Relevant bibliographies by topics / Endocryne tumour

Academic literature on the topic 'Endocryne tumour'

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Published: 11 March 2023

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Journal articles on the topic "Endocryne tumour"

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Lenzen, S., G. Klöppel, S. Zielmann, and U. Panten. "Secretory, enzymatic, and morphological characterization of rat pancreatic endocrine tumours induced by streptozotocin and nicotinamide." Acta Endocrinologica 109, no. 3 (July 1985): 361–68. http://dx.doi.org/10.1530/acta.0.1090361.

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Abstract. Rat pancreatic endocrine tumours were induced by administration of streptozotocin plus nicotinamide. Fifteen to eighteen months later tumours with wet weights of 0.1 to 224 mg were isolated. These tumours were compared with normal rat pancreatic islets. Insulin release from perifused tumours was stimulated by d-glucose, l-leucine, 2-ketoisocaproate, and d-glyceraldehyde, potentiated by theophylline and inhibited by norepinephrine. Compared with isolated rat pancreatic islets, however, insulin secretory responsiveness to glucose stimulation and insulin content were reduced in tumour tissue. Hypoglycaemia in tumour bearing rats and impaired diffusion of insulin out of the tumours may explain this difference. The pattern of enzyme activities observed in tumour tissue was typical for pancreatic endocrine tissue. The activities of succinate dehydrogenase, the two types of the monoamine oxidase, and α-glucosidase were in the normal range in tumour tissue. Only the activities of 5'nucleotidase and glutamate dehydrogenase were decreased. Immunocytochemical analysis of the tumours revealed that they contained an average of 91% B-cells. In addition 8% of D-cells were encountered. Proportions of A-cells and PP-cells ranged below 1%. Thus this endocrine tumour of the pancreas with a high proportion of functionally intact B-cells is an interesting model for studying regulation of secretion and endocrine tumour development.
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Asa, Sylvia L., William Singer, Kalman Kovacs, Eva Horvath, David Murray, Nicholas Colapinto, and Michael O. Thorner. "Pancreatic endocrine tumour producing growth hormone-releasing hormone associated with multiple endocrine neoplasia type I syndrome." Acta Endocrinologica 115, no. 3 (July 1987): 331–37. http://dx.doi.org/10.1530/acta.0.1150331.

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Abstract. We report the first documentation of GHRH production by a tumour associated with proven multiple endocrine neoplasia (MEN). A 30-year-old woman had hypoglycaemia, hyperparathyroidism, and pituitary adenoma with hyperprolactinaemia. Serum growth hormone elevation was attributed to hypoglycaemia but plasma GHRH was elevated. Subtotal pancreatectomy revealed multiple endocrine tumours and nesidioblastosis. Immunohistochemistry demonstrated insulin, glucagon, and somatostatin in several tumours. GHRH was localized in the largest one and was released from that tumour in vitro. Post-operative plasma GH returned to normal. Excess secretion of humoural factors by one tumour may stimulate growth of other tumours in MEN syndromes. The prevalence of GHRH in MEN-I tumours remains to be established.
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Turner, HE, Z. Nagy, KC Gatter, MM Esiri, AL Harris, and JA Wass. "Angiogenesis in pituitary adenomas - relationship to endocrine function, treatment and outcome." Journal of Endocrinology 165, no. 2 (May 1, 2000): 475–81. http://dx.doi.org/10.1677/joe.0.1650475.

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Angiogenesis has been shown to be related to tumour behaviour, prognosis and response to treatment in many different tumour types. The aim of this study was to examine the relationship between angiogenesis and tumour behaviour and response to treatment in pituitary adenomas. The microvessel density (MVD) of pituitary tumours was assessed by counting blood vessels labelled with 3 different endothelial markers using antibodies to CD31, factor eight-related antigen and biotinylated Ulex europaeus (agglutinin I UEAI). One hundred and forty-two surgically removed pituitary adenomas (46 GH secreting, 6 microprolactinomas, 19 macroprolactinomas, 18 ACTH secreting and 53 functionless tumours) were carefully characterized and assessed. There was a significant negative correlation between age and MVD of GH secreting tumours (R(2)=33.8, P=0.005). Age was not related to MVD in other tumour types. Pre-treatment hormone production by the adenomas was related to MVD in prolactinomas (P<0.05), but not in GH secreting tumours. Invasive prolactinomas were significantly more vascular than non-invasive tumours (P<0.05). Drug treatment with metyrapone or bromocriptine did not appear to influence tumour angiogenesis. Surgical cure was more likely in macroprolactinomas and in ACTH secreting tumours with lower MVD. These results show that factors related to angiogenesis are very important in determining a number of clinical features of pituitary tumours, in particular the invasiveness of macroprolactinomas, the effect of age in tumours secreting GH and the outcome of surgical treatment in macroprolactinomas and ACTH secreting tumours.
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Sarkadi, Balázs, Vince Kornél Grolmusz, Henriett Butz, Annamária Kövesdi, István Likó, Gábor Nyirő, Péter Igaz, and Attila Patócs. "Molekuláris genetikai vizsgálatok az örökletes endokrinológiai tumor szindrómák klinikai diagnosztikájában." Orvosi Hetilap 159, no. 7 (February 2018): 285–92. http://dx.doi.org/10.1556/650.2018.31036.

