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[PMID]:27531415
[Au] Autor:Massereau E; Cheynet F; Bénateau H; Veyssière A; Bencheman Y; Gallucci A; Hammoutène S; Chossegros C
[Ad] Endereço:Service de stomatologie et de chirurgie maxillofaciale, hôpital de la Conception, 147, boulevard Baille, 13005 Marseille, France; Service d'odontologie, hôpital de la Timone, 264, rue Saint-Pierre, 13385 Marseille, France. Electronic address: eugeniemassereau@hotmail.fr.
[Ti] Título:[Chondromatose of the temporomandibular joint: Multicentric study and clarification from 14 cases].
[Ti] Título:Chondromatose de l'articulation temporomandibulaire : étude multicentrique et mise au point à partir de 14 cas..
[So] Source:Rev Stomatol Chir Maxillofac Chir Orale;117(4):234-9, 2016 Sep.
[Is] ISSN:2213-6541
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:INTRODUCTION: The aim of our study was to analyse a series of patients suffering from temporomandibular joint (TMJ) chondromatosis treated in 2 departments of stomatology and maxillofacial surgery (University hospitals of the Conception in Marseille and of Caen) and to make a general review of this disease. MATERIAL AND METHODS: We conducted a retrospective study including all the patients treated for a TMJ chondromatosis in one of these 2 departments. Following parameters were analyzed: sex, ages at discovery and at surgery, symptoms, side, imaging, histology, recurrence and any other events considered as relevant. RESULTS: Fourteen patients could be included: 85.7 % were women. Average age at diagnosis was 40.14 (σ = 13.82; IC95: 32.90-47.38) (41 for women [σ = 14.74; IC95: 33.28-48.72] and 35 years for men [σ = 5.66, IC95: 27.16-42.84]). Average age at surgery was 40.86 (σ = 14.18; IC95: 33.43-48.28). There was no predominance of side; 57.14 % of the patients had a joint syndrome, 57.14 % a tumor syndrome, 28.57 % had pain and 14.29 % had headaches. Panoramic X-ray was informative in 3 cases only. CT scan showed intra-articular calcifications in half of the cases only but arthrosic modifications in all the cases. Magnetic resonance imaging (MRI) constantly showed intra-articular cartilage fragments. When histology was performed, it found the synovial to be normal in one case and multiple nodules with clear cartilaginous differentiation in another case. One patient suffered from a second contralateral localization 10 years later. DISCUSSION: Chondromatosis has a slow evolution and is asymptomatic for a long time. MRI allows to evoke the diagnosis and to locate precisely the osteochondromas. Diagnosis is confirmed by histology that highlights a synovial metaplasia and more or less calcified chondromas. The main differential diagnosis to be eliminated because of prognostic reasons is the synovial chondrosarcoma. Treatment consists in surgical removing of the chondromas. Evolution is usually favorable.
[Mh] Termos MeSH primário: Condromatose Sinovial
Condromatose
Transtornos da Articulação Temporomandibular
[Mh] Termos MeSH secundário: Adulto
Condromatose/diagnóstico
Condromatose/epidemiologia
Condromatose/cirurgia
Condromatose Sinovial/diagnóstico
Condromatose Sinovial/epidemiologia
Condromatose Sinovial/cirurgia
Feminino
Seres Humanos
Masculino
Meia-Idade
Recidiva
Estudos Retrospectivos
Articulação Temporomandibular/patologia
Articulação Temporomandibular/cirurgia
Transtornos da Articulação Temporomandibular/diagnóstico
Transtornos da Articulação Temporomandibular/epidemiologia
Transtornos da Articulação Temporomandibular/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170421
[Lr] Data última revisão:
170421
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160818
[St] Status:MEDLINE


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[PMID]:27513781
[Au] Autor:Paparo F; Massarelli M; Cordeschi R; Sciannameo V; Spallaccia F
[Ad] Endereço:Department of Maxillo-Facial Surgery, Azienda Ospedaliera "S. Maria" di Terni.
