Database : MEDLINE
Search on : multiple and endocrine and neoplasia and type and 2b [Words]
References found : 762 [refine]
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[PMID]: 29457255
[Au] Autor:Thomas N; Glod J; Derse-Anthony C; Baple EL; Osborne N; Sturley R; Vaidya B; Newbold K; Brooke A
[Ad] Address:Department of Endocrinology, Royal Devon and Exeter NHS Foundation Trust, Exeter, UK.
[Ti] Title:Pregnancy on vandetanib in metastatic medullary thyroid carcinoma associated with multiple endocrine neoplasia type 2B.
[So] Source:Clin Endocrinol (Oxf);, 2018 Feb 19.
[Is] ISSN:1365-2265
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:LETTER
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1111/cen.13577

  2 / 762 MEDLINE  
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[PMID]: 29182461
[Au] Autor:Kreps EO; Van Herzeele I; Callewaert BL
[Ad] Address:a Department of Ophthalmology , Ghent University Hospital , Ghent , Belgium.
[Ti] Title:Diagnosis of multiple endocrine neoplasia type 2B and management of its ocular features.
[So] Source:Ophthalmic Genet;39(2):268-270, 2018 Apr.
[Is] ISSN:1744-5094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: To describe ocular and vascular findings in a patient with multiple endocrine neoplasia type 2B. MATERIALS AND METHODS: Case report of a 31-year-old male who was referred for ocular assessment following diagnosis of a carotid artery dissection and multiple vascular anomalies. RESULTS: Clinical examination revealed a marfanoid habitus, myelinated corneal nerve fibers, neuromas in the perilimbal area, conjunctival hyperemia with peripheral corneal neovascularization, and posterior blepharitis. Diagnosis of multiple endocrine neoplasia type 2B was confirmed by genetic testing of the RET proto-oncogene. Genetic screening for hereditary aortic and peripheral vasculopathies failed to reveal an underlying cause for the vascular findings. We noted improvement of the ocular surface disease with topical corticosteroids and oral tetracyclines. CONCLUSIONS: Ophthalmologists play a vital role in recognizing this rare but lethal malignancy. We report on a patient with apart from characteristic ocular findings also staphylococcal hypersensitivity and widespread systemic vasculopathy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:In-Data-Review
[do] DOI:10.1080/13816810.2017.1408849

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[PMID]: 29394980
[Au] Autor:Erdem I; Duman D; Eroglu S; Agca M; Erdagi A; Turker H; Hazar A
[Ad] Address:Department of Pulmonary Medicine, Sureyyapasa Chest Diseases and Thoracic Surgery Training and Research Hospital, Istanbul, Turkey.
[Ti] Title:Endobronchial Mucosal Neuroma with Sarcoidosis.
[So] Source:J Coll Physicians Surg Pak;28(2):162-163, 2018 Feb.
[Is] ISSN:1681-7168
[Cp] Country of publication:Pakistan
[La] Language:eng
[Ab] Abstract:A first case of endobronchial mucosal neuroma with sarcoidosis is hereby reported. A 67-year female patient, who was diagnosed as sarcoidosis previously, was admitted to our hospital with symptoms of dyspnea, chest pain and fatigue. Middle lobe atelectasis and endobronchial lesion were observed in thorax computed tomography (CT). Fiberoptic bronchoscopy revealed polypoid lesions and histopathological examination of biopsy material showed clustered nerve bundles consistent with mucosal neuroma and non-necrotising granulomas consistent with sarcoidosis. Mucosal neuromas are pathognomonic features of multiple endocrine neoplasia (MEN) type 2B. But other components of MEN type 2B such as medullary tyroid carcinoma or pheochromocytoma were not detected in our patient. Hence, a diagnosis of solitary mucosal neuroma and sarcoidosis in the bronchi was made.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180203
[Lr] Last revision date:180203
[St] Status:In-Process
[do] DOI:10.29271/jcpsp.2018.02.162

