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991.
Filippo Gagliardi Alfio Spina Lina Raffaella Barzaghi Michele Bailo Marco Losa Maria Rosa Terreni Pietro Mortini 《Pituitary》2016,19(3):277-285
Purpose
Granular cell tumors of the neurohypophysis are rare, solitary lesions, mostly presenting in the adult age. They rarely grow to a sufficient size to cause mass effect related symptoms and they may be found in most cases incidentally at autopsy. Because of their rarity as of now they have been described only as case reports or included in small clinical series.Methods
We report a series of 11 patients, who underwent surgery for granular cell tumors of the neurohypophysis between 1996 and 2013 in a single center.Results
Mean follow-up time after treatment was 92.2 months (range 9–231 months). Mean age at surgery was 40.7 years (range 12–66 years). There were 7 males (63.6 %) and 4 females (36.4 %). Main symptoms at presentation were: hyperprolactinemia (72.7 %), visual impairment (45.5 %) and headache (36 %). Except for 2 patients, all the others underwent surgery as primary treatment at our Institution, through a transsphenoidal (54.5 %) or a transcranial approach (45.5 %). Overall- and progression-free survival times for the entire series (calculated from the time of diagnosis) were 112.9 and 100.5 months respectively. There was one case of perioperative death in a patient who had undergone repeat transcranial surgery for residual tumor.Conclusions
Although extremely rare, granular cell tumors of the neurohypophysis have to be considered in the differential diagnosis of suprasellar masses, to avoid misleading interpretation and consequent wrong therapeutic management. Early diagnosis, extensive tumor removal, opportune indication of adjuvant radiotherapy are the keys to manage these cases.992.
993.
Moi P Faà V Marini MG Asunis I Ibba G Cao A Rosatelli MC 《British journal of haematology》2004,126(6):881-884
The silent beta-thalassemia mutation, beta(+)-101C-->T, is the only mutation currently described in the distal beta-globin CACCC box. We present a novel mutation, a C-->G transversion, in the same position. Expression analysis in heterozygous subjects demonstrated that the mutation determines a 20% reduction in the output of the beta-globin gene. DNA-protein interaction and transactivation analysis correlated the decrease in the beta-globin synthesis with the reduced binding and transactivation of EKLF to the mutant promoter. These data predict that the beta-101C-->G mutation will display a silent thalassemia phenotype similar to that of the beta-101C-->T mutation. 相似文献
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995.
Ismael Nilo Lino de Queiroz Ana Luíza Gomes Quinderé José Ariévilo Gurgel Rodrigues Edfranck de Sousa Oliveira Vanderlei Natássia Albuquerque Ribeiro Renata Line da Conceição Rivanor Kátia Alves Ribeiro Chistiane Oliveira Coura Karuza Maria Alves Pereira Hellíada Vasconcelos Chaves Mirna Marques Bezerra Ianna Wivianne Fernandes de Araújo Norma Maria Barros Benevides 《Inflammation research》2015,64(12):971-982
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Intergenerational influences on the growth of Maya children: The effect of living conditions experienced by mothers and maternal grandmothers during their childhood 下载免费PDF全文
998.
Consistent copy number changes and recurrent PRKAR1A mutations distinguish Melanotic Schwannomas from Melanomas: SNP‐array and next generation sequencing analysis 下载免费PDF全文
Lu Wang Ahmet Zehir Justyna Sadowska Nengyi Zhou Marc Rosenblum Klaus Busam Narasimhan Agaram William Travis Maria Arcila Snjezana Dogan Michael F. Berger Donavan T. Cheng Marc Ladanyi Khedoudja Nafa Meera Hameed 《Genes, chromosomes & cancer》2015,54(8):463-471
Melanotic Schwannomas (MS) are rare tumors that share histological features with melanocytic tumors and schwannomas. However, their genetics are poorly understood. To elucidate the genetic characteristics of MS, we performed genome‐wide studies in a series of cases. Twelve MS cases were available for the study. Genomic DNAs extracted from formalin‐fixed paraffin embedded tumor tissues were subjected to copy number (CN) and allelic imbalance (AI) analysis by Single Nucleotide Polymorphism (SNP)‐array and screened for mutations in coding exons of 341 key cancer‐associated genes using a hybrid capture‐based next‐generation sequencing (NGS) assay. Sanger sequencing was used to further verify recurrent mutations detected by NGS study. SNP‐array analysis revealed remarkably stereotypic chromosomal abnormalities in MS. Hypodiploidy was common, typically involving monosomies of chromosomes 1, 2, and 17. All 12 samples showed mutations in PRKAR1A gene, including 2 cases with 2 mutations each. The 14 mutations were scattered across PRKAR1A, and most were inactivating mutations. AI on 17q, presenting as loss of heterozygosity with or without CN losses, combined with a PRKAR1A mutation was observed in 9/12 MS cases. The remaining 3 cases included the two samples harboring two mutations in PRKAR1A. MS exhibits a stereotypic pattern of chromosomal losses. In contrast, melanomas are typically characterized by the presence of multiple CN aberrations, without demonstrable differences in the frequency of losses and gains. Inactivation of both alleles of PRKAR1A by “two hits” observed in almost all cases underscores the central role of PRKAR1A in the pathogenesis of this neoplasm. © 2015 Wiley Periodicals, Inc. 相似文献
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1000.