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Journal articles on the topic 'Endocryne tumour'

Author: Grafiati
Published: 11 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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9

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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10

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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11

Chung, Daniel C., Alison P. Smith, David N. Louis, Fiona Graeme-Cook, Andrew L. Warshaw, and Andrew Arnold. "Analysis of the retinoblastoma tumour suppressor gene in pancreatic endocrine tumours." Clinical Endocrinology 47, no. 5 (November 1997): 523–28. http://dx.doi.org/10.1046/j.1365-2265.1997.2861110.x.

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12

Stridsberg, M., K. Öberg, Q. Li, U. Engström, and G. Lundqvist. "Measurements of chromogranin A, chromogranin B (secretogranin I), chromogranin C (secretogranin II) and pancreastatin in plasma and urine from patients with carcinoid tumours and endocrine pancreatic tumours." Journal of Endocrinology 144, no. 1 (January 1995): 49–59. http://dx.doi.org/10.1677/joe.0.1440049.

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Abstract Chromogranins and/or secretogranins constitute a family of water-soluble acidic glycoproteins that are present in almost all endocrine, neuroendocrine and neuronal tissue. Antibodies against chromogranins have been widely used for immunohistochemical staining of endocrine tissue and tumours of neuroendocrine origin. Furthermore, measurements of circulating chromogranin A have been used as a reliable marker for neuroendocrine tumour growth. In this study, we describe the development of specific antibodies against chromogranin A, chromogranin B (secretogranin I), chromogranin C (secretogranin II) and pancreastatin. The antibodies were used for immunohistochemical staining of normal and neoplastic neuroendocrine tissue and development of reliable radioimmunoassays for chromogranin A, chromogranin B, chromogranin C and pancreastatin. In 44 patients with carcinoid tumours, 17 patients with sporadic endocrine pancreatic tumours and 11 patients with endocrine pancreatic tumours and the multiple endocrine neoplasia 1 syndrome, plasma measurements revealed elevated chromogranin A levels in 99%, elevated chromogranin B in 88%, elevated chromogranin C in 6% and elevated pancreastatin in 46% of the patients. Urinary measurements revealed elevated levels in 39%, 15%, 14% and 33% of the patients respectively. Gel permeation chromatography of plasma and urine showed that circulating chromogranin A, and immunoreactive fragments of chromogranin A, had a higher molecular weight distribution than the chromogranin A fragments excreted to the urine. Furthermore, it was noted that most of the patients excreting chromogranin A fragments to the urine had previously been treated with streptozotocin, a cytotoxic agent known to induce renal tubular dysfunction. The antibodies raised proved useful for immunohistochemical staining and visualised endocrine cells in pancreatic islets, adrenal medulla and the small intestine as well as in endocrine pancreatic tumours, pheochromocytoma and midgut carcinoid tumours. In conclusion, the antibodies raised were useful for both immunohistochemical staining of normal tissue and endocrine tumours as well as development of specific radioimmunoassays for plasma measurements of the different chromogranins. Furthermore, we show that plasma measurements of chromogranin A and B were superior to measurements of chromogranin C and pancreastatin and plasma measurements of the different chromogranins were more reliable as markers for tumour growth than the corresponding urine measurements. Journal of Endocrinology (1995) 144, 49–59
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13

Nisa, Zaibun, and Soha El Shiekh. "A retrospective analysis of Estrogen Receptors in Breast Cancer and its comparison with national standards." Gazette of Medical Sciences 3, no. 1 (March 2, 2022): 70–73. http://dx.doi.org/10.46766/thegms.oncol.22020601.

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Estrogen receptor (ER) positive tumours are more common than ER negative tumours and tend to have a better prognosis. These tumours respond well to endocrine therapy as compared to ER negative tumours, thus avoiding the harmful effects of chemotherapy. Moreover, since ER positive tumours are associated with slow tumour growth and low histology grade, it increases the overall survival.
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14

Guidetti, Elena, Monica Cevenini, Maria Luigia Cipollini, Martina Ferrata, Paola Tomassetti, and Roberto Corinaldesi. "MEN1 syndrome: an anusual case." Clinical Management Issues 6, no. 1S (October 13, 2015): 23–28. http://dx.doi.org/10.7175/cmi.v6i1s.493.

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Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant endocrine disorder and is characterised by the concurrent appearance of adenomas of the parathyroid glands, neuroendocrine-enteropancreatic tumours, and pituitary adenomas, as well as other types of less frequent tumours, such as adrenal cortical tumours, carcinoid tumours, lipomas, etc. Two different forms, familial and sporadic, have been described. The gene responsible, MEN1, consists of 10 exons encoding a 610-amino acid protein known as menin. The MEN1 syndrome is caused by inactivating mutations in MEN1 tumour suppressor gene. The combination of clinical and genetic investigation helps in the diagnosis. Genetic testing has been advocated to identify MEN1 carriers of the MEN1 families for the purpose of earlier detection of tumours. We present a patient with traditionally described manifestations of MEN1 (a parathyroid hyperplasia associated with a pancreatic neuroendocrine tumour and a gastrinoma), but with a negative genetic test for the MEN1 mutation.
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15

Andersson, T., B. Eriksson, A. Hemmingsson, B. Jung, E. Lindh, K. Å. Thuomas, and K. Öberg. "Effect of Interferon on T1 Relaxation Times of Liver Metastases from Endocrine Gastrointestinal Tumours." Acta Radiologica 29, no. 1 (January 1988): 21–25. http://dx.doi.org/10.1177/028418518802900105.