[Ti] Título:Chondromatosis of the Temporomandibular Joint as a Consequence of Persistent Long-Lasting Joint Dysfunction: Late Diagnosis of a Rare Occurrence.
[So] Source:J Craniofac Surg;27(7):e636-e637, 2016 Oct.
[Is] ISSN:1536-3732
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The authors present a rare patient of right synovial chondromatosis (SC) of the temporomandibular joint in which diagnosis was late and delay led to SC extension to the cranial base. Synovial chondromatosis is a rare benign disorder characterized by multiple cartilaginous free-floating nodules originated from the synovial membrane of large articular joints of the body. Differential diagnosis is with neoplasm and radical surgical removal is essential. The patient came to the authors' observation complaining about long-lasting temporomandibular joint dysfunction. The patient already underwent either functional or medical therapy in times without any improvement. Clinical examination showed limited mouth opening and swelling of the right preauricolar region with no signs of facial nerve palsy and without paresthesia or hearing loss. No history of recent trauma was recorded. Magnetic resonance imaging showed a mucous-like hyperintense mass with small hypointense spots inside. A preoperative computed tomography scan was performed and showed a mass extending from the superior aspect of the temporomandibular joint to the glenoid fossa, which was partially eroded. The patient underwent either open joint surgery or arthroscopy of the superior joint space and a large number of chondrocytes were removed. No complications were recorded postoperatively and the patient completely recovered after 6 months. Histology confirmed the diagnosis of synovial condromatosys of the right temporomandibular joint.
[Mh] Termos MeSH primário: Condromatose/diagnóstico
Diagnóstico Tardio
Transtornos da Articulação Temporomandibular/diagnóstico
Síndrome da Disfunção da Articulação Temporomandibular/diagnóstico
Articulação Temporomandibular/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Artroscopia
Condromatose/etiologia
Diagnóstico Diferencial
Feminino
Seguimentos
Seres Humanos
Imagem por Ressonância Magnética
Síndrome da Disfunção da Articulação Temporomandibular/complicações
Fatores de Tempo
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:160812
[St] Status:MEDLINE


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[PMID]:27240490
[Au] Autor:Salinas-Torres VM; Salinas-Torres RA
[Ad] Endereço:Departamento de Genética Médica, Hospital General de Tijuana ISESALUD, Baja California, Mexico. Electronic address: vm_salinas7@hotmail.com.
[Ti] Título:Otofaciocervical syndrome and metachondromatosis in a girl: Presentation of a novel association and remarks on clinical variability of branchial-arch disorders.
[So] Source:Int J Pediatr Otorhinolaryngol;85:19-21, 2016 Jun.
[Is] ISSN:1872-8464
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Otofaciocervical syndrome (OFCS) is a rare disorder characterized by facial, ear, branchial, and musculoskeletal anomalies, along with hearing loss and mild intellectual disability. Clinically, its distinction from branchiootorenal syndrome can be difficult. To date, the coexistence of OFCS and metachondromatosis has not been reported. Here, we describe a sporadic patient with both OFCS and metachondromatosis. This novel association prompts us to do some remarks on the clinical variability of branchial-arch disorders; in fact, our observations are consistent with the highly variable expressivity of OFCS and illustrate the need of a more accurate characterization of these branchial-arch disorders. In the meantime, involvement of clavicles, scapulae and shoulders remains a distinctive feature of OFCS.