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Abstract: The common features of hereditary endocrine tumour syndromes or multiple endocrine neoplasias (MEN) are the association of various tumours of different endocrine organs in one patient or within the same family. Different types can be distinguished from among which type 1 and type 2 are the most common. The mode of inheritance is autosomal dominant, meaning that there is a 50% chance to inherit the pathogenic alteration. The pathogenic variants of genes responsible for MEN syndromes have also been identified in sporadic endocrine tumours and many cases initially referred to as sporadic have been later categorized as familiar based on genetic analysis. The main role of the molecular genetic analysis in these syndromes is to identify the pathogenic variant, then, after appropriate genetic counseling, to perform the genetic screening of first-degree relatives. Following molecular genetic analysis, the state-of-the-art clinical follow-up of the clinically healthy mutation carriers may decrease or even prevent the morbidity and mortality. Due to technological developments in recent years, the molecular genetic analysis of hereditary tumour syndromes has also been changed. Using next generation based sequencing methods in routine clinical diagnostics, the number of pathogenic genes in endocrine tumours has also increased. The present review focuses on the genetic background of hereditary endocrine tumour syndromes and the recently used molecular biological methods will also be presented. Orv Hetil. 2018; 159(7): 285–292.
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Arnold, R., R. Benning, C. Neuhaus, M. Rolwage, and M. E. Trautmann. "Gastroenteropancreatic Endocrine Tumours: Effect of Sandostatin® on Tumour Growth." Digestion 54, no. 1 (1993): 72–75. http://dx.doi.org/10.1159/000201081.

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Igaz, Péter. "Genetics of neuroendocrine tumours, hereditary tumour syndromes." Orvosi Hetilap 154, no. 39 (September 2013): 1541–48. http://dx.doi.org/10.1556/oh.2013.29706.

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Neuroendocrine tumours occur in some hereditary tumour syndromes, and the molecular pathophysiological mechanisms involved in these are also important in their sporadic counterparts which representing the majority of neuroendocrine tumours. These syndromes include multiple endocrine neoplasia type 1, von Hippel–Lindau syndrome, neurofibromatosis type 1 and tuberous sclerosis. All these follow an autosomal dominant inheritance. The primarily affected molecular pathways are Ras-MAPK signalling, hypoxia induced factor 1α, and mTOR signalling that are also involved in sporadic tumours and may even represent potential molecular targets of therapy. In this review, the major characteristics of hereditary tumour syndromes, their molecular genetics and the pathophysiological mechanisms involved in sporadic tumours are discussed. Orv. Hetil., 2013, 154, 1541–1548.
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Marques, Pedro, Ashley B. Grossman, and Márta Korbonits. "The tumour microenvironment of pituitary neuroendocrine tumours." Frontiers in Neuroendocrinology 58 (July 2020): 100852. http://dx.doi.org/10.1016/j.yfrne.2020.100852.

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8

Dimitriadis, Georgios K., Anna Angelousi, Martin O. Weickert, Harpal S. Randeva, Gregory Kaltsas, and Ashley Grossman. "Paraneoplastic endocrine syndromes." Endocrine-Related Cancer 24, no. 6 (June 2017): R173—R190. http://dx.doi.org/10.1530/erc-17-0036.

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The majority of neoplasms are responsible for symptoms caused by mass effects to surrounding tissues and/or through the development of metastases. However, occasionally neoplasms, with or without endocrine differentiation, acquire the ability to secrete a variety of bioactive substances or induce immune cross-reactivity with the normal tissues that can lead to the development of characteristic clinical syndromes. These syndromes are named endocrine paraneoplastic syndromes when the specific secretory components (hormones, peptides or cytokines) are unrelated to the anticipated tissue or organ of origin. Endocrine paraneoplastic syndromes can complicate the patient’s clinical course, response to treatment, impact prognosis and even be confused as metastatic spread. These syndromes can precede, occur concomitantly or present at a later stage of tumour development, and along with the secreted substances constitute the biological ‘fingerprint’ of the tumour. Their detection can facilitate early diagnosis of the underlying neoplasia, monitor response to treatment and/or detect early recurrences following successful initial management. Although when associated with tumours of low malignant potential they usually do not affect long-term outcome, in cases of highly malignant tumours, endocrine paraneoplastic syndromes are usually associated with poorer survival outcomes. Recent medical advances have not only improved our understanding of paraneoplastic syndrome pathogenesis in general but also enhanced their diagnosis and treatment. Yet, given the rarity of endocrine paraneoplastic syndromes, there is a paucity of prospective clinical trials to guide management. The development of well-designed prospective multicentre trials remains a priority in the field in order to fully characterise these syndromes and provide evidence-based diagnostic and therapeutic protocols.
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de Sá, Sandra Valéria, Maria Lúcia Corrêa-Giannella, Márcio Carlos Machado, Jean Jorge S. de Souza, Maria Adelaide Albergaria Pereira, Rosely Antunes Patzina, Sheila Aparecida Coelho Siqueira, Marcel Cerqueira César Machado, and Daniel Giannella-Neto. "Somatostatin receptor subtype 5 (SSTR5) mRNA expression is related to histopathological features of cell proliferation in insulinomas." Endocrine-Related Cancer 13, no. 1 (March 2006): 69–78. http://dx.doi.org/10.1677/erc.1.00962.

