO, and other styles
27

A., F. "Pancréas endocrine : les cellules β dormantes". Médecine des Maladies Métaboliques 5, № 4 (2011): 437. http://dx.doi.org/10.1016/s1957-2557(11)70283-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
28

Ailhaud, G. "L'adipocyte, cellule sécrétrice et endocrine." médecine/sciences 14, no. 8-9 (1998): 858. http://dx.doi.org/10.4267/10608/1157.

Full text
APA, Harvard, Vancouver, ISO, and other styles
29

Modigliani, E., and L. Gattégno. "Le lymphocyte est une cellule endocrine." médecine/sciences 3, no. 5 (1987): 275. http://dx.doi.org/10.4267/10608/3678.

Full text
APA, Harvard, Vancouver, ISO, and other styles
30

Bouzakri, K., P. Plomgaard, and T. Berney. "Insulinorésistance : communication cellule musculaire-pancréas endocrine." Médecine des Maladies Métaboliques 5, no. 3 (2011): 322. http://dx.doi.org/10.1016/s1957-2557(11)70252-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Shakya, Manita, Taha Yildirim, and Iris Lindberg. "Increased expression and retention of the secretory chaperone proSAAS following cell stress." Cell Stress and Chaperones 25, no. 6 (2020): 929–41. http://dx.doi.org/10.1007/s12192-020-01128-7.

Full text
Abstract:
Abstract The secretory pathway of neurons and endocrine cells contains a variety of mechanisms designed to combat cellular stress. These include not only the unfolded protein response pathways but also diverse chaperone proteins that collectively work to ensure proteostatic control of secreted and membrane-bound molecules. One of the least studied of these chaperones is the neural- and endocrine-specific molecule known as proSAAS. This small chaperone protein acts as a potent anti-aggregant both in vitro and in cellulo and also represents a cerebrospinal fluid biomarker in Alzheimer’s disease. In the present study, we have examined the idea that proSAAS, like other secretory chaperones, might represent a stress-responsive protein. We find that exposure of neural and endocrine cells to the cell stressors tunicamycin and thapsigargin increases cellular proSAAS mRNA and protein in Neuro2A cells. Paradoxically, proSAAS secretion is inhibited by these same drugs. Exposure of Neuro2A cells to low concentrations of the hypoxic stress inducer cobalt chloride, or to sodium arsenite, an oxidative stressor, also increases cellular proSAAS content and reduces its secretion. We conclude that the cellular levels of the small secretory chaperone proSAAS are positively modulated by cell stress.
APA, Harvard, Vancouver, ISO, and other styles
32

Papewalis, C., B. Jacobs, M. Wuttke, and M. Schott. "Cellular Therapies in Endocrine Diseases." Experimental and Clinical Endocrinology & Diabetes 116, S 01 (2008): S33—S39. http://dx.doi.org/10.1055/s-2008-1081489.

Full text
APA, Harvard, Vancouver, ISO, and other styles
33

Nosé, Vània. "Molecular and Cellular Endocrine Pathology." American Journal of Surgical Pathology 25, no. 7 (2001): 974–75. http://dx.doi.org/10.1097/00000478-200107000-00024.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Duvillié, Bertrand. "Quelles cellules souches pour une réparation du pancréas endocrine ?" médecine/sciences 29, no. 8-9 (2013): 744–48. http://dx.doi.org/10.1051/medsci/2013298013.

Full text
APA, Harvard, Vancouver, ISO, and other styles
35

Spada, Anna, Lucia Vallar, and Giovanni Faglia. "Cellular alterations in pituitary tumors." European Journal of Endocrinology 130, no. 1 (1994): 43–52. http://dx.doi.org/10.1530/eje.0.1300043.

Full text
Abstract:
Spada A, Vallar L, Faglia G. Cellular alterations in pituitary tumors. Eur J Endocrinol 1994;130:43–52. ISSN 0804–4643 In the last few years, molecular studies on pituitary adenomas have yielded evidence supporting a primary pituitary origin of these tumors. Although the existence of genomic alterations in tumoral cells is strongly suggested by the fact that almost all pituitary adenomas are monoclonal in origin, structural genetic abnormalities such as rearrangement, deletion or mutation, which could result in transcriptional activation, have been identified in a minority of tumors. As far as the possible loss of anti-oncogenes in pituitary tumors is concerned, gene alterations have not been found in the p53 nor in the retinoblastoma gene, while loss of chromosome 1 1q13 sequences, which contain the deduced location of the yet uncloned MEN-1 gene, has been reported in a subset of GH-secreting adenomas. With regard to the activation of dominant oncogenes in the process of tumor formation, activating mutations of either the Gs α-subunit or the ras gene have been identified in a large proportion of GH-secreting adenomas and in individual particularly invasive tumours, respectively. Promoting agents such as hypothalamic neurohormones and growth factors may be required for the selective growth of genetically altered cells. In this respect, it is worth noting that receptor/postreceptor alterations occurring in pituitary tumors may cause an increased action of stimulatory neurohormones with growth promoting properties as well as defective action of inhibitory inputs. Anna Spada, Institute of Endocrine Sciences, Pad. Granelli Ospedale Maggiore IRCCS, via F Sforza 35, Milano 20122, Italy
APA, Harvard, Vancouver, ISO, and other styles
36