  4 / 762 MEDLINE  
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[PMID]: 29077903
[Au] Autor:Raue F; Dralle H; Machens A; Bruckner T; Frank-Raue K
[Ad] Address:Endocrine Practice Heidelberg, Molecular Genetic Laboratory, Heidelberg, Germany.
[Ti] Title:Long-Term Survivorship in Multiple Endocrine Neoplasia Type 2B diagnosed before and in the new Millennium.
[So] Source:J Clin Endocrinol Metab;, 2017 Oct 25.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: Recent long-term outcome and survival data are lacking for patients with multiple endocrine neoplasia type 2B (MEN2B). Objectives: To analyze long-term MEN2B outcome and define prognostic factors. Design, Setting, and Participants: Retrospective comparative study of 75 patients with MEN2B from two German tertiary referral centers. Patients diagnosed and treated before and after 2000 were compared for demographic, biochemical, surgical, and outcome parameters. Intervention: Surgery. Main Outcome measure: Long-term survival. Results: We identified 7 familial and 68 de novo cases of MEN2B; 61 cases exhibited the RET M918T genotype (two others exhibited A883F and E768D/L790T mutations). Surgery was performed at a mean age of 16.4±11.2 years. Tumor stages at diagnosis were (n=71 patients): stage I: 15%; stage II: 6%; stage III: 35%; stage IV: 44%. The mean follow up was 9.6±9.0 years. Outcomes were: n=15 (20%) cured, n= 9 (12%) minimal residual disease, n=19 (25%) metastatic disease, and n=10 (13%) no information. Medullary thyroid cancer (MTC) caused 22 (29%) deaths at 7.3±6.2 years after diagnosis (mean age 22.9±10.7 years). Overall survival rates at 5, 10, and 20 years were 85%, 74%, and 58%, respectively. After 2000 (vs. before 2000), significantly more patients were in stages I and II (32% vs. 11%), more were cured (43% vs. 20%), and we observed a higher survival trend (p=0.058). The only prognostic factor was tumor stage at diagnosis. Conclusion: Patients with MEN2B developed MTC at an early age with wide ranging aggressiveness, but the outcome was generally better after 2000 than before 2000.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[St] Status:Publisher
[do] DOI:10.1210/jc.2017-01884

  5 / 762 MEDLINE  
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[PMID]: 29066504
[Au] Autor:Grey J; Winter K
[Ad] Address:J Grey, Management, Association for Multiple Endocrine Neoplasia Disorders, Tunbridge Wells, United Kingdom of Great Britain and Northern Ireland jo.grey@amend.org.uk.
[Ti] Title:Patient quality of life and prognosis in MEN2.
[So] Source:Endocr Relat Cancer;, 2017 Oct 24.
[Is] ISSN:1479-6821
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Multiple endocrine neoplasia type 2 (MEN2) refers to the autosomal dominant neuroendocrine tumour syndromes, MEN type 2A (MEN2A) and MEN type 2B (MEN2B). They are typified by the development of medullary thyroid carcinoma (MTC), phaeochromocytoma and parathyroid hyperplasia in MEN2A, and MTC, phaeochromocytomas, ganglioneuromatosis and skeletal abnormalities in MEN2B. The aggressiveness of MTC is variable according to genotype, and although it is still the major cause of mortality in both conditions, prognosis has improved dramatically in those diagnosed and treated at a young age thanks to predictive genetic testing. Nevertheless, metastatic MTC, ganglioneuromatosis and a variety of other negative clinical and psychosocial impacts on quality of life and/or prognosis in MEN2 persist. In the absence at time of writing of any large scale research into quality of life specifically in MEN2, this review includes data from patient surveys and anonymised patient anecdotes from the records of the Association for Multiple Endocrine Neoplasia Disorders (AMEND), for whom the authors work. We recommend that these patients are cared for only in centres of expertise able to provide expert diagnosis, treatment and continuity of care, including psychological and transition support. Only in this way can the clinical advances of the last two and half decades be built upon further to ensure that the care of these complex, lifelong patients can be considered truly holistic.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171025
[Lr] Last revision date:171025
[St] Status:Publisher