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Insulinomas are rare endocrine neoplasias that constitute the most frequent islet cell tumours. Somatostatin (SST) analogs are tentatively used to inhibit insulin secretion and control tumour growth in patients with local invasion or inoperative metastasis, but variable responses have been reported. Data regarding somatostatin receptor (SSTR) subtypes expression in insulinomas are conflicting. In this study, we evaluated 16 cases of primary insulinomas (including four primary plurihormonal tumours) and two hepatic metastases. Histopathological and immunohistochemical analysis for some features associated with tumour aggressiveness and semi-quantitative RT-PCR for SSTR1-5 and real-time qPCR for SSTR5 were performed. SSTR subtypes 1, 3, and 5 were expressed in 100%, SSTR2 in 89%, and SSTR4 only in 22% of the insulinomas. SSTR5 mRNA was positively correlated with histopathological features related to tumour aggressiveness (large tumour diameter, well-differentiated endocrine tumour with uncertain behaviour and higher number of cells with nuclear atypia). SSTR5 mRNA expression in primary insulinomas was lower than in primary plurihormonal tumours (P < 0.05). The observed positive correlation between SSTR5 expression and tumour size suggests that the use of SST analogues more specific to SSTR5 in the treatment of insulinomas deserves attention.
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Madeira, I., B. Terris, M. Voss, A. Denys, A. Sauvanet, J.-F. Flejou, V. Vilgrain, J. Belghiti, P. Bernades, and P. Ruszniewski. "Prognostic factors in patients with endocrine tumours of the duodenopancreatic area." Gut 43, no. 3 (September 1, 1998): 422–27. http://dx.doi.org/10.1136/gut.43.3.422.

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Background—The development of endocrine tumours of the duodenopancreatic area (ETDP) is thought to be slow, but their natural history is not well known. The aim of this study was to determine the factors that influence survival of patients with ETDP.Patients/Methods—Eighty two patients with ETDP (44 non-functioning tumours, 23 gastrinomas, seven calcitonin-secreting tumours, four glucagonomas, three insulinomas, one somatostatinoma) followed from October 1991 to June 1997 were included in the study. The following factors were investigated: primary tumour size, hormonal clinical syndrome, liver metastases, lymph node metastases, extranodular/extrahepatic metastases, progression of liver metastases, local invasion, complete resection of the primary tumour, and degree of tumoral differentiation. The prognostic significance of these factors was investigated by uni- and multi-variate analysis.Results—Twenty eight patients (34%) died within a median of 17 months (range 1–110) from diagnosis. Liver metastases (p = 0.001), lymph node metastases (p = 0.001), progression of liver metastases (p<0.00001), lack of complete resection of the primary tumour (p = 0.001), extranodular/extrahepatic metastases (p = 0.001), local invasion (p = 0.001), primary tumour size ⩾3 cm (p = 0.001), non-functioning tumours (p = 0.02), and poor tumoral differentiation (p = 0.006) were associated with an unfavourable outcome by univariate analysis. Multivariate analysis identified only liver metastases (risk ratio (RR) = 8.3; p<0.0001), poor tumoral cell differentiation (RR = 8.1; p = 0.0001), and lack of complete resection of the primary tumour (RR = 4.8; p = 0.0007) as independent risk factors. Five year survival rates were 40 and 100% in patients with and without liver metastases, 85 and 42% in patients with and without complete resection of primary tumour, and 17 and 71% in patients with poor and good tumour cell differentiation respectively.Conclusion—Liver metastases are a major prognostic factor in patients with ETDP. Progression of liver metastases is also an important factor which must be taken into account when deciding on the therapeutic approach. The only other independent prognostic factors are tumoral cell differentiation and complete resection of the primary tumour.
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Dissertations / Theses on the topic "Endocryne tumour"

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BRAGANTINI, Emma. "Prognostic significance of cytokeratin 19 in pancreatic endocrine tumours." Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337410.

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Presupposti. La prognosi delle neoplasie endocrine pancreatiche è difficile da stabilire nonostante la recente classificazione dell’OMS. Studi recenti hanno evidenziato il potenziale ruolo prognostico di alcuni marcatori come CK19, CD99 e P27. Scopo. Valutare il ruolo prognostico dell’espressione di CK19 nelle neoplasie endocrine pancreatiche. Materiali e metodi. Sono state analizzate 149 neoplasie endocrine pancreatiche per l’espressione immunoistochimica di CK19 utilizzando tissue array. Risultati. La presenza di CK19 è stata riscontrata in 100/149 (67,1%) e in 26 su 35 (74.2%) corrispondenti metastasi sia linfonodali che viscerali. E’ stata evidenziata una correlazione statisticamente significativa tra espressione di CK19 e le dimensioni del tumore, lo stato linfonodale, la presenza di metastasi, la sopravvivenza a cinque anni, e con i sottogruppi della classificazione OMS che mostrano una prognosi peggiore (carcinomi endocrini ben differenziati e carcinomi endocrini poco differenziati) Conclusioni: Il presente studio conferma l’associazione dell’espressione di CK19 con le dimensioni del tumore, lo status linfonodale, la presenza di metastasi, la sopravvivenza a cinque anni, e con i sottogruppi della OMS2004 che mostrano una prognosi peggiore. L’analisi multivariata non ha confermato il ruolo della CK19 come marcatore prognostico indipendente. Possiamo quindi concludere che CK19 può essere utilizzato come marcatore di malignità ma non come marcatore prognostico indipendente.
Aim: Pancreatic endocrine tumours are rare neoplasm, whose behaviour is difficult to predict. Recent 2004 WHO classification gives clear criteria to define prognosis of PET, but despite these criteria some tumours show a more aggressive course. Recent studies lighted the role of some immunohistochemical markers as CK19, CD99, P27 as prognostic marker in pancreatic endocrine. The aim of this study was to evaluate the prognostic value of CK19 expression in PETs. Methods and results: 149 PETs and 35 mached metastases were studied using tissue array technology and evaluating immunohistochemical expression of CK19. The presence of CK 19 was detected in a total of 100/149 primitive tumours (67.1%) and 26/35 (74.2%) metastases both in lymph node and in other sites. The difference between the prevalence of CK 19 in metastasis and primitive tumours was not significant. There was a strong correlation between presence of CK 19 in the primitive and its matched metastasis (Fisher's test; P = 0.0012). The results were statistically compared with follow up data, showing a significant correlation with with tumour dimension, lymph node status, presence of metastasis, 5 years survival, and with the subgroups of WHO 2004 classification that have a worse prognosis (WDEC and PDEC). When the WHO parameter was added to the model, ck19 was no longer significantly associated with survival. Furthermore, ck19 expression was not significantly associated with survival when evaluated in single WHO subgroups. Conclusions: We conclude that ck19 can be used as a malignancy marker and index but they are not an independent prognostic markers
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Restany, Alain. "Les tumeurs endocrines du pancréas à sécrétions multiples : considérations pathogéniques et thérapeutiques." Montpellier 1, 1988. http://www.theses.fr/1988MON11263.

