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This thesis investigates the role of Crim1, a transmembrane protein that is expressed in a number of areas in the vertebrate embryo including the developing kidney, eye, testis and spinal cord, which we believe