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Eight patients with liver metastases from endocrine gastrointestinal tumours were examined with magnetic resonance imaging of the liver before and during treatment with interferon. T1, T2 and tumour size were measured and compared with tumour marker levels and symptomatic improvement or deterioration. Before therapy all tumours showed a long T1 and T2, in comparison to normal liver and fat, and during therapy they all showed a decrease in T1. As no change in liver T1 and fat T1 occurred, the decreased tumour T1 is considered to be a therapy effect. This cannot be fully explained but is possibly due to a reduction in tumour growth rate during interferon treatment. There was no certain correlation between tumour T1 and tumour marker levels or symptomatic changes.
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16

Reed, NS. "Endocrine Tumours." British Journal of Cancer 72, no. 1 (July 1995): 252–53. http://dx.doi.org/10.1038/bjc.1995.317.

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17

Whimster, W. F. "Endocrine Tumours." Postgraduate Medical Journal 62, no. 723 (January 1, 1986): 73. http://dx.doi.org/10.1136/pgmj.62.723.73.

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18

Andersson, T., B. Eriksson, A. Hemmingsson, P. G. Lindgren, and K. Öberg. "Angiography, Computed Tomography, Magnetic Resonance Imaging and Ultrasonography in Detection of Liver Metastases from Endocrine Gastrointestinal Tumours." Acta Radiologica 28, no. 5 (September 1987): 535–39. http://dx.doi.org/10.1177/028418518702800507.

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Twenty-five patients with endocrine tumours (13 with endocrine pancreatic tumours and 12 with carcinoids) were examined with angiography, computed tomography, magnetic resonance imaging and ultrasonography. Seventeen patients had liver metastases and were followed between 3 and 66 months with serial examinations during treatment with chemotherapeutic agents and interferon. The efficiency of the various techniques to detect metastases was investigated. Analysis of changes in tumour size during treatment was made to see if treatment effects could be monitored with radiologic examinations. Ultrasonography was the best non-invasive method for detection of metastases and is recommended as standard method for imaging in this group of patients. Angiography was even better showing extremely small metastases, less than 5 mm, and is recommended in selected cases. With one exception, no significant change in tumour size was noted in spite of clear laboratory and clinical signs of therapy effect indicating that tumour size determination is not useful for therapy monitoring in this type of disease.
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19

Wickramasuriya, P. K. H., D. C. Rajapakshe, P. Lambiyas, and L. Y. P. Randunu. "Pancreatic neuro-endocrine tumour." Journal of the Ruhunu Clinical Society 22, no. 1 (December 15, 2017): 29. http://dx.doi.org/10.4038/jrcs.v22i1.33.

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20

Kann, P. H., E. Balakina, D. Ivan, D. K. Bartsch, S. Meyer, K.-J. Klose, Th Behr, and P. Langer. "Natural course of small, asymptomatic neuroendocrine pancreatic tumours in multiple endocrine neoplasia type 1: an endoscopic ultrasound imaging study." Endocrine-Related Cancer 13, no. 4 (December 2006): 1195–202. http://dx.doi.org/10.1677/erc.1.01220.

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Endoscopic ultrasound (EUS) enables detection and localization of pancreatic neuroendocrine tumours. Even small tumours down to a diameter of 1–2 mm can be visualized. Since such small tumours usually cannot be detected by computed tomography (ct), magnetic resonance imaging (mri) and somatostatin receptor scintigraphy (srs), and experience with EUS imaging is limited, there is no clear evidence for clinical management in multiple endocrine neoplasia type 1 (MEN1). Knowledge about the natural course of growth and metastatic distribution is mandatory to come to appropriate clinical decisions and guidelines. This prospective study was aimed to assess the natural course of small (<15 mm) neuroendocrine pancreatic tumours without clinical symptoms due to endocrine activity or mechanical problems and without clear indication for surgical therapy in MEN1 by EUS. A total of 82 asymptomatic tumours <15 mm (5.9 ± 3.2 mm diameter at baseline) in 20 patients with MEN1-disease (8 female/12 male, 43 ± 13 years) were studied over a period of 20 ± 12 months (33.8 patient years, 106.7 tumour years) by EUS. Change in largest diameter of each tumour and annual tumour incidence rate in the patients’ cohort were calculated. Increase of largest tumour diameter was found to be 1.3 ± 3.2% per month, annual tumour incidence rate 0.62 new tumours per patient year. In one patient, rapid progressive pancreatic manifestation of MEN1 was observed. There was no evidence in ct and/or srs and/or mri for metastatic disease in all patients. Only 4/84 (4.8%) pancreatic tumours could be visualized by computed tomography, 5/79 (6.3%) by somatostatin receptor imaging and 4/39 (10.3%) by magnetic resonance imaging. Small asymptomatic neuroendocrine pancreatic tumours in MEN1 usually seem to grow slowly. Annual tumour incidence rate is low. However, faster growing tumours and patients with rapidly progressive disease can be observed. Risk for obvious metastatic disease from asymptomatic neuroendocrine pancreatic tumours <15 mm in MEN1 seems to be low.
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21