Marx, C., S. R. Bornstein, and G. W. Wolkersdörfer. "Cellular immune-endocrine interaction in adrenocortical tissues." European Journal of Clinical Investigation 30 (December 2000): 1–5. http://dx.doi.org/10.1046/j.1365-2362.2000.0300s3001.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
37

Rolim, Ana Luiza R., Susan C. Lindsey, Ilda S. Kunii, et al. "Ion channelopathies in endocrinology: recent genetic findings and pathophysiological insights." Arquivos Brasileiros de Endocrinologia & Metabologia 54, no. 8 (2010): 673–81. http://dx.doi.org/10.1590/s0004-27302010000800002.

Full text
Abstract:
Ion channels serve diverse cellular functions, mainly in cell signal transduction. In endocrine cells, these channels play a major role in hormonal secretion, Ca2+-mediated cell signaling, transepithelial transport, cell motility and growth, volume regulation and cellular ionic content and acidification of lysosomal compartments. Ion channel dysfunction can cause endocrine disorders or endocrine-related manifestations, such as pseudohypoaldosteronism type 1, Liddle syndrome, Bartter syndrome, persistent hyperinsulinemic hypoglycemia of infancy, neonatal diabetes mellitus, cystic fibrosis, Dent's disease, hypomagnesemia with secondary hipocalcemia, nephrogenic diabetes insipidus and, the most recently genetically identified channelopathy, thyrotoxic hypokalemic periodic paralysis. This review briefly recapitulates the membrane action potential in endocrine cells and offers a short overview of known endocrine channelopathies with focus on recent progress regarding the pathophysiological mechanisms and functional genetic defects.
APA, Harvard, Vancouver, ISO, and other styles
38

Demoreuil, C., A. Thirot-Bidault, C. Dagher, et al. "Carcinome endocrine peu différencié à grandes cellules des voies biliaires extrahépatiques." Gastroentérologie Clinique et Biologique 33, no. 3 (2009): 194–98. http://dx.doi.org/10.1016/j.gcb.2009.01.005.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Radon, K., D. Jung, D. M. Rose, D. Parera, J. Konietzko, and L. Vollrath. "CELLULAR PHONES AND HUMAN ENDOCRINE AND IMMUNOLOGICAL AXIS." Epidemiology 9, Supplement (1998): S109. http://dx.doi.org/10.1097/00001648-199807001-00353.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Das, Diptatanu, and Shantanu Das. "Endocrine Disruptor—A threat to the animal world." International Academic Publishing House 24 (April 30, 2021): 10–23. http://dx.doi.org/10.52756/ijerr.2021.v24.002.

Full text
Abstract:
Various types of naturally occurring and artificially made chemicals cause disruption of endocrine processes among animals. They mimic biochemically with hormones and interfere with the normal signaling and activity of the endocrine system, causing enormous changes at the cellular level of animals from lower to higher organisms, including human being. These modified regulations of cellular activities as a result of endocrine disruptors have severe implications at the organismal level. Types and adverse effects of these natural and synthetic agents, especially estrogenic compounds causing biological threats have been discussed in details in this review.
APA, Harvard, Vancouver, ISO, and other styles
41

Auernhammer, Christoph J., and Christian J. Strasburger. "Effects of growth hormone and insulin-like growth factor I on the immune system." European Journal of Endocrinology 133, no. 6 (1995): 635–45. http://dx.doi.org/10.1530/eje.0.1330635.