  6 / 762 MEDLINE  
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[PMID]: 29049491
[Au] Autor:Alegría-Landa V; Jo-Velasco M; Robledo M; Requena L
[Ad] Address:Department of Dermatology, Fundación Jiménez Diaz, Universidad Autónoma, Madrid, Spain.
[Ti] Title:Dermal Hyperneury and Multiple Sclerotic Fibromas in Multiple Endocrine Neoplasia Type 2A Syndrome.
[So] Source:JAMA Dermatol;, 2017 Oct 18.
[Is] ISSN:2168-6084
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Multiple endocrine neoplasia type 2 (MEN 2) syndrome is an autosomal dominant, hereditary cancer disorder caused by germline mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band 10q11.21. Two distinct clinical forms have been described as the following phenotypes: multiple endocrine neoplasia type 2A (MEN 2A) and multiple endocrine neoplasia type 2B (MEN 2B) syndromes. The common and necessary nexus that defines these 2 phenotypes is the presence of medullary thyroid carcinoma (MTC). The familial MTC type of MEN 2 syndrome was included within the spectrum of MEN 2A syndrome. Cutaneous manifestations of MEN 2A syndrome include macular amyloidosis, whereas MEN 2B syndrome is traditionally linked to multiple mucosal neuromas. Objectives: To describe a family with cutaneous manifestations not previously described in patients with MEN 2A syndrome and to discuss the association of this disorder with Cowden syndrome. Design, Setting, and Participants: Clinicopathologic correlation of cutaneous lesions and genetic studies in 11 members of a family with familial MTC. Interventions: Cutaneous lesions were histopathologically and immunohistochemically studied. Genetic screening for a germline mutation at the RET gene was performed in 11 family members. Main Outcomes and Measures: Identification of cutaneous lesions not previously described in patients with MEN 2A syndrome. Results: This family of 11 individuals with familial MTC type of MEN 2A syndrome demonstrated the moderate risk RET p.Val804Met (protein valine at residue 804 replaced by methionine) genetic mutation, with 2 of the relatives presenting with dermal hyperneury, cutaneous lesions classically described in MEN 2B syndrome, and 1 relative also showing multiple sclerotic fibromas, a cutaneous manifestation of PTEN (phosphatase and tensin homologue) hamartoma-tumor syndrome. Conclusions and Relevance: Dermal hyperneury and multiple sclerotic fibromas should be added to the list of cutaneous manifestations of patients with the familial MTC type of MEN 2A syndrome.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171019
[Lr] Last revision date:171019
[St] Status:Publisher
[do] DOI:10.1001/jamadermatol.2017.3959

  7 / 762 MEDLINE  
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[PMID]: 28925363
[Au] Autor:Bennaceur-Griscelli A; Hadoux J; Féraud O; Opolon P; Divers D; Gobbo E; Schlumberger M; Griscelli F; Turhan AG
[Ad] Address:INSERM U935, Université Paris Sud, 94800, Villejuif, France; ESTeam Paris Sud, INSERM U935, Université Paris Sud, Université Paris-Saclay, 94800, Villejuif, France; INGESTEM National IPSC Infrastructure, 94800 Villejuif, France; Division of Hematology, Paris Sud University Hospitals, Le Kremlin Bicê
[Ti] Title:Generation of an induced pluripotent stem cell line from a patient with hereditary multiple endocrine neoplasia 2B (MEN2B) syndrome with "highest risk" RET mutation.
[So] Source:Stem Cell Res;23:154-157, 2017 Aug.
[Is] ISSN:1876-7753
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Multiple Endocrine Neoplasia Type 2B (MEN2B) is a cancer-predisposing syndrome that affects patients with germline RET mutations. The clinical spectrum of the syndrome includes medullary thyroid carcinoma (MTC) and pheochromocytoma. Currently, there is no satisfactory model recapitulating all the features of the disease especially at the level of stem cells. We generated induced pluripotent stem cells (iPSCs) from a patient with RET mutation at codon 918 who developed pheochromocytoma and MTC. These iPSC had normal karyotype, harboured the RET mutation and expressed pluripotency hallmarks. A comprehensive pathological assessment of teratoma was performed after injection in immunodeficient mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 170919
[Lr] Last revision date:170919
[St] Status:In-Process

  8 / 762 MEDLINE  
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[PMID]: 28610401
[Au] Autor:Younis E
[Ad] Address:King Hussein Cancer center (KHCC), Amman, Jordan. Email: EYounis@KHCC.JO
[Ti] Title:Oncogenesis of Thyroid Cancer
[So] Source:Asian Pac J Cancer Prev;18(5):1191-1199, 2017 05 01.
[Is] ISSN:2476-762X
[Cp] Country of publication:Thailand
[La] Language:eng
[Ab] Abstract:Thyroid neoplasms encompass a variety of lesions that range from benign adenomas to malignancies. These latter can be well-differentiated, poorly differentiated or undifferentiated (anaplastic) carcinomas. More than 95% of thyroid cancers are derived from thyroid follicular cells, while 2-3% (medullary thyroid cancers, MTC) originate from calcitonin producing C-cells. Over the last decade, investigators have developed a clearer understanding of genetic alterations underlying thyroid carcinogenesis. A number of point mutations and translocations are involved, not only in its tumorigenesis, but also as have potential use as diagnostic and prognostic indicators and therapeutic targets. Many occur in genes for several important signaling pathways, in particular the mitogen-activated protein kinase (MAPK) pathway. Sporadic (isolated) lesions account for 75% of MTC cases, while inherited MTC, often in association with multiple endocrine neoplasia (MEN) type 2A and 2B syndromes, constitute the remainder. However, non-MEN familial MTC may also occur. Advances in genetic testing have revolutionized the management of MTC, with prospects of genetic screening, testing and early prophylactic thyroidectomy. Ethical concerns of these advances are addressed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1706
[Cu] Class update date: 170829
[Lr] Last revision date:170829
[St] Status:Publisher

