PMC:2812425 / 1310-3011 JSONTXT

{"project":"MyTest","denotations":[{"id":"19633868-17189459-29215954","span":{"begin":474,"end":475},"obj":"17189459"},{"id":"19633868-11077991-29215955","span":{"begin":477,"end":478},"obj":"11077991"},{"id":"19633868-1493643-29215956","span":{"begin":728,"end":729},"obj":"1493643"},{"id":"19633868-11077991-29215957","span":{"begin":787,"end":788},"obj":"11077991"},{"id":"19633868-9529355-29215958","span":{"begin":950,"end":951},"obj":"9529355"},{"id":"19633868-10995566-29215959","span":{"begin":953,"end":954},"obj":"10995566"},{"id":"19633868-16098013-29215960","span":{"begin":993,"end":994},"obj":"16098013"},{"id":"19633868-11386754-29215961","span":{"begin":1033,"end":1034},"obj":"11386754"},{"id":"19633868-10507724-29215962","span":{"begin":1220,"end":1221},"obj":"10507724"},{"id":"19633868-17075716-29215963","span":{"begin":1365,"end":1366},"obj":"17075716"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Introduction\nGingival fibromatosis (gingival hyperplasia) may result from systemic medication with calcium-channel blockers, cyclosporin, dilantin, and phenytoin, or it may be hereditary. In severe cases, the gingival enlargement may cover the crowns of teeth and cause severe functional and esthetic concerns. Hereditary gingival fibromatosis (HGF) is a rare condition that can occur as an isolated disease or as part of a number of syndromes or chromosomal abnormalities [1, 2]. The onset of gingival overgrowth generally coincides with the eruption of the permanent incisors, infrequently with the eruption of the primary dentition, and it rarely presents already at birth. Among the non-syndromic HGFs, autosomal recessive [3] and autosomal dominant inheritance have been described [2]. Linkage studies have localized loci for autosomal dominant non-syndromic forms of gingival fibromatosis (adHGF) to chromosomes 2p21–p22 (GINGF1, OMIM 135300) [4, 5], 2p22.3–p23.3 (GINGF3, OMIM 609955) [6], and 5q13–q22 (GINGF2, OMIM 605544) [7]. Delineation of chromosome 2p13–p21 duplication in a patient with HGF in association with mental retardation and facial dysmorphism suggested another HGF locus on chromosome 2p13–p21 [8]. Recently, an apparently maternally inherited form of gingival fibromatosis was mapped to chromosome 11p15 in two unrelated Chinese families [9]. The molecular basis of HGF remains largely unknown. One mutation in the SOS1 (son of sevenless one) gene (OMIM 182530) has been identified at the GINGF1 locus in a single adHGF family. Diagnosis of HGF is based on medical history and clinical examination, since there are currently no specific immunohistochemical markers available."}

{"project":"2_test","denotations":[{"id":"19633868-17189459-29215954","span":{"begin":474,"end":475},"obj":"17189459"},{"id":"19633868-11077991-29215955","span":{"begin":477,"end":478},"obj":"11077991"},{"id":"19633868-1493643-29215956","span":{"begin":728,"end":729},"obj":"1493643"},{"id":"19633868-11077991-29215957","span":{"begin":787,"end":788},"obj":"11077991"},{"id":"19633868-9529355-29215958","span":{"begin":950,"end":951},"obj":"9529355"},{"id":"19633868-10995566-29215959","span":{"begin":953,"end":954},"obj":"10995566"},{"id":"19633868-16098013-29215960","span":{"begin":993,"end":994},"obj":"16098013"},{"id":"19633868-11386754-29215961","span":{"begin":1033,"end":1034},"obj":"11386754"},{"id":"19633868-10507724-29215962","span":{"begin":1220,"end":1221},"obj":"10507724"},{"id":"19633868-17075716-29215963","span":{"begin":1365,"end":1366},"obj":"17075716"}],"text":"Introduction\nGingival fibromatosis (gingival hyperplasia) may result from systemic medication with calcium-channel blockers, cyclosporin, dilantin, and phenytoin, or it may be hereditary. In severe cases, the gingival enlargement may cover the crowns of teeth and cause severe functional and esthetic concerns. Hereditary gingival fibromatosis (HGF) is a rare condition that can occur as an isolated disease or as part of a number of syndromes or chromosomal abnormalities [1, 2]. The onset of gingival overgrowth generally coincides with the eruption of the permanent incisors, infrequently with the eruption of the primary dentition, and it rarely presents already at birth. Among the non-syndromic HGFs, autosomal recessive [3] and autosomal dominant inheritance have been described [2]. Linkage studies have localized loci for autosomal dominant non-syndromic forms of gingival fibromatosis (adHGF) to chromosomes 2p21–p22 (GINGF1, OMIM 135300) [4, 5], 2p22.3–p23.3 (GINGF3, OMIM 609955) [6], and 5q13–q22 (GINGF2, OMIM 605544) [7]. Delineation of chromosome 2p13–p21 duplication in a patient with HGF in association with mental retardation and facial dysmorphism suggested another HGF locus on chromosome 2p13–p21 [8]. Recently, an apparently maternally inherited form of gingival fibromatosis was mapped to chromosome 11p15 in two unrelated Chinese families [9]. The molecular basis of HGF remains largely unknown. One mutation in the SOS1 (son of sevenless one) gene (OMIM 182530) has been identified at the GINGF1 locus in a single adHGF family. Diagnosis of HGF is based on medical history and clinical examination, since there are currently no specific immunohistochemical markers available."}