Full text
Abstract:
Auernhammer CJ, Strasburger CJ. Effects of growth hormone and insulin-like growth factor I on the immune system. Eur J Endocrinol 1995;133:635–45. ISSN 0804–4643 Growth hormone-releasing hormone (GHRH). growth hormone (GH), prolactin (PRL) and insulin-like growth factor I (IGF-I) are synthesized and secreted by various immunocompetent cells. In addition, GHRH, GH, PRL and IGF-I receptors are expressed on immune cells. Growth hormone, PRL and IGF-I stimulate the proliferation of immunocompetent cells and modulate humoral and cellular immune functions, i.e. immunoglobuline secretion of B cells, thymulin secretion of thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst and killing capacity of neutrophils and macrophages. No clinically significant cellular or humoral immunodeficiency has been found in GH-deficient patients. However, several immunological parameters and functions are altered in GH-deficient patients when compared to normal controls. The data available to date indicate that endocrine and pleiotropic para- and autocrine mechanisms of action are involved in a neuropeptide immune network, including GH PRL and IGF-I as modulators of immune function. Christian J Strasburger, Medizinische Klinik, Klinikum Innenstadt der LMU, Ziemssenstr. 1, 80336 Munich, Germany
APA, Harvard, Vancouver, ISO, and other styles
42

Ghadouane, M., M. Zannoud, M. Alami, et al. "Tumeur neuro-endocrine à petites cellules de la vessie. Une nouvelle observation." Annales d'Urologie 37, no. 2 (2003): 75–78. http://dx.doi.org/10.1016/s0003-4401(03)00009-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Anract, J., P. Bories, V. Goffin, et al. "Rôle du CaSR dans la différenciation neuro-endocrine des cellules tumorales prostatiques." Progrès en Urologie 29, no. 13 (2019): 662. http://dx.doi.org/10.1016/j.purol.2019.08.080.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Weckman, Andrea, Antonio Di Ieva, Fabio Rotondo, et al. "Autophagy in the endocrine glands." Journal of Molecular Endocrinology 52, no. 2 (2014): R151—R163. http://dx.doi.org/10.1530/jme-13-0241.

Full text
Abstract:
Autophagy is an important cellular process involving the degradation of intracellular components. Its regulation is complex and while there are many methods available, there is currently no single effective way of detecting and monitoring autophagy. It has several cellular functions that are conserved throughout the body, as well as a variety of different physiological roles depending on the context of its occurrence in the body. Autophagy is also involved in the pathology of a wide range of diseases. Within the endocrine system, autophagy has both its traditional conserved functions and specific functions. In the endocrine glands, autophagy plays a critical role in controlling intracellular hormone levels. In peptide-secreting cells of glands such as the pituitary gland, crinophagy, a specific form of autophagy, targets the secretory granules to control the levels of stored hormone. In steroid-secreting cells of glands such as the testes and adrenal gland, autophagy targets the steroid-producing organelles. The dysregulation of autophagy in the endocrine glands leads to several different endocrine diseases such as diabetes and infertility. This review aims to clarify the known roles of autophagy in the physiology of the endocrine system, as well as in various endocrine diseases.
APA, Harvard, Vancouver, ISO, and other styles
45

Ptasznik, Andrzej, Gillian M. Beattie, Martin I. Mally, Vincenzo Cirulli, Ana Lopez, and Alberto Hayek. "Phosphatidylinositol 3-Kinase Is a Negative Regulator of Cellular Differentiation." Journal of Cell Biology 137, no. 5 (1997): 1127–36. http://dx.doi.org/10.1083/jcb.137.5.1127.

Full text
Abstract:
Phosphatidylinositol 3-kinase (PI3K) has been shown to be an important mediator of intracellular signal transduction in mammalian cells. We show here, for the first time, that the blockade of PI3K activity in human fetal undifferentiated cells induced morphological and functional endocrine differentiation. This was associated with an increase in mRNA levels of insulin, glucagon, and somatostatin, as well as an increase in the insulin protein content and secretion in response to secretagogues. Blockade of PI3K also increased the proportion of pluripotent precursor cells coexpressing multiple hormones and the total number of terminally differentiated cells originating from these precursor cells. We examined whether any of the recently described modulators of endocrine differentiation could participate in regulating PI3K activity in fetal islet cells. The activity of PI3K was inversely correlated with the hepatocyte growth factor/scatter factor–induced downregulation or nicotinamideinduced upregulation of islet-specific gene expression, giving support to the role of PI3K, as a negative regulator of endocrine differentiation. In conclusion, our results provide a mechanism for the regulation of hormone-specific gene expression during human fetal neogenesis. They also suggest a novel function for PI3K, as a negative regulator of cellular differentiation.
APA, Harvard, Vancouver, ISO, and other styles
46

Ueno, Takayuki, Norikazu Masuda, Shunji Kamigaki, et al. "Differential Involvement of Autophagy and Apoptosis in Response to Chemoendocrine and Endocrine Therapy in Breast Cancer: JBCRG-07TR." International Journal of Molecular Sciences 20, no. 4 (2019): 984. http://dx.doi.org/10.3390/ijms20040984.