[Mh] Termos MeSH primário: Neoplasias Ósseas/complicações
Síndrome Brânquio-Otorrenal/complicações
Condromatose/complicações
Exostose Múltipla Hereditária/complicações
[Mh] Termos MeSH secundário: Neoplasias Ósseas/diagnóstico por imagem
Braquidactilia/diagnóstico por imagem
Braquidactilia/etiologia
Síndrome Brânquio-Otorrenal/diagnóstico por imagem
Pré-Escolar
Condromatose/diagnóstico por imagem
Exostose Múltipla Hereditária/diagnóstico por imagem
Feminino
Rim Fundido/diagnóstico por imagem
Rim Fundido/etiologia
Seres Humanos
Neuropeptídeos
Radiografia
Escoliose/diagnóstico por imagem
Escoliose/etiologia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptides); 98035-79-1 (small cardioactive peptide A)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160601
[St] Status:MEDLINE


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[PMID]:26984661
[Au] Autor:McFarlane J; Knight T; Sinha A; Cole T; Kiely N; Freeman R
[Ti] Título:Exostoses, enchondromatosis and metachondromatosis; diagnosis and management.
[So] Source:Acta Orthop Belg;82(1):102-5, 2016 Mar.
[Is] ISSN:0001-6462
[Cp] País de publicação:Belgium
[La] Idioma:eng
[Ab] Resumo:We describe a 5 years old girl who presented to the multidisciplinary skeletal dysplasia clinic following excision of two bony lumps from her fingers. Based on clinical examination, radiolographs and histological results an initial diagnosis of hereditary multiple exostosis (HME) was made. Four years later she developed further lumps which had the radiological appearance of enchondromas. The appearance of both exostoses and enchondromas suggested a possible diagnosis of metachondromatosis. Genetic testing revealed a splice site mutation at the end of exon 11 on the PTPN11 gene, confirming the diagnosis of metachondromatosis. While both single or multiple exostoses and enchondromas occur relatively commonly on their own, the appearance of multiple exostoses and enchondromas together is rare and should raise the differential diagnosis of metachondromatosis. Making this diagnosis is important as the lesions in metachondromatosis may spontaneously resolve and therefore surgical intervention is often unnecessary. We discuss the diagnostic findings, genetic causes, treatment and prognosis of this rare condition of which less than thirty cases have previously been reported.
[Mh] Termos MeSH primário: Neoplasias Ósseas/genética
Condromatose/genética
Encondromatose/genética
Exostose Múltipla Hereditária/genética
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
[Mh] Termos MeSH secundário: Neoplasias Ósseas/diagnóstico
Pré-Escolar
Condromatose/diagnóstico
Encondromatose/diagnóstico
Exostose Múltipla Hereditária/diagnóstico
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.3.48 (PTPN11 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160317
[Lr] Data última revisão:
160317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160318
[St] Status:MEDLINE


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[PMID]:26174433
[Au] Autor:Sareen A; D'souza MM; Reddy KB; Kanojia RK; Kumar A
[Ad] Endereço:Lady Hardinge Medical College, New Delhi, India.
[Ti] Título:Genochondromatosis type I: A clinicoradiological study of four family members.
[So] Source:Am J Med Genet A;167A(11):2758-66, 2015 Nov.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genochondromatosis is an extremely rare autosomal dominant disorder, which manifests during childhood and tends to regress in adult life. The bony lesions are symmetrically distributed with characteristic localization at the metaphysis of proximal humerus and distal femur. Two types have been described based on the involvement of clavicle. Usually asymptomatic, sometimes patients may present with pathological fractures. In this communication, we describe four members of a family with Genochondromatosis type I, with some additional clinical and radiological findings not reported previously.
[Mh] Termos MeSH primário: Neoplasias Ósseas/diagnóstico por imagem
Neoplasias Ósseas/patologia
Condromatose/diagnóstico por imagem
Condromatose/patologia
Síndromes Neoplásicas Hereditárias/diagnóstico por imagem
Síndromes Neoplásicas Hereditárias/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Diagnóstico Diferencial
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Linhagem
Radiografia
Rádio (Anatomia)/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150716
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.37247


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[PMID]:24875294
[Au] Autor:Bowen ME; Ayturk UM; Kurek KC; Yang W; Warman ML
[Ad] Endereço:Orthopaedic Research Laboratories, Boston Children's Hospital, Boston, Massachusetts, United States of America.
