2004
Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1
Busygina V, Suphapeetiporn K, Marek LR, Stowers RS, Xu T, Bale AE. Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1. Human Molecular Genetics 2004, 13: 2399-2408. PMID: 15333582, DOI: 10.1093/hmg/ddh271.Peer-Reviewed Original ResearchConceptsDNA cross-linking agentsNucleotide excision repairDNA damage-induced mutationsTumor suppressor geneDamage-induced mutationsDrosophila homologGenomic integrityHuman meninMutant fliesBiochemical functionsTranscriptional modulationNuclear proteinsDrosophila modelProtein 50Novel memberExcision repairNull allelesMolecular mechanismsCancer genesHistone deacetylaseSuppressor geneHomozygous inactivationMnn1Normal fliesGenes
1991
Allelic loss on chromosome 11 in hereditary and sporadic tumors related to familial multiple endocrine neoplasia type 1.
Bale A, Norton J, Wong E, Fryburg J, Maton P, Oldfield E, Streeten E, Aurbach G, Brandi M, Friedman E. Allelic loss on chromosome 11 in hereditary and sporadic tumors related to familial multiple endocrine neoplasia type 1. Cancer Research 1991, 51: 1154-7. PMID: 1671755.Peer-Reviewed Original ResearchConceptsFamilial multiple endocrine neoplasia type 1Multiple endocrine neoplasia type 1Anterior pituitary tumorsPancreatic islet tumorsIslet tumorsPituitary tumorsAllelic lossType 1Autosomal dominant disorderMalignant gastrinomaBronchial carcinoidParathyroid glandsParathyroid tumorsAnterior pituitaryLoss of heterozygosityTumorsPancreatic isletsSporadic tumorsDominant disorderMEN1 genePatientsRestriction fragment length polymorphismFragment length polymorphismHomozygous inactivationInformative restriction fragment length polymorphisms