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Bonnavion, Rémy. "Study of the effects of Men1 disruption in mouse pancreatic endocrine progenitors during development and adult life." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10144/document.

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Le syndrome des Néoplasies Endocriniennes Multiples de type I (NEM1) est une maladie tumorale héréditaire rare caractérisée par l'apparition de tumeurs notamment du pancréas endocrine. Le gène de prédisposition est le suppresseur de tumeur MEN1, généralement retrouvé muté sur un des 2 allèles au niveau germinal chez les patients NEM1. Les tumeurs endocrines pancréatiques sont rares mais souvent métastatiques lors du diagnostic. Ces tumeurs forment un groupe hétérogène de par le type d'hormone qu'elles peuvent sécréter. Le développement et l'évolution de ces tumeurs sont encore très mal compris. L'origine cellulaire des différents types de tumeurs endocrines pancréatiques reste énigmatique, notamment en ce qui concerne les tumeurs exprimant des hormones non pancréatiques tels que les gastrinomes. Mon projet de thèse s'est articulé autour de la caractérisation d'un nouveau modèle murin d'invalidation du gène Men1 spécifiquement dans les cellules progénitrices endocrine pancréatiques Ngn3+ (PEPs), le modèle PancEndoMen1 KO. Ces travaux nous ont permis de démontrer que les gastrinomes pancréatiques liés à l'inactivation du gène Men1, avaient pour origines les cellules pancréatiques endocrines elles-mêmes. De plus, les souris PancEndoMen1 KO, développent des altérations de prolifération différentes suivant les lignages endocrines. De surcroît, l'invalidation du gène Men1 soit dans les cellules progénitrices pancréatiques, soit dans les cellules PEPs conduit au développement de tumeurs caractérisées par une altération de leur différentiation endocrine. Ainsi, mes travaux de thèse ont permis de mieux renseigner l'histogenèse des tumeurs endocrines pancréatiques en adressant le rôle dans la tumorigenèse de l'invalidation de Men1 dans les cellules PEPs au cours du développement
Multiple Endocrine Neoplasia Type I syndrome (MEN1) is a rare hereditary tumoral disease characterized by the apparition of tumors in multiple endocrine organs including the endocrine pancreas. MEN1 patients generally carry a germinal mutation on one allele of the predisposing gene to the disease, the tumor suppressor MEN1. Pancreatic endocrine tumors are rare, slowly evolving and often present with metastasis at diagnosis. These tumors constitute a heterogeneous group defined by their hormonal secretions. Evolution and development of these tumors is far from being understood. The cell of origin of the different pancreatic endocrine tumor types is enigmatic, notably for tumors secreting non-pancreatic hormones such as gastrinomas. My thesis project was structured toward the characterization of a new murine model allowing the specific disruption of the Men1 gene in Ngn3+ pancreatic endocrine progenitors, the PancEndoMen1 KO model. The combined study of this new model and previous model generated in the team, allowed us to demonstrate that pancreatic gastrinomas related to Men1 inactivation, originate from the endogenous pancreatic endocrine cells. In parallel, our results demonstrated that the mutant mice having Men1-deficient Ngn3+-progenitors resulted in differential cell proliferation alterations in different pancreatic endocrine cells. Importantly, Men1-disruption in either pancreatic endocrine or pan-pancreatic progenitors displayed tumors with impaired differentiation features. Thus, this thesis works allowed to better characterize pancreatic endocrine tumors histogenesis by addressing the role of pancreatic endocrine progenitors targeted Men1 disruption during development in tumorigenesis
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Kaboré, Moussa. "Contribution à l'étude des tumeurs neuro-endocrines : à propos d'un cas de "tumeur carcinoi͏̈de" de l'ovaire, avec dissémination péritonéale." Bordeaux 2, 1989. http://www.theses.fr/1989BOR25283.