[Ti] Título:SHP2 regulates chondrocyte terminal differentiation, growth plate architecture and skeletal cell fates.
[So] Source:PLoS Genet;10(5):e1004364, 2014.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss of PTPN11/SHP2 in mice or in human metachondromatosis (MC) patients causes benign cartilage tumors on the bone surface (exostoses) and within bones (enchondromas). To elucidate the mechanisms underlying cartilage tumor formation, we investigated the role of SHP2 in the specification, maturation and organization of chondrocytes. Firstly, we studied chondrocyte maturation by performing RNA-seq on primary chondrocyte pellet cultures. We found that SHP2 depletion, or inhibition of the ERK1/2 pathway, delays the terminal differentiation of chondrocytes from the early-hypertrophic to the late-hypertrophic stage. Secondly, we studied chondrocyte maturation and organization in mice with a mosaic postnatal inactivation of Ptpn11 in chondrocytes. We found that the vertebral growth plates of these mice have expanded domains of early-hypertrophic chondrocytes that have not yet terminally differentiated, and their enchondroma-like lesions arise from chondrocytes displaced from the growth plate due to a disruption in the organization of maturation and ossification zones. Furthermore, we observed that lesions from human MC patients also display disorganized chondrocyte maturation zones. Next, we found that inactivation of Ptpn11 in Fsp1-Cre-expressing fibroblasts induces exostosis-like outgrowths, suggesting that loss of SHP2 in cells on the bone surface and at bone-ligament attachment sites induces ectopic chondrogenesis. Finally, we performed lineage tracing to show that exostoses and enchondromas in mice likely contain mixtures of wild-type and SHP2-deficient chondrocytes. Together, these data indicate that in patients with MC, who are heterozygous for inherited PTPN11 loss-of-function mutations, second-hit mutations in PTPN11 can induce enchondromas by disrupting the organization and delaying the terminal differentiation of growth plate chondrocytes, and can induce exostoses by causing ectopic chondrogenesis of cells on the bone surface. Furthermore, the data are consistent with paracrine signaling from SHP2-deficient cells causing SHP2-sufficient cells to be incorporated into the lesions.
[Mh] Termos MeSH primário: Cartilagem/metabolismo
Diferenciação Celular/genética
Comunicação Parácrina/genética
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/genética
Neoplasias Ósseas/patologia
Cartilagem/patologia
Condrócitos/metabolismo
Condrócitos/patologia
Condrogênese/genética
Condroma/genética
Condroma/patologia
Condromatose/genética
Condromatose/patologia
Exostose/genética
Exostose/patologia
Exostose Múltipla Hereditária/genética
Exostose Múltipla Hereditária/patologia
Lâmina de Crescimento
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Camundongos
Osteogênese/genética
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, mouse)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140531
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1004364


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[PMID]:23929766
[Au] Autor:Kim HK; Feng GS; Chen D; King PD; Kamiya N
[Ad] Endereço:Texas Scottish Rite Hospital for Children, Dallas, TX, USA; Orthopaedic Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA.
[Ti] Título:Targeted disruption of Shp2 in chondrocytes leads to metachondromatosis with multiple cartilaginous protrusions.
[So] Source:J Bone Miner Res;29(3):761-9, 2014 Mar.
[Is] ISSN:1523-4681
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metachondromatosis is a benign bone disease predominantly observed in the hands and feet of children or young adults demonstrating two different manifestations: a cartilage-capped bony outgrowth on the surface of the bone called exostosis and ectopic cartilaginous nodules inside the bone called enchondroma. Recently, it has been reported that loss-of-function mutations of the SHP2 gene, which encodes the SHP2 protein tyrosine phosphatase, are associated with metachondromatosis. The purpose of this study was to investigate the role of SHP2 in postnatal cartilage development, which is largely unknown. We disrupted Shp2 during the postnatal stage of mouse development in a chondrocyte-specific manner using a tamoxifen-inducible system. We found tumor-like nodules on the hands and feet within a month after the initial induction. The SHP2-deficient mice demonstrated an exostosis-like and enchondroma-like phenotype in multiple bones of the hands, feet, and ribs as assessed by X-ray and micro-computed tomography (CT). Histological assessment revealed the disorganization of the growth plate cartilage, a cartilaginous protrusion from the epiphyseal bone, and ectopic cartilage nodules within the bones, which is consistent with the pathological features of metachondromatosis in humans (ie, both exostosis and enchondroma). At molecular levels, we observed an abundant expression of Indian hedgehog protein (IHH) and fibroblast growth factor 2 (FGF2) and impaired expression of mitogen-activated protein kinases (MAPK) in the affected cartilage nodules in the SHP2-deficient mice. In summary, we have generated a mouse model of metachondromatosis that includes manifestations of exostosis and enchondroma. This study provides a novel model for the investigation of the pathophysiology of the disease and advances the understanding of metachondromatosis. This model will be useful to identify molecular mechanisms for the disease cause and progression as well as to develop new therapeutic strategies in the future.
[Mh] Termos MeSH primário: Neoplasias Ósseas/patologia
Cartilagem/metabolismo
Condrócitos/citologia
Condromatose/patologia
Exostose Múltipla Hereditária/patologia
Domínios de Homologia de src/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/metabolismo
Condrócitos/metabolismo
Condromatose/metabolismo
Exostose Múltipla Hereditária/metabolismo
Sistema de Sinalização das MAP Quinases
Camundongos
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1409
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130810
[St] Status:MEDLINE
[do] DOI:10.1002/jbmr.2062


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[PMID]:23863940
[Au] Autor:Yang W; Wang J; Moore DC; Liang H; Dooner M; Wu Q; Terek R; Chen Q; Ehrlich MG; Quesenberry PJ; Neel BG
[Ad] Endereço:Department of Orthopaedics, Brown University Alpert Medical School and Rhode Island Hospital, Providence, Rhode Island 02903, USA. wyang@lifespan.org
[Ti] Título:Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling.
[So] Source:Nature;499(7459):491-5, 2013 Jul 25.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The tyrosine phosphatase SHP2, encoded by PTPN11, is required for the survival, proliferation and differentiation of various cell types. Germline activating mutations in PTPN11 cause Noonan syndrome, whereas somatic PTPN11 mutations cause childhood myeloproliferative disease and contribute to some solid tumours. Recently, heterozygous inactivating mutations in PTPN11 were found in metachondromatosis, a rare inherited disorder featuring multiple exostoses, enchondromas, joint destruction and bony deformities. The detailed pathogenesis of this disorder has remained unclear. Here we use a conditional knockout (floxed) Ptpn11 allele (Ptpn11(fl)) and Cre recombinase transgenic mice to delete Ptpn11 specifically in monocytes, macrophages and osteoclasts (lysozyme M-Cre; LysMCre) or in cathepsin K (Ctsk)-expressing cells, previously thought to be osteoclasts. LysMCre;Ptpn11(fl/fl) mice had mild osteopetrosis. Notably, however, CtskCre;Ptpn11(fl/fl) mice developed features very similar to metachondromatosis. Lineage tracing revealed a novel population of CtskCre-expressing cells in the perichondrial groove of Ranvier that display markers and functional properties consistent with mesenchymal progenitors. Chondroid neoplasms arise from these cells and show decreased extracellular signal-regulated kinase (ERK) pathway activation, increased Indian hedgehog (Ihh) and parathyroid hormone-related protein (Pthrp, also known as Pthlh) expression and excessive proliferation. Shp2-deficient chondroprogenitors had decreased fibroblast growth factor-evoked ERK activation and enhanced Ihh and Pthrp expression, whereas fibroblast growth factor receptor (FGFR) or mitogen-activated protein kinase kinase (MEK) inhibitor treatment of chondroid cells increased Ihh and Pthrp expression. Importantly, smoothened inhibitor treatment ameliorated metachondromatosis features in CtskCre;Ptpn11(fl/fl) mice. Thus, in contrast to its pro-oncogenic role in haematopoietic and epithelial cells, Ptpn11 is a tumour suppressor in cartilage, acting through a FGFR/MEK/ERK-dependent pathway in a novel progenitor cell population to prevent excessive Ihh production.
[Mh] Termos MeSH primário: Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Condromatose/metabolismo
Condromatose/patologia
Exostose Múltipla Hereditária/metabolismo
Exostose Múltipla Hereditária/patologia
Proteínas Hedgehog/metabolismo
Células Mesenquimais Estromais/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/deficiência
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/tratamento farmacológico
Neoplasias Ósseas/genética
Cartilagem/metabolismo
Cartilagem/patologia
Catepsina K/deficiência
Catepsina K/genética
Catepsina K/metabolismo
Divisão Celular
Linhagem da Célula
Condromatose/tratamento farmacológico
Condromatose/genética
Exostose Múltipla Hereditária/tratamento farmacológico
Exostose Múltipla Hereditária/genética
Fatores de Crescimento de Fibroblastos/metabolismo
Deleção de Genes
Regulação da Expressão Gênica/efeitos dos fármacos
Genes Supressores de Tumor/fisiologia
Proteínas Hedgehog/antagonistas & inibidores
Sistema de Sinalização das MAP Quinases
Macrófagos/metabolismo
Células Mesenquimais Estromais/citologia
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Monócitos/metabolismo
Osteoclastos/metabolismo
Osteopetrose/genética
Osteopetrose/metabolismo
Osteopetrose/patologia
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Parathyroid Hormone-Related Protein); 0 (ihh protein, mouse); 62031-54-3 (Fibroblast Growth Factors); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, mouse); EC 3.4.22.38 (Cathepsin K); EC 3.4.22.38 (Ctsk protein, mouse)
[Em] Mês de entrada:1308
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130719
[St] Status:MEDLINE
[do] DOI:10.1038/nature12396


  9 / 48 MEDLINE  
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[PMID]:23863941
[Au] Autor:Zaidi M; Méndez-Ferrer S
[Ti] Título:Cell biology: tumour stem cells in bone.
[So] Source:Nature;499(7459):414-6, 2013 Jul 25.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Condromatose/metabolismo
Condromatose/patologia
Exostose Múltipla Hereditária/metabolismo
Exostose Múltipla Hereditária/patologia
Proteínas Hedgehog/metabolismo
Células Mesenquimais Estromais/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/deficiência
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:COMMENT; NEWS
[Nm] Nome de substância:
0 (Hedgehog Proteins); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, mouse)
[Em] Mês de entrada:1308
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130719
[St] Status:MEDLINE
[do] DOI:10.1038/nature12412


  10 / 48 MEDLINE  
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[PMID]:23613356
[Au] Autor:Lee YS; Dan J; Ryu KJ; Kim BK; Han SH; Kim HJ
[Ad] Endereço:Department of Orthopaedic Surgery, CHA Gumi Medical Center, School of Medicine, CHA University, Gumi-si, Kyungsangbuk-do, Republic of Korea.
[Ti] Título:Case of genochondromatosis type I in an 8-year-old boy.
[So] Source:Am J Med Genet A;161A(6):1513-6, 2013 Jun.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias Ósseas/genética
Condromatose/genética
Fraturas do Fêmur/patologia
Fêmur/patologia
Fraturas Espontâneas/patologia
Síndromes Neoplásicas Hereditárias/genética
[Mh] Termos MeSH secundário: Neoplasias Ósseas/diagnóstico por imagem
Criança
Condromatose/diagnóstico por imagem
Fraturas do Fêmur/genética
Fraturas Espontâneas/genética
Seres Humanos
Masculino
Síndromes Neoplásicas Hereditárias/diagnóstico por imagem
Fenótipo
Radiografia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1604
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130425
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.35924



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