Raverot, Gerald, Emmanuel Jouanneau, and Jacqueline Trouillas. "MANAGEMENT OF ENDOCRINE DISEASE: Clinicopathological classification and molecular markers of pituitary tumours for personalized therapeutic strategies." European Journal of Endocrinology 170, no. 4 (April 2014): R121—R132. http://dx.doi.org/10.1530/eje-13-1031.

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Pituitary tumours, the most frequent intracranial tumour, are historically considered benign. However, various pieces of clinical evidence and recent advances in pathological and molecular analyses suggest the need to consider these tumours as more than an endocrinological disease, despite the low incidence of metastasis. Recently, we proposed a new prognostic clinicopathological classification of these pituitary tumours, according to the tumour size (micro, macro and giant), type (prolactin, GH, FSH/LH, ACTH and TSH) and grade (grade 1a, non-invasive; 1b, non-invasive and proliferative; 2a, invasive; 2b, invasive and proliferative and 3, metastatic). In addition to this classification, numerous molecular prognostic markers have been identified, allowing a better characterisation of tumour behaviour and prognosis. Moreover, clinical and preclinical studies have demonstrated that pituitary tumours could be treated by some chemotherapeutic drugs or new targeted therapies. Our improved classification of these tumours should now allow the identification of prognosis markers and help the clinician to propose personalised therapies to selected patients presenting tumours with a high risk of recurrence.
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22

Berwaerts, J. "A pseudo-endocrine suprasellar tumour: review of primitive neuroectodermal tumours in adults." Endocrine Related Cancer 5, no. 4 (December 1, 1998): 303–10. http://dx.doi.org/10.1677/erc.0.0050303.

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23

Clifton-Bligh, Rory. "Oncogenes (and tumour suppressors) in endocrine tumours - current diagnostics and future approaches." Pathology 41 (January 2009): 29. http://dx.doi.org/10.1097/01268031-200941001-00062.

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24

Clifton-Bligh, Rory. "Oncogenes (and tumour suppressors) in endocrine tumours – current diagnostics and future approaches." Pathology 41 (January 2009): 18. http://dx.doi.org/10.1097/01268031-200941001-00044.

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25

Konings, Gonda, Niina Saarinen, Bert Delvoux, Loes Kooreman, Pasi Koskimies, Camilla Krakstad, Kristine Fasmer, et al. "Development of an Image-Guided Orthotopic Xenograft Mouse Model of Endometrial Cancer with Controllable Estrogen Exposure." International Journal of Molecular Sciences 19, no. 9 (August 28, 2018): 2547. http://dx.doi.org/10.3390/ijms19092547.

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Endometrial cancer (EC) is the most common gynaecological malignancy in Western society and the majority of cases are estrogen dependent. While endocrine drugs proved to be of insufficient therapeutic value in the past, recent clinical research shows promising results by using combinational regimens and pre-clinical studies and identified potential novel endocrine targets. Relevant pre-clinical models can accelerate research in this area. In the present study we describe an orthotopic and estrogen dependent xenograft mouse model of EC. Tumours were induced in one uterine horn of female athymic nude mice using the well-differentiated human endometrial adenocarcinoma Ishikawa cell line—modified to express the luciferase gene for bioluminescence imaging (BLI). BLI and contrast-enhanced computed-tomograph (CE-CT) were used to measure non-invasive tumour growth. Controlled estrogen exposure was achieved by the use of MedRod implants releasing 1.5 μg/d of 17β-estradiol (E2) in ovariectomized mice. Stable E2 serum concentration was demonstrated by LC-MS/MS. Induced tumours were E2 responsive as increased tumour growth was observed in the presence of E2 but not placebo, assessed by BLI, CE-CT, and tumour weight at sacrifice. Metastatic spread was assessed macroscopically by BLI and histology and was seen in the peritoneal cavity, in the lymphovascular space, and in the thoracic cavity. In conclusion, we developed an orthotopic xenograft mouse model of EC that exhibits the most relevant features of human disease, regarding metastatic spread and estrogen dependency. This model offers an easy to manipulate estrogen dosage (by simply adjusting the MedRod implant length), image-guided monitoring of tumour growth, and objectively measurable endpoints (including tumour weight). This is an excellent in vivo tool to further explore endocrine drug regimens and novel endocrine drug targets for EC.
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Bajaj, Anubha. "The Genetic Multiplicity- Multiple Endocrine Neoplasia type I." International Journal of Infection Prevention 1, no. 2 (February 5, 2020): 1–13. http://dx.doi.org/10.14302/issn.2690-4837.ijip-20-3176.