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L', Hopital François. "Tumeur endocrine pancréatique secrétant calcitonine et glucagon." Clermont-Ferrand 1, 1987. http://www.theses.fr/1987CLF11048.

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Après urappel sur les tumeurs endocrines du pancréas, la somatostatine, la calcitonine et le calcitonine gene related peptide (CGRP), l' auteur décrit une observation de tumeurs endocrines pancréatiques sécrétant calcitonine et glucagon (dosages radio-immunologiques et immunocytochimie), s' exprimant sous la forme : d' un processus tumoral hépatique (métastases), de diarrhée, de flushs, d' épisodes d' hypoglycémie, et traitées par la somatostatine retard. Il s' agit de la première observation décrite de tumeur pancréatique associant calcitonine et glucagon, les épisodes d' hypoglycémie sont expliqués par une sécrétion inappropriée d' insuline. L' auteur note enfin l' absence d' efficacité de la somatostine retard sur l' hyperglucagonémie (en opposition avec les données de la littérature) et sur l' hypercalcitoninémie (en accord avec les données de la littérature).
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Cuny, Thomas. "New regulatory mechanisms in the growth of endocrine tumors : digestive neuroendocrine tumors, pitiutary adenomas." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5061.

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Bien que rares, les tumeurs endocrines développées chez l'Homme demeurent problèmatiques. Une meilleure compréhension des mécanismes qui régulent leur croissance constitue un objectif essentiel pour identifier des cibles thérapeutiques nouvelles.Dans la première partie de cette thèse, nous avons étudié l'impact du microenvironnement tumoral (MeT), définit par l'ensemble des facteurs qui encerclent la niche tumorale primitive, sur la croissance des tumeurs endocrines digestives. In vitro, nous observons un effet prolifératif réciproque entre des fibroblastes, l'une des cellules pivots du MeT, et des lignées cellulaires humaines de tumeurs endocrines pancréatiques, tel qu'il est susceptible d'exister in situ. Dans une seconde partie, nous avons montré que le pegvisomant, un antagoniste du récepteur de l'hormone de croissance utilisé chez des patients atteint d'adénome hypophysaire somatotrope, n'a pas d'effet prolifératif in vitro sur les cellules somatotropes adénomateuses
Although rare, endocrine tumors developed in Humans remain problematic, such as a better understanding of their regulatory mechanisms of growth represent a step forward to identify new therapeutical targets.In the first part of this thesis, we investigated the impact of the tumor microenvironment (TME), as defined by the factors surrounding the tumor primitive niche, on the growth of human digestive endocrine tumors. We, here, showed the occurrence of a reciprocal proliferation between human fibroblasts, a key cell within the TME, and human pancreatic neuroendocrine tumor cell lines, suggesting that human fibroblasts may constitue a new therapeutical target of interest in the TME of digestive endocrine tumors. In a second part, we showed that pegvisomant (PEG), a growth hormone receptor antagonist currently used in patients with GH-secreting pituitary adenoma, did not impact in vitro the proliferation rate of GH-secreting adenoma cells and therefore is suitable in patients with a persisting GH-secreting pituitary adenoma residue after surgery
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Villaume, Karine. "Mécanismes de l'angiogenèse associée aux tumeurs endocrine digestives : rôle du VEGF." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10189/document.

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Les tumeurs endocrines digestives sont des tumeurs hypervasculaires, ce qui suggère l'existence d'un processus d'angiogenèse tumorale actif. Les mécanismes de l'angiogenèse tumorale associée aux tumeurs endocrines digestives sont complexes. Deux processus semblent coexister : les tumeurs les mieux différenciées sont capables de récapituler les propriétés pro-angiogéniques des cellules endocrines normales alors que les tumeurs moins différenciées et plus agressives sont associées à un processus d angiogenèse non spécifique, développé en réponse à l'hypoxie. Dans ces deux processus, le VEGF joue vraisemblablement un rôle important, dans la mesure où il fait partie intégrante du programme de différenciation endocrine. L'objectif de notre travail a été de mieux comprendre les mécanismes de sa régulation dans les cellules endocrines digestives tumorales et d'analyser son rôle dans la croissance tumorale, à travers une double approche expérimentale, in vitro et in vivo ; Nos résultats nous ont permis de : (a) montrer la complexité de la régulation de la synthèse et de la sécrétion du VEGF par les cellules endocrines néoplasiques, qui implique plusieurs voies de signalisation (PI3K/Akt/mTOR et p38/MAPK), dont les rôles respectifs varient selon le type de cellule étudiée ; (b) confirmer expérimentalement la dissociation entre expression du VEGF et capacités angiogéniques d'une part, propriétés invasives et métastatiques d'autre part ; (c) montrer expérimentalement que l'inhibition de l'angiogenèse peut contribuer à l'effet antitumoral de substances d'intérêt thérapeutique dans les tumeurs endocrines digestives
Digestive endocrine tumors are hypervascular tumors, likely to be associated with an active angiogenic process. The mechanisms of tumor angiogenesis in digestive endocrine tumors are complex. Two processes seem to coexist: well differentiated tumors are able to recapitulate the pro-angiogenic capacities of normal endocrine cells whereas less differentiated and more aggressive tumors are associated with a non specific angiogenic process, in response to hypoxia. In both processes, VEGF is likely to play an important role, since it is constitutively expressed by normal peptide-secreting endocrine cells, as part of their specific differentiation program. Our aim was to evaluate the mechanisms of regulation of VEGF synthesis and secretion by neoplastic digestive endocrine tumors and to analyze its role in tumor progression, through an in vitro and in vivo experimental approach. We were able to demonstrate that: (a) the regulation of VEGF synthesis and secretion is complex and involves several pathways (PI3K/Akt/mTOR and p38/MAPK), with different roles according to the cell studied; (b) there is a dissociation between VEGF expression and angiogenic capacities, on one hand, and invasive and metastatic properties, on the other hand; (c) the inhibition of angiogenesis may contribute to the anti-tumoral effect of several drugs of therapeutic interest in digestive endocrine tumors
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Hessman, Ola. "Genetic studies of endocrine abdominal tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5026-1/.