  9 / 762 MEDLINE  
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[PMID]: 28504695
[Au] Autor:Lines KE; Stevenson M; Filippakopoulos P; Müller S; Lockstone HE; Wright B; Grozinsky-Glasberg S; Grossman AB; Knapp S; Buck D; Bountra C; Thakker RV
[Ad] Address:Academic Endocrine Unit, OCDEM, University of Oxford, Churchill Hospital, Headington, Oxford, UK.
[Ti] Title:Epigenetic pathway inhibitors represent potential drugs for treating pancreatic and bronchial neuroendocrine tumors.
[So] Source:Oncogenesis;6(5):e332, 2017 May 15.
[Is] ISSN:2157-9024
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cancer is associated with alterations in epigenetic mechanisms such as histone modifications and methylation of DNA, and inhibitors targeting epigenetic mechanisms represent a novel class of anti-cancer drugs. Neuroendocrine tumors (NETs) of the pancreas (PNETs) and bronchus (BNETs), which may have 5-year survivals of <50% and as low as 5%, respectively, represent targets for such drugs, as >40% of PNETs and ~35% of BNETs have mutations of the multiple endocrine neoplasia type 1 (MEN1) gene, which encodes menin that modifies histones by interacting with histone methyltransferases. We assessed 9 inhibitors of epigenetic pathways, for their effects on proliferation, by CellTiter Blue assay, and apoptosis, by CaspaseGlo assay, using 1 PNET and 2 BNET cell lines. Two inhibitors, referred to as (+)-JQ1 (JQ1) and PFI-1, targeting the bromo and extra terminal (BET) protein family which bind acetylated histone residues, were most effective in decreasing proliferation (by 40-85%, P<0.001) and increasing apoptosis (by 2-3.6 fold, P<0.001) in all 3 NET cell lines. The anti-proliferative effects of JQ1 and PFI-1 remained present for at least 48 hours after removal of the compound. JQ1, but not PFI-1, had cell cycle effects, assessed by propidium iodide staining and flow cytometry, resulting in increased and decreased proportions of NET cells in G1, and S and G2 phases, respectively. RNA Sequencing analysis revealed that these JQ1 effects were associated with increased histone 2B expression, and likely mediated through altered activity of bromodomain-containing (Brd) proteins. Assessment of JQ1 in vivo, using a pancreatic beta cell-specific conditional Men1 knockout mouse model that develops PNETs, revealed that JQ1 significantly reduced proliferation (by ~50%, P<0.0005), assessed by bromodeoxyuridine incorporation, and increased apoptosis (by ~3 fold, P<0.0005), assessed by terminal deoxynucleotidyl transferase dUTP nick end labelling, of PNETs. Thus, our studies demonstrate that BET protein inhibitors may provide new treatments for NETs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 170816
[Lr] Last revision date:170816
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1038/oncsis.2017.30

  10 / 762 MEDLINE  
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[PMID]: 28483157
[Au] Autor:Beylerian M; Hoffart L; Denis D
[Ad] Address:Service d'ophtalmologie, CHU-Hôpital Nord, chemin des Bourrely, 13915 Marseille cedex 20, France. Electronic address: mariebeylerian@hotmail.fr.
[Ti] Title:Hypertrophie bilatérale des nerfs cornéens compliquée de glaucome dans le cadre d'une néoplasie endocrinienne multiple de type 2B (NEM2B) chez un enfant. [Bilateral corneal nerve hypertrophy associated with glaucoma in a boy with multiple endocrine neoplasia type 2B].
[So] Source:J Fr Ophtalmol;40(5):e149-e151, 2017 May.
[Is] ISSN:1773-0597
[Cp] Country of publication:France
[La] Language:fre
[Pt] Publication type:LETTER
[Em] Entry month:1705
[Cu] Class update date: 170521
[Lr] Last revision date:170521
[St] Status:In-Data-Review


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