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Multiple endocrine neoplasia type 1 (MEN1) is a syndrome emerging from characteristic mutations of MEN1 gene with concurrently enunciated multiple endocrine and tumours and associated non-endocrine neoplasm. Previously designated as Werner’s syndrome, MEN1 syndrome denominates genomic mutation within chromosome 11q13 or a tumour suppressor gene with a distinctive protein product nomenclated as “menin”. MEN1 syndrome demonstrates an autosomal dominant pattern of disease inheritance where genomic mutations delineate a comprehensive (100%) disease penetrance. MEN1 gene was initially identified in 1997 upon chromosome 11q13. Although twelve genetic mutations were primarily identified, currently beyond eighteen hundred genomic mutations are scripted1, 2. MEN1 syndrome is comprised of diverse combination of twenty or more endocrine and non-endocrine tumours exemplifying a classic triad of pituitary, parathyroid and pancreatic neoplasm. Diverse non endocrine tumours enunciated with MEN1 syndrome are denominated with meningioma, ependymoma or angiofibroma1, 2. Endocrine tumours are discerned on account of excessive hormonal secretion engendered from various neoplasm or on account of neoplastic evolution. Approximately 10% instances can occur due to a de-novo genomic variant. Offspring of an individual with MEN1 syndrome quantifies a 50% possibility of inheriting the genomic variant. Cogent prenatal diagnosis can be determined in instances where specific genomic variant of a particular family is known. Physical, psychological and social restrictions are prevalent with MEN1 syndrome. Heterozygotes with MEN1 genetic variant are denominated as carriers and manifest a two- fold possible mortality1, 2.
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Schott, Matthias. "Immunesurveillance by dendritic cells: potential implication for immunotherapy of endocrine cancers." Endocrine-Related Cancer 13, no. 3 (September 2006): 779–95. http://dx.doi.org/10.1677/erc.1.01133.

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Dendritic cells (DCs) are highly efficient antigen-presenting cells in the immune system with the potential to regulate the system and induce a cytotoxic T-cell response. As a proof of principle, a multitude of animal and human studies has demonstrated that immunization with antigen-loaded DCs may lead to anti-tumour immune responses with tumour regression and rejection of cancer. The identification of tumour antigens that can be recognized by T lymphocytes has facilitated the development of new protocols and enabled immunologists to monitor immune responses. However, to date, long-term clinical effects on larger numbers of cancer patients are missing, and there is no generally accepted DC generation or activation protocol. This review will focus on the most important findings on the role of DCs within the immune system and how to generate and activate these cells in order to induce cytotoxic immunity in non-endocrine and endocrine malignancies. Recently, we and other researchers reported on DC vaccinations in patients with endocrine malignancies mainly in metastasized medullary thyroid carcinoma resulting in tumour-specific immunity and partial clinical responses in some cases. Based on these and other in vitro data, new DC vaccination protocols for the treatment of patients with endocrine tumours have now been conducted.
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28

Bosman, Fred T. "Endocrine cells in non-endocrine tumours." Journal of Pathology 159, no. 3 (November 1989): 181–82. http://dx.doi.org/10.1002/path.1711590302.

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29

Wright, Nicholas A. "Endocrine cells in non-endocrine tumours." Journal of Pathology 161, no. 1 (May 1990): 85–87. http://dx.doi.org/10.1002/path.1711610114.

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30

Gui, Xianyong, Ziran Meng, Yarrow J. McConnell, Shuhong Liu, Vincent G. Falck, Lloyd A. Mack, and Walley J. Temple. "Differing expression profiles of Notch/enterocyte and Wnt/secretory lineage signallings are associated with morphological diversity of appendiceal tumours." Journal of Clinical Pathology 70, no. 1 (July 1, 2016): 40–50. http://dx.doi.org/10.1136/jclinpath-2016-203645.

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BackgroundTumours of appendix, including classic carcinoid tumour (CCT), goblet cell carcinoid (GCC), low-grade appendiceal mucinous neoplasm, high-grade appendiceal mucinous neoplasm/mucinous carcinoma (MCA) and non-mucinous adenocarcinoma (NMA), show different and sometimes mixed morphological features. It was hypothesised that these tumours originate from common tumour stem cell(s) with potential of various cell lineage differentiation. In normal intestinal epithelium, absorptive lineage (enterocytes) differentiation is driven by Notch-Hes1 pathway, while secretory lineage is driven by Wnt-Math1 pathway and further separated by different downstream signallings into three sublineages (Gfi1-Klf4/Elf3 for goblet cells, Gfi1-Sox9 for Paneth cells and Ngn3-Pdx1/Beta2/Pax4 for enteroendocrine cells).MethodsThe expressions of various signalling proteins in different appendiceal tumours were detected by immunohistochemistry on tumour tissue microarray.ResultsCCT showed reduced Hes1/Elf3 and Sox9/Klf4 coupled with elevated Math1, in keeping with endocrine phenotype. As compared with CCT, GCC showed higher Klf4 and similar Ngn3/Pax4, indicative of a shift of differentiation towards goblet cells as well as endocrine cells. GCC displayed a Notch signalling similar to adenocarcinoma. Mucinous tumours showed lower Elf3 than normal appendiceal epithelium and higher Math1/Gfi1/Klf4, suggestive of a differentiation towards less enterocytes but more goblet cells. NMA showed Notch signalling similar to other glandular tumours, but lower Klf4. However, some seemingly paradoxical changes were also observed, probably suggesting gene mutations and/or our incomplete understanding of the intestinal cell differentiation.ConclusionsWnt/secretory lineage protein and Notch/absorptive lineage protein expression profiles are generally associated with the tumour cell differentiation and morphological diversity of common appendiceal tumours.
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31

de Herder, W. W., E. P. Krenning, C. H. J. Van Eijck, and S. W. J. Lamberts. "Considerations concerning a tailored, individualized therapeutic management of patients with (neuro)endocrine tumours of the gastrointestinal tract and pancreas." Endocrine-related cancer 11, no. 1 (March 2004): 19–34. http://dx.doi.org/10.1677/erc.0.0110019.

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Endocrine tumours of the gastrointestinal tract and pancreas may present at different disease stages with either hormonal or hormone-related symptoms/syndromes, or without hormonal symptoms. They may occur either sporadically or as part of hereditary syndromes. In the therapeutic approach to a patient with these tumours, excessive hormonal secretion and/or its effects should always be controlled first. Tumour-related deficiencies or disorders should also be corrected. Subsequently, control should be aimed at the tumour growth. Surgery is generally considered as first-line therapy for patients with localized disease, as it can be curative. However, in patients with metastatic disease the role of first-line surgery is not clearly established and other therapies should be considered, such as non-surgical cytoreductive therapies, biotherapy (with somatostatin analogues or interferon-alpha), embolization and chemoembolization of liver metastases, chemotherapy (with single or multiple dose regimens) and peptide receptor-targeted radiotherapy. The delicate balance of the use of the different therapeutical options in patients with endocrine tumours of the gastrointestinal tract and pancreas emphasizes the importance of team approach and team expertise.
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32

Carter, D. C. "Pancreatic endocrine tumours." BMJ 294, no. 6572 (March 7, 1987): 593–94. http://dx.doi.org/10.1136/bmj.294.6572.593.

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33

Kölby, L., O. Nilsson, and H. Ahlman. "Gastroduodenal Endocrine Tumours." Scandinavian Journal of Surgery 93, no. 4 (December 2004): 317–23. http://dx.doi.org/10.1177/145749690409300411.

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34

Wank, Stephen A. "Gastrointestinal Endocrine Tumours." Gastroenterology 114, no. 5 (May 1998): 1107. http://dx.doi.org/10.1016/s0016-5085(98)70337-3.

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35

de Herder, W. W., and S. W. J. Lamberts. "Gut endocrine tumours." Best Practice & Research Clinical Endocrinology & Metabolism 18, no. 4 (December 2004): 477–95. http://dx.doi.org/10.1016/j.beem.2004.08.003.

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36

Sarwar, N., J.-S. Kim, J. Jiang, D. Peston, H. D. Sinnett, P. Madden, J. M. Gee, et al. "Phosphorylation of ERα at serine 118 in primary breast cancer and in tamoxifen-resistant tumours is indicative of a complex role for ERα phosphorylation in breast cancer progression." Endocrine-Related Cancer 13, no. 3 (September 2006): 851–61. http://dx.doi.org/10.1677/erc.1.01123.

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Oestrogen receptor-α (ERα) is an important prognostic marker in breast cancer and endocrine therapies are designed to inhibit or prevent ERα activity. In vitro studies have indicated that phosphorylation of ERα, in particular on serine 118 (S118), can result in activation in a ligand-independent manner, thereby potentially contributing to resistance to endocrine agents, such as tamoxifen and aromatase inhibitors. Here we report the immunohistochemistry (IHC) of S118 phosphorylation in 301 primary breast tumour biopsies. Surprisingly, this analysis shows that S118 phosphorylation is higher in more differentiated tumours, suggesting that phosphorylation at this site is associated with a good prognosis in patients not previously treated with endocrine agents. However, we also report that S118 phosphorylation was elevated in tumour biopsies taken from patients who had relapsed following tamoxifen treatment, when compared to pre-treatment biopsies. Taken together, these data are consistent with the view that S118 phosphorylation is a feature of normal ERα function and that increases in levels of phosphorylation at this site may play a key role in the emergence of endocrine resistance in breast cancer.
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37

Thuróczy, J., F. J. van Sluijs, H. S. Kooistra, G. Voorhout, J. A. Mol, J. S. van der Linde‐Sipman, and A. Rijnberk. "Multiple endocrine neoplasias in a dog: Corticotrophic tumour, bilateral adrenocortical tumours, and pheochromocytoma." Veterinary Quarterly 20, no. 2 (April 1998): 56–61. http://dx.doi.org/10.1080/01652176.1998.9694839.