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Larsson, Gunnel. "Quality of Life in Patients with Endocrine Gastrointestinal Tumours." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4916-6/.

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Tsolakis, Apostolos V. "Characterization of Endocrine Cells and Tumours in the Stomach." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8804.

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Books on the topic "Endocryne tumour"

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Donal, O'Shea, and Bloom Stephen Robert, eds. Gastrointestinal endocrine tumours. London: Baillière Tindall, 1996.

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H, Clark Orlo, and American Cancer Society, eds. Endocrine tumors. Hamilton, Ont: BC Decker, 2003.

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1936-, Mazzaferri Ernest L., and Samaan Naguib A. 1925-, eds. Endocrine tumors. Boston: Blackwell Scientific Publications, 1993.

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Chapman, Catherine Eluned. Radioimmunodetection of endocrine tumours. Birmingham: University of Birmingham, 1987.

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Socinski, Mark A. Endocrine tumours and malignancies. London: Mosby-Wolfe, 1996.

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Andrew, Arnold, ed. Endocrine neoplasms. Boston: Kluwer Academic Publishers, 1997.

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M, Polak Julia, and Bloom Stephen Robert, eds. Endocrine tumours: The pathobiology ofregulatory peptide-producing tumours. Edinburgh: Churchill Livingstone, 1985.

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Solcia, Enrico, Günter Klöppel, and Leslie H. Sobin. Histological Typing of Endocrine Tumours. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59655-1.

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M, Polak Julia, and Bloom Stephen Robert, eds. Endocrine tumours: The pathobiology of regulatory peptide-producing tumours. Edinburgh: Churchill Livingstone, 1985.

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Surgical pathology of endocrine and neuroendocrine tumors. New York, NY: Humana Press, 2009.

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Book chapters on the topic "Endocryne tumour"

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Asa, Sylvia L. "Corticotroph Tumor." In Endocrine Pathology, 144–48. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5034.

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Asa, Sylvia L. "Lactotroph Tumor." In Endocrine Pathology, 465–67. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5037.

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Asa, Sylvia L. "Mammosomatotroph Tumor." In Endocrine Pathology, 481–83. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5038.

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Asa, Sylvia L. "Somatotroph Tumor." In Endocrine Pathology, 746–49. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5053.

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Asa, Sylvia L. "Thyrotroph Tumor." In Endocrine Pathology, 805–7. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5055.

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Asa, Sylvia L. "Gonadotroph Tumor." In Endocrine Pathology, 336–38. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5036.

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Klopfleisch, Robert. "Endocrine Tumors." In Veterinary Oncology, 217–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41124-8_12.

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Krausz, Yodphat. "Endocrine Tumors." In Hybrid PET/CT and SPECT/CT Imaging, 475–511. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-92820-3_13.

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Kruseman, A. C. Nieuwenhuijzen. "Endocrine Tumors." In Application of Monoclonal Antibodies in Tumor Pathology, 255–63. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3299-9_14.

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Brandt, Mary. "Endocrine Tumors." In Pearls and Tricks in Pediatric Surgery, 443–48. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51067-1_63.

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Conference papers on the topic "Endocryne tumour"

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Chopra, Seema. "Sclerosing sex cord stromal tumour of the ovary: A rare variant of ovarian neoplasms in childhood and adolescence." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685321.

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Case Report: 19 yr old unmarried girl c/o abdominal distension, loss of appetite and Irregular menstrual cycles x 5 months. USG: gross ascites, liver, Lobulated isoechoic mass in right adnexa, 7x5 cm, abutting right ovary. CA125: 1297 U/ml. FNAC Degenerated crushed cells & stromal fragments. Few scattered benign oval/spindle cells. Laparoscopy f/b laparotomy: 6 litres of straw colored asciic fluid drained. Uterus, left adnexa normal. Rt ovarian mass 6x7 cm, bilobed, arising from ovary. Solid, stuck in POD Adherent to gut. Right oophrectomy done. CA-125: 22 u/ml on day 6 post op. HPE – Sclerosing stromal tumor. Discussion: Sclerosing sex cord stromal tumour of the ovary is a rare tumor; accounts for 6% of ovarian stromal tumors Over a 100 reported tumors in literature. 80% of SST seen in second and third decade of life. Essentially a benign tumour, Usually a unilateral nonfunctioning tumor. Few cases with elevated serum CA-125 and hormonal abnormalities have been reported. Endocrine alterations caused by secretion of estrogen, progesterone or testosterone; induction of precocious puberty. Conclusion: Unilateral oophrectomy is the treatment. No recurrence of the tumor in the patients treated by oophorectomy or by conservative resection of the tumor. Excision of the tumor isfollowed by normal menses, pregnancy has also been reported.
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Qurbanova R.Sh., Asadova Sh.Sh., Vahabova Sh.B., Qurbanova R. Sh ,. Asadova Sh Sh ,. Vahabova Sh B. "CLİNİCAL AND MORPHOLOGİCAL PATTERNS OF ENDOCCRİNE-CELL CARSİNOMA OF UTERİ." In THE FIRST INTERNATIONAL SCIENTIFIC – PRACTICAL VIRTUAL CONFERENCE IN MODERN & SOCIAL SCIENCES: NEW DIMENSIONS, APPROACHES AND CHALLENGES. IRETC, 2022. http://dx.doi.org/10.36962/mssndac-01-11.

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The relevance of the problem. The endicrine-cell carsinoma of corpus uteri and of the cervex uteri remains insufficiently studied, from clinical and proqnosis point of view insignificant group of malignant epithelial organ tumors. The purpose of the study. Taking into consideration all stated above, as the goal of current investigation has been appeared complex statistic, clinic, laboratory-instrumental and morphological study of this cancer with comparative analysis of results in different types of treatment, and also including progression and prognosis of the process. Material and methods. 405 cases of endocrine cell carcinoma of corpus uteri were identified within 2016- 2021. Complaints, anamnesis and clinical stages of the process approximately didn’t differ from the analogous groups of comparison of patient by the moment of appeal for the specialized aid. The obtained results and their discussion. It was determined that the fraquancy of countering of the endocrine cell carcinoma of corpus uteri is 26,1%, but the cancer of cervix uteri 12,7% from total number patients, respectively. It was proved that there exists the direct correlation between the frequency of endocrine cell carcinoma of corpus uteri and anatomical section of organ. In 56,0% od cases primary tumor origin is situated in lower segment of corpus, circus cervix or proximal part of cervical canal. “Carcinoids” and “Small cell homomorphous solid squamous cell and glandular carcinoids” were encountered most frequently among histotypes and the versions. Morphologically in tumor tissue were revealed mono and double specialized apudocytes, producing olygopeptides and amines with paraendocrine effects. Proceeding from secretory status of the endocrine tumor component were distinguished following clinical-morphological subgroups of endocrine cell carcinoma of corpus utseri: 1) with prevailing secretion of peptides (excluding the somatostatin); 2) with prevailing secretion of amines and somatostatin; 3) with similar secretion of peptides and amines. It was proved that, there is direct close correlation between prevailing hormonal status and clinical progression of endocrine-cell carcinoma of corpus uteri. Despite of somatostatin predominant secretion of oligopeptides by the tumor accelerates clinical progression, and brings to early and multidirectional metastases. On the contrary, with prevailing secretion of amines (serotonin, melatonin) and somatostatin the process doesn’t improving, and metastases, also, recurrences after radical therapy isn’t seen. It was revealed, that when choosing the tactic of radical treatment, side by side with the other factors, must be taken into consideration the hormonal status of endocrine-cell carcinoma of corpus uteri. High prevalence of secretion of oligopeptides in endocrine-cell carcinoma of corpus uteri can be useful in direct indication for choosing of complex or combinative treatment with necessary use radical surgical operation. Keywords: distinguished following clinical-morphological subgroups.
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Larionov, A., D. Faratian, H. Caldwell, A. Sims, A. Fawkes, L. Murphy, L. Renshaw, J. Dixon, and J. Dixon. "miRNA Profiling of Endocrine-Resistant Breast Tumours." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5130.

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Larionov, A., D. Faratian, H. Caldwell, A. Sims, A. Fawkes, L. Murphy, L. Renshaw, J. Dixon, and J. Dixon. "Gene Expression Profiles of Endocrine Resistant Breast Tumours." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5132.

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Larionov, A., D. Faratian, H. Caldwell, A. Sims, A. Fawkes, L. Murphy, L. Renshaw, J. Dixon, and J. Dixon. "Genes Regulated by miRNA in Endocrine-Resistant Breast Tumours." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5149.

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Herold, Kevan. "Abstract IA09: Checkpoint inhibitor-induced autoimmune diabetes and endocrine syndromes." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-ia09.

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Bianchini, G., L. Pusztai, T. Iwamoto, CM Kelly, M. Zambetti, A. Fasolo, G. Del Conte, L. Santarpia, WF Symmans, and L. Gianni. "S1-7: Molecular Tumor Characteristics Influence Adjuvant Endocrine Treatment Outcome." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-s1-7.

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Paulinelli, Régis Resende, Luiz Fernando Jubé Ribeiro, Thauana Dias Santos, Elisana Maria Santos Caires, Marilha Gabriella Martins Pontes, and Bruna Morais Faria. "ONCOPLASTIC MAMMAPLASTY WITH DISGUISED GEOMETRIC COMPENSATION." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2020.

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Objective: To evaluate the results and follow-up of retrospective cohort of patients submitted to a new technique of oncoplastic mammaplasty, referred to as disguised geometric compensation mammaplasty (DGCM), which is suitable for tumors involving the glandular tissue in the lateral or medial pillars of the mammaplasty. Materials and Methods: A total of 25 patients with breast tumor involving the pillars of the mammaplasty were included, of whom 20 (80.00%) had invasive ductal carcinoma, 3 (12.00%) had phyllodes tumor, 1 (4.00%) had invasive lobular carcinoma, and 1 (4.00%) had in situ ductal carcinoma. Preoperative markings followed the “Wise-pattern” technique. The resection of the tumor in the pillar of the mammaplasty, preserving the overlying skin, was geometrically compensated with a correspondent area coming from the lower poles, which folds over itself and maintains the skin vascularity in the pillar. One patient was converted to classic geometric compensation due to a positive skin margin in the frozen section. Other patient combined a classic geometric compensation for the inner quadrants and DGCM for the outer quadrants in the same breast. One patient decided to submit to a bilateral mastectomy after adjuvant chemotherapy because of a BRCA2 mutation. Immediate fat grafting was done in one case. Approval from the ethics committee: n. 2.322.212. Results: Mean age was 46.96±9.53 years. Mean clinical tumor size was 47.21±22.16 mm before chemotherapy and 36.67±22.5 mm after chemotherapy. There were 11 (44.00%) locally advanced and 1 (4.00%) multicentric tumor. Nine (36.00%) patients were submitted to neoadjuvant chemotherapy. Adjuvant chemotherapy, endocrine therapy, and radiotherapy were indicated according to the necessity. Ptosis was corrected in all cases. The aesthetic results were rated as excellent or good in 21 cases (95.45%) by the Harvard scale and the BCCT.core. Three patients have not returned for the aesthetic evaluation after surgery. The BREAST-Q scores for the satisfaction with the breasts and satisfaction with outcomes were 81.50 (±15.00) and 90.44 (±11.70), respectively. Intraoperative frozen sections were done in 12 (48%) cases. There were two (8.00%) positive margins. One focus of DCIS in the skin margin was treated with radiotherapy, and the other positive margin was treated with re-excision. The complications were: three (12.00%) small wound dehiscences, two (8.00%) small skin necrosis, and two (8.00%) local hyperemia treated with antibiotics, two (8.00%) enlarged scars, and one (4.00%) small hematoma. There were not reoperations to treat complications. There was 1 (4.00%) local recurrence in the breast and axilla after 11 months, treated with radical mastectomy, and 1 (4.00%) metastasis to the brain after 3 months. No deaths were observed within a mean follow-up time of 16.28±11.39 months. Conclusion: The technique allowed breast conservation in situations requiring large resection in the pillars of the mammaplasty, with a high rate of free margins, correction of ptosis, satisfactory symmetry, and few complications.
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Freitas, Paola Ferreira, Juliana Costa Souza, Andre Mattar, Jorge Yoshinori Shida, and Luiz Henrique Gebrim. "NEOAJUVANT ENDOCRINE THERAPY IN BREAST CANCER: THE FIRST RESULTS OF 59 PATIENTS." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1086.

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Introduction: Luminal breast cancer cases, those with positive hormone receptors and human epidermal growth factor (HER 2) negative range around 70% of cases and it is known to be more frequent in older patients. Out of the neoadjuvant therapies, neoadjuvant endocrine therapy (NET) has been gaining more ground due to fewer side effects and tumor downstaging, making it possible for advanced breast cancer tumor patients to undergo breast conservation surgery (BCS). Objectives: To evaluate clinical and pathological response in women that underwent NET with Anastrozole (ANAS) at Pérola Byington Hospital (CRSM), a breast cancer reference center in São Paulo, Brazil. To determine the BCS (breastconserving surgery) rate after NET and the rate of disease progression during treatment. Methods: CRSM patients from 2018 to 2019 that underwent NET for luminal breast cancer with HER 2 negative were identified and data were reviewed. Results: 59 patients were identified, among which only 34 patients underwent breast surgery. All patients were treated with ANAS 1mg/daily. The median age was 63.5 years and average time on treatment was 203.5 days (approximately 6.78 months). Clinical stage at presentation was 3% Stage I, 6% Stage IIA, 32% stage IIB, 43% stage IIIA and 18% stage IIIB. After NET we found pathologic complete response (pCR) in 3% of the cases. and pathological downstage in different stages: Stage I 15%, Stage IIA 24%, Stage IIB 26%, stage IIB 26%, Stage IIIA 29% and stage IIIB 3%. During treatment 6.78% patients progressed, and all of them received chemotherapy. After NET 71% were submitted to adjuvant chemotherapy. The change for BCS was 19.35%. During surgical treatment patients 74% were submitted to axillary dissection and 26% had sentinel node biopsy (SNB). The average number of SNB removed was 5.33. No patients had to stop the medication due to toxicity. Conclusions: NET is still underutilized, having its optimal period of drug administration range around 8 to 12 months. It has been very important in aiding patients obtain better outcomes allowing for BCS while having fewer side effects when compared to neoadjuvant chemotherapy.
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Garcia, Cathy, Jaffarguriqbal Singh, Lauren Lawres, Sherry Agabiti, Daniel B. Burkhardt, Alexander Tong, Rebecca Cardone, Richard G. Kibbey, Smita Krishnaswamy, and Mandar D. Muzumdar. "Abstract LT013: Endocrine-exocrine signaling is a driver of obesity-associated pancreatic ductal adenocarcinoma." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-lt013.

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Reports on the topic "Endocryne tumour"

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Klapperich, Catherine, and Jennifer Rosen. Barriers to Therapy: A Novel 3-D Model to Study the Effect of Tumor Interstitial Pressure on Endocrine-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada475124.

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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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