Full text
Abstract:
Endocrine therapy is an essential component in the curative treatment of hormone receptor (HR)-positive breast cancer. To improve treatment efficacy, the addition of metronomic chemotherapy has been tested and shown to improve therapeutic effects. To better understand cellular reactions to metronomic chemoendocrine therapy, we studied autophagy-related markers, beclin 1 and LC3, and apoptosis-related markers, TUNEL and M30, in pre- and post-treatment cancer tissues from a multicenter neoadjuvant trial, JBCRG-07, in which oral cyclophosphamide plus letrozole were administered to postmenopausal patients with HR-positive breast cancer. Changes in the levels of markers were compared with those following neoadjuvant endocrine therapy according to clinical response. Apoptosis, in addition to autophagy-related markers, increased following metronomic chemoendocrine therapy and such increases were associated with clinical response. By contrast, following endocrine therapy, the levels of apoptosis-related markers did not increase regardless of clinical response, whereas the levels of autophagy-related markers increased. Furthermore, levels of the apoptosis-related marker, M30, decreased in responders of endocrine therapy, suggesting that the induction of apoptosis by metronomic chemoendocrine therapy was involved in the improved clinical outcome compared with endocrine therapy. In conclusion, metronomic chemoendocrine therapy induced a different cellular reaction from that of endocrine therapy, including the induction of apoptosis, which is likely to contribute to improved efficacy compared with endocrine therapy alone.
APA, Harvard, Vancouver, ISO, and other styles
47

Carter, David. "Cellular transcriptomics – the next phase of endocrine expression profiling." Trends in Endocrinology & Metabolism 17, no. 5 (2006): 192–98. http://dx.doi.org/10.1016/j.tem.2006.05.004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Cinti, Saverio. "Organo endocrino adiposo 2020: stato dell’arte." L'Endocrinologo 21, no. 4 (2020): 270–76. http://dx.doi.org/10.1007/s40619-020-00757-5.

Full text
Abstract:
Sommario I tessuti adiposi bianco e bruno sono organizzati a formare un vero e proprio organo. Essi svolgono funzioni diverse ma collaborano grazie alla loro plasticità che permette la reciproca conversione. Ciò implica una nuova proprietà per le cellule mature. Il sottocutaneo della ghiandola mammaria fornisce un altro esempio perché queste cellule adipose si trasformano in ghiandole durante la gravidanza. L’organo adiposo nell’obesità va incontro a flogosi inducendo insulino-resistenza, patogeneticamente coinvolta nel diabete Tipo 2. L’organo adiposo collabora con quelli della digestione formando un sistema che è in grado di controllare diversi aspetti nutrizionali e quindi denominato sistema nutrizionale.
APA, Harvard, Vancouver, ISO, and other styles
49

JIANG, YU, and WEIQUN WANG. "POTENTIAL MECHANISMS OF CANCER PREVENTION BY WEIGHT CONTROL." Biophysical Reviews and Letters 03, no. 03 (2008): 421–37. http://dx.doi.org/10.1142/s1793048008000824.

Full text
Abstract:
Weight control via dietary caloric restriction and/or physical activity has been demonstrated in animal models for cancer prevention. However, the underlying mechanisms are not fully understood. Body weight loss due to negative energy balance significantly reduces some metabolic growth factors and endocrinal hormones such as IGF-1, leptin, and adiponectin, but enhances glucocorticoids, that may be associated with anti-cancer mechanisms. In this review, we summarized the recent studies related to weight control and growth factors. The potential molecular targets focused on those growth factors- and hormones-dependent cellular signaling pathways are further discussed. It appears that multiple factors and multiple signaling cascades, especially for Ras-MAPK-proliferation and PI3K-Akt-anti-apoptosis, could be involved in response to weight change by dietary calorie restriction and/or exercise training. Considering prevalence of obesity or overweight that becomes apparent over the world, understanding the underlying mechanisms among weight control, endocrine change and cancer risk is critically important. Future studies using "-omics" technologies will be warrant for a broader and deeper mechanistic information regarding cancer prevention by weight control.
APA, Harvard, Vancouver, ISO, and other styles
50

El Mesbahi, O., A. Beaudoin, C. Louvet, and A. De Gramont. "Syndrome de lyse tumorale après chimiothérapie pour carcinome colique endocrine à petites cellules." La Revue de Médecine Interne 25, no. 10 (2004): 768–69. http://dx.doi.org/10.1016/j.revmed.2004.06.008.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Cellules endocrines' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography