The Association of Bronchial Carcinoid and Pluriglandular Adenomatosis

Williams, E. D.; Celestin, Louis-Cyril

doi:10.1136/thx.17.2.120

Cited by 110 publications

(18 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a total of only 33 cases reported in literature, information on metastases is available, with 24% lymph node metastases and 12% distant metastases (Underdahl et al 1953, Williams & Celestin 1962, Dry et al 1975, Farhangi et al 1987, Shepherd 1991, Murat et al 1997, Sachithanandan et al 2005, Snabboon et al 2005, Lourenco-Jr et al 2007, Abe et al 2008, Divisi et al 2008, Waldmann et al 2009, Fabbri et al 2010, Matsuda et al 2010, Montero et al 2010.…”

Section: Natural History and Prognostic Factors: Pulmonary Carcinoidsmentioning

confidence: 99%

Thoracic and duodenopancreatic neuroendocrine tumors in multiple endocrine neoplasia type 1: natural history and function of menin in tumorigenesis

Pieterman¹,

Conemans²,

Dreijerink³

et al. 2014

Endocrine-Related Cancer

View full text Add to dashboard Cite

Mutations of the multiple endocrine neoplasia type 1 (MEN1) gene lead to loss of function of its protein product menin. In keeping with its tumor suppressor function in endocrine tissues, the majority of the MEN1-related neuroendocrine tumors (NETs) show loss of heterozygosity (LOH) on chromosome 11q13. In sporadic NETs, MEN1 mutations and LOH are also reported, indicating common pathways in tumor development. Prevalence of thymic NETs (thNETs) and pulmonary carcinoids in MEN1 patients is 2-8%. Pulmonary carcinoids may be underreported and research on natural history is limited, but disease-related mortality is low. thNETs have a high mortality rate. Duodenopancreatic NETs (dpNETs) are multiple, almost universally found at pathology, and associated with precursor lesions. Gastrinomas are usually located in the duodenal submucosa while other dpNETs are predominantly pancreatic. dpNETs are an important determinant of MEN1-related survival, with an estimated 10-year survival of 75%. Survival differs between subtypes and apart from tumor size there are no known prognostic factors. Natural history of nonfunctioning pancreatic NETs needs to be redefined because of increased detection of small tumors. MEN1-related gastrinomas seem to behave similar to their sporadic counterparts, while insulinomas seem to be more aggressive. Investigations into the molecular functions of menin have led to new insights into MEN1-related tumorigenesis. Menin is involved in gene transcription, both as an activator and repressor. It is part of chromatin-modifying protein complexes, indicating involvement of epigenetic pathways in MEN1-related NET development. Future basic and translational research aimed at NETs in large unbiased cohorts will clarify the role of menin in NET tumorigenesis and might lead to new therapeutic options.

show abstract

Section: Natural History and Prognostic Factors: Pulmonary Carcinoidsmentioning

confidence: 99%

Thoracic and duodenopancreatic neuroendocrine tumors in multiple endocrine neoplasia type 1: natural history and function of menin in tumorigenesis

Pieterman¹,

Conemans²,

Dreijerink³

et al. 2014

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…7,8 Nonendocrine mesenchymal tumors, such as lipomas, angiofibromas, and collagenomas, have also been shown to be associated with MEN1 and MEN1 gene alterations. 8 -10 Leiomyomata have been occasionally documented in MEN1 patients, 8,[11][12][13][14] and loss of heterozygosity (LOH) at the MEN1 locus was recently shown in two esophageal leiomyomata from one MEN1 patient. 15 MEN1 gene inactivation in lung or uterine leiomyomata, however, has not been studied.…”

mentioning

confidence: 99%

Multiple Leiomyomas of the Esophagus, Lung, and Uterus in Multiple Endocrine Neoplasia Type 1

McKeeby

Zhuang

et al. 2001

The American Journal of Pathology

View full text Add to dashboard Cite

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary disorder characterized by multiple parathyroid, pancreatic, duodenal, and pituitary neuroendocrine tumors. Nonendocrine mesenchymal tumors, such as lipomas, collagenomas, and angiofibromas have also been reported. MEN1-associated neuroendocrine and some mesenchymal tumors have documented MEN1 gene alterations on chromosome 11q13. To test whether the MEN1 gene is involved in the pathogenesis of multiple smooth muscle tumors, we examined the 11q13 loss of heterozygosity (LOH) and clonality patterns in 15 leiomyomata of the esophagus, lung, and uterus from five patients with MEN1. Forty sporadic uterine leiomyomata were also studied for 11q13 LOH. LOH analysis was performed using four polymorphic DNA markers at the MEN1 gene locus; D11S480, PYGM, D11S449, and INT-2. The gene for multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant tumor syndrome, has been mapped to chromosome 11q13 1 and recently identified. 2 The MEN1 gene is thought to act as a tumor suppressor based on the presence of inherited inactivating mutations in the constitutional DNA of affected family members accompanied by the loss of the wild-type allele in associated tumors. 2-4 Somatic inactivation of the MEN1 gene has been also documented in a subset of sporadic counterpart parathyroid, enteropancreatic, and pulmonary endocrine tumors, and mesenchymal tumors. 5 MEN1 patients typically present first with primary hyperparathyroidism resulting from multiple parathyroid tumors caused by MEN1 gene alterations. 6 Neuroendocrine tumors of the pancreas, duodenum, anterior pituitary gland, stomach, and lung are other tumors that are an integral part of MEN1. 7,8 Nonendocrine mesenchymal tumors, such as lipomas, angiofibromas, and collagenomas, have also been shown to be associated with MEN1 and MEN1 gene alterations. 8 -10 Leiomyomata have been occasionally documented in MEN1 patients, 8,[11][12][13][14] and loss of heterozygosity (LOH) at the MEN1 locus was recently shown in two esophageal leiomyomata from one MEN1 patient. 15 MEN1 gene inactivation in lung or uterine leiomyomata, however, has not been studied. To test whether MEN1 gene alterations are involved in the development of multiple smooth muscle tumors in MEN1 patients, we analyzed 15 leiomyomata from five patients with documented MEN1 germline mutations for LOH at the MEN1 gene locus. To assess whether MEN1 gene alterations are present in sporadic smooth muscle tumors, we analyzed 40 sporadic uterine leiomyomata for MEN1 gene deletion for comparison. Furthermore, to evaluate whether MEN1-associated leiomyomata arise as independent clonal events at different anatomical sites within an organ, the patterns of 11q13 LOH in different tumors from individual patients

show abstract

“…This is exemplified by a patient reported by Zollinger, Elliot, Endahl, Grant, Goswitz, and Taft (1962), who remained well and underwent a successful pregnancy seven years after total gastrectomy for a malignant ulcerogenic tumour of the pancreas and by the patient reported in the present paper who remained well 21 months after gastric radiotherapy despite the presence of widespread glandular and hepatic metastases noted before the course of radiotherapy. The diagnostic difficulty between the two tumours may be further complicated by (a) the affinity of the ulcerogenic tumour for silver stains in some patients (Mieher, Hartsock, Goekas, Ballard, and Frame, 1962;Sanchez and Sommers, 1960), and, conversely, by the lack of silver staining potential in the odd patient with a carcinoid; (b) the association between ulcerogenic tumour and carcinoid present in the same patient (Gerber and Shields, 1960;Williams and Celestin, 1962); (c) the allegedly high incidence of peptic ulceration in patients with metastatic carcinoid disease (MacDonald, 1956;Horsley and Golden, 1957;Lemmer, 1942); and (d)the occasional presence of hyperserotoninuria in patients with ulcerogenic pancreatic tumours, particularly those in whom steatorrhoea is the dominant clinical feature (Espiner and Beaven, 1962). Despite the foregoing, however, we believe that the histological features of an ulcerogenic tumour of the pancreas are sufficiently characteristic to permit a correct diagnosis in the vast majority of cases, and that the correct diagnosis should virtually always be possible if the histological features are considered in conjunction with the clinical story and the acid secretory data derived from the augmented histamine test.…”

Section: Discussionmentioning

confidence: 99%

Malignant Zollinger-Ellison syndrome in a Bantu woman with a prolonged remission after gastric radiotherapy

Bank¹,

Marks²,

Sealy³

et al. 1965

Gut

View full text Add to dashboard Cite

The Association of Bronchial Carcinoid and Pluriglandular Adenomatosis

Cited by 110 publications

References 18 publications

Thoracic and duodenopancreatic neuroendocrine tumors in multiple endocrine neoplasia type 1: natural history and function of menin in tumorigenesis

Thoracic and duodenopancreatic neuroendocrine tumors in multiple endocrine neoplasia type 1: natural history and function of menin in tumorigenesis

Multiple Leiomyomas of the Esophagus, Lung, and Uterus in Multiple Endocrine Neoplasia Type 1

Malignant Zollinger-Ellison syndrome in a Bantu woman with a prolonged remission after gastric radiotherapy

Contact Info

Product

Resources

About