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38

Arnold, R., M. E. Trautmann, W. Creutzfeldt, R. Benning, M. Benning, C. Neuhaus, R. Jurgensen, et al. "Somatostatin analogue octreotide and inhibition of tumour growth in metastatic endocrine gastroenteropancreatic tumours." Gut 38, no. 3 (March 1, 1996): 430–38. http://dx.doi.org/10.1136/gut.38.3.430.

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39

Buchfelder, M., R. Fahlbusch, M. Walther, and K. Mann. "Endocrine disturbances in suprasellar germinomas." Acta Endocrinologica 120, no. 3 (March 1989): 337–42. http://dx.doi.org/10.1530/acta.0.1200337.

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Abstract. The authors have investigated hypothalamicpituitary function in 8 patients (aged 9–27 years) with surgically and histologically proven suprasellar germinomas. Diabetes insipidus was found in 7 patients. All the patients had hypogonadism and hypocortisolism as judged by dynamic endocrine testing. Hypothyroidism was found in 6. Moreover, growth hormone secretion, as assessed by insulin-induced hypoglycemia, was defective in all patients. Comparison of results of insulin-induced hypoglycemia testing and stimulation tests by CRH and GHRH suggested that all patients had a primary supra-hypohypophyseal lesion rather than a primary pituitary defect. The authors conclude that suprasellar germinomas, although uncommon, should be included in the differential diagnosis of juvenile suprasellar tumours and in cases suggestive of idiopathic diabetes insipidus, even if neuroradiological investigation fails to demonstrate a discrete tumour.
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40

Kimura, Shioko, and Anthony Glover. "Editorial - Endocrine Tumor." Molecular and Cellular Endocrinology 469 (July 2018): 1–2. http://dx.doi.org/10.1016/j.mce.2018.04.017.

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41

Wang, Jichen. "Endocrine tumor abdomen." European Journal of Radiology 62, no. 3 (June 2007): 315–16. http://dx.doi.org/10.1016/j.ejrad.2007.02.039.

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42

Grötzinger, Carsten. "Tumour Biology of Gastroenteropancreatic Neuroendocrine Tumours." Neuroendocrinology 80, no. 1 (2004): 8–11. http://dx.doi.org/10.1159/000080732.

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43

Beghelli, Stefania, Giuseppe Pelosi, Giuseppe Zamboni, Massimo Falconi, Calogero Iacono, Cesare Bordi, and Aldo Scarpa. "Pancreatic endocrine tumours: evidence for a tumour suppressor pathogenesis and for a tumour suppressor gene on chromosome 17p." Journal of Pathology 186, no. 1 (September 1998): 41–50. http://dx.doi.org/10.1002/(sici)1096-9896(199809)186:1<41::aid-path172>3.0.co;2-l.

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44

Moncho-Amor, Veronica, Probir Chakravarty, Christophe Galichet, Robin Lovell-Badge, and Karine Rizzoti. "Sox2 Is Required Independently in Both Stem and Differentiated Cells for Pituitary Tumour Genesis in P27 Null Mice." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A510. http://dx.doi.org/10.1210/jendso/bvab048.1043.

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Abstract Tumour development can depend on cell intrinsic dysfunction, but, in some cases, extrinsic factors are important drivers. Here, we have established a genetically tractable model demonstrating that the same gene is relevant both cell-autonomously and non-cell-autonomously for tumorigenesis. P27, a cell cycle inhibitor, is also able to drive repression of the transcription factor Sox2. This interaction plays a crucial role during development of p27-/- pituitary tumours because loss of one copy of Sox2 impairs tumorigenesis (1). However, SOX2 is expressed in both endocrine and stem cells (SC), and its contribution to tumorigenesis in either cell type is unknown. We have thus explored the cellular origin and mechanisms underlying endocrine tumorigenesis in p27-/- pituitaries. We found that pituitary hyperplasia is associated with reduced cellular differentiation, in parallel with increased levels of SOX2 in stem and endocrine cells. Using conditional loss-of-function and lineage tracing approaches, we show that SOX2 is required cell-autonomously in p27-/- endocrine cells for these to give rise to tumours, and in SCs for promotion of tumorigenesis. This is supported by studies deleting the Sox2 regulatory region 2 (Srr2), the target of P27 repressive action. Single cell transcriptomic analysis further reveals that activation of a SOX2-dependent MAPK pathway in SCs is important for tumorigenesis. Altogether, our data highlight different aspects of the role of SOX2 following loss of p27, according to cellular context, and uncover an unexpected SOX2-dependent tumour-promoting role for SCs. Our results imply that targeting SCs, in addition to tumour cells, may represent an efficient anti-tumoral strategy in certain contexts. (1) Li H, et al. (2012) p27(Kip1) directly represses Sox2 during embryonic stem cell differentiation. Cell Stem Cell 11(6):845-852.
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45

Harding, Brian, Manuel C. Lemos, Anita A. C. Reed, Gerard V. Walls, Jeshmi Jeyabalan, Michael R. Bowl, Hilda Tateossian, et al. "Multiple endocrine neoplasia type 1 knockout mice develop parathyroid, pancreatic, pituitary and adrenal tumours with hypercalcaemia, hypophosphataemia and hypercorticosteronaemia." Endocrine-Related Cancer 16, no. 4 (December 2009): 1313–27. http://dx.doi.org/10.1677/erc-09-0082.

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Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized in man by parathyroid, pancreatic, pituitary and adrenal tumours. The MEN1 gene encodes a 610-amino acid protein (menin) which is a tumour suppressor. To investigate the in vivo role of menin, we developed a mouse model, by deleting Men1 exons 1 and 2 and investigated this for MEN1-associated tumours and serum abnormalities. Men1+/− mice were viable and fertile, and 220 Men1+/− and 94 Men1+/+ mice were studied between the ages of 3 and 21 months. Survival in Men1+/− mice was significantly lower than in Men1+/+ mice (<68% vs >85%, P<0.01). Men1+/− mice developed, by 9 months of age, parathyroid hyperplasia, pancreatic tumours which were mostly insulinomas, by 12 months of age, pituitary tumours which were mostly prolactinomas, and by 15 months parathyroid adenomas and adrenal cortical tumours. Loss of heterozygosity and menin expression was demonstrated in the tumours, consistent with a tumour suppressor role for the Men1 gene. Men1+/− mice with parathyroid neoplasms were hypercalcaemic and hypophosphataemic, with inappropriately normal serum parathyroid hormone concentrations. Pancreatic and pituitary tumours expressed chromogranin A (CgA), somatostatin receptor type 2 and vascular endothelial growth factor-A. Serum CgA concentrations in Men1+/− mice were not elevated. Adrenocortical tumours, which immunostained for 3-β-hydroxysteroid dehydrogenase, developed in seven Men1+/− mice, but resulted in hypercorticosteronaemia in one out of the four mice that were investigated. Thus, these Men1+/− mice are representative of MEN1 in man, and will help in investigating molecular mechanisms and treatments for endocrine tumours.
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46

Pal, Tuya, Alexander Liede, Margot Mitchell, Alain Calender, and Steven A. Narod. "Intestinal Carcinoid Tumours in a Father and Daughter." Canadian Journal of Gastroenterology 15, no. 6 (2001): 405–9. http://dx.doi.org/10.1155/2001/908056.

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Familial cases of carcinoid tumours that are not associated with any known syndrome or disease are extremely rare. All cases reported in the world literature have involved carcinoid tumours of the gastrointestinal tract. Two cases of carcinoid tumours of the small intestine in a father and daughter are presented. Laboratory analyses did not support the hypothesis that the occurrence of carcinoid tumours in this family is a variant of the multiple endocrine neoplasia type 1 syndrome. A review of the literature on familial occurrence of intestinal carcinoid tumours in the absence of any other known carcinoid tumour-predisposing genetic syndrome is provided.
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47

Mills, Jonathan, and William Dalleywater. "Thyroid cancer." InnovAiT: Education and inspiration for general practice 11, no. 4 (March 1, 2018): 212–17. http://dx.doi.org/10.1177/1755738017752742.

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Thyroid neoplasms represent the most-common endocrine tumour and constitute an extremely varied spectrum of disease. At the most severe end, they may have a very poor prognosis. Malignant thyroid tumours constitute around 1% of cancers and cancer-specific deaths in the UK, with just under 3000 new diagnoses each year and around 350 deaths annually in the UK alone. Although the incidence has doubled over the last 20 years, the mortality rate among men has not changed, although survival rates have improved in women. Thyroid cancer originates from follicular or parafollicular thyroid cells that can give rise to cancer that is well-differentiated to poorly differentiated. Most tumours retain endocrine differentiation, however, and may cause problematic symptoms from aberrant hormone levels.
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48

Savvoukidis, Theodoros, Silke Cameron, and Giuliano Ramadori. "Sixty-eight consecutive cases of neuroendocrine tumor treated with somatostatin analogues: A 20-year single-center experience." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e14707-e14707. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14707.

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e14707 Background: Neuroendocrine tumours (NET) arise from enterochromaffine and related cells found in epithelial organs throughout the body. Hormone related symptoms in neuroendocrine tumours are well treated with somatostatin analogues. Previous experience has demonstrated some antiproliferative activity of somatostatin analogues in the treatment of NET. Methods: In the last 20 years 68 patients with histologically proven NET were treated: primaries in small bowel (27), pancreas (17), rectum (9), appendix (5), lung (4), unknown (3), extra- adrenal abdominal paragangliomas (2) and stomach (1). The mean age of first diagnosis was 56 years. All of them received somatostatin analogues in long acting depot administration (or combination interferon/somatostatin analogues) for a minimum period of two months and a maximum of 139 months. Somatostatin therapy was started in patients with endocrine-active tumours immediately after the diagnosis and in patients with endocrine-inactive tumours after an observation time of 3 months without therapy if progress was observed. Tumor size was assessed every 3 months after begin of therapy. Results: Best responses were a stable disease in 46 of 68 patients (68%) and a partial remission in 2 (3%). Twenty of 68 patients (29%) showed progress. The responses achieved were in small bowel 20/27; pancreas 14/17; rectum 7/9; appendix 4/5 and lung 3/4. The median duration of response was 34 months. Conclusions: Our results document that treatment with somatostatin analogues prolongs time to progression in NET. Stabilisation of tumour mass itself is a relevant outcome for patients with NET. The benefit of somatostin analogues is indipendent to use of chemotherapy. Because of its efficacy and the good tolerability somatostatin analogues can be considered a first line treatment option.
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49

Culig, Z., H. Steiner, G. Bartsch, and A. Hobisch. "Mechanisms of endocrine therapy-responsive and -unresponsive prostate tumours." Endocrine-Related Cancer 12, no. 2 (June 2005): 229–44. http://dx.doi.org/10.1677/erc.1.00775a.

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Several options for the endocrine treatment of non-organ-confined prostate cancer are available. They include surgical or medical removal of androgenic hormones or administration of non-steroidal anti-androgens. However, tumour progression after a period of remission of the disease inevitably occurs in virtually all patients. The androgen receptor (AR) is, in various tumour models, implicated in the development of therapy resistance but molecular mechanisms that by-pass the receptor have also been described. Adaptation mechanisms relevant to tumour recurrence include up-regulation of AR mRNA and protein, overexpression of AR coactivators, increased activation of mutated receptors by steroids and anti-androgens, and ligand-independent activation. For research studies, sublines that respond to but do not depend on androgen for their proliferation were generated. Coactivators SRC-1, TIF-2, RAC3, p300, CBP, Tip60, and gelsolin are highly expressed in endocrine therapy-resistant prostate cancer. AR point mutations are increasingly detected in relapsed cancers and contribute to the failure of endocrine therapy in a subgroup of patients. Ligand-independent activation of the AR by HER-2/neu and interleukin-6 is associated with activation of the signalling pathway of mitogen-activated protein kinase. Increased activity of intracellular kinases may affect cellular events in both an AR-dependent and -independent manner. Mitogen-activated protein kinases are strongly phosphorylated in endocrine therapy-resistant prostate tumours. Similarly, activation of the AR by phosphorylated protein kinase B, Akt, has also been reported in prostate cancer. Activation of the Akt pathway contributes to increased survival of prostate tumour cells.
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50

De Sousa, Sunita M. C., Mark J. McCabe, Kathy Wu, Tony Roscioli, Velimir Gayevskiy, Katelyn Brook, Lesley Rawlings, et al. "Germline variants in familial pituitary tumour syndrome genes are common in young patients and families with additional endocrine tumours." European Journal of Endocrinology 176, no. 5 (May 2017): 635–44. http://dx.doi.org/10.1530/eje-16-0944.

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Objective Familial pituitary tumour syndromes (FPTS) account for 5% of pituitary adenomas. Multi-gene analysis via next-generation sequencing (NGS) may unveil greater prevalence and inform clinical care. We aimed to identify germline variants in selected patients with pituitary adenomas using a targeted NGS panel. Design We undertook a nationwide cross-sectional study of patients with pituitary adenomas with onset ≤40 years of age and/or other personal/family history of endocrine neoplasia. A custom NGS panel was performed on germline DNA to interrogate eight FPTS genes. Genome data were analysed via a custom bioinformatic pipeline, and validation was performed by Sanger sequencing. Multiplex ligation-dependent probe amplification (MLPA) was performed in cases with heightened suspicion for MEN1, CDKN1B and AIP mutations. The main outcomes were frequency and pathogenicity of rare variants in AIP, CDKN1B, MEN1, PRKAR1A, SDHA, SDHB, SDHC and SDHD. Results Forty-four patients with pituitary tumours, 14 of whom had a personal history of other endocrine tumours and/or a family history of pituitary or other endocrine tumours, were referred from endocrine tertiary-referral centres across Australia. Eleven patients (25%) had a rare variant across the eight FPTS genes tested: AIP (p.A299V, p.R106C, p.F269F, p.R304X, p.K156K, p.R271W), MEN1 (p.R176Q), SDHB (p.A2V, p.S8S), SDHC (p.E110Q) and SDHD (p.G12S), with two patients harbouring dual variants. Variants were classified as pathogenic or of uncertain significance in 9/44 patients (20%). No deletions/duplications were identified in MEN1, CDKN1B or AIP. Conclusions A high yield of rare variants in genes implicated in FPTS can be found in selected patients using an NGS panel. It may also identify individuals harbouring more than one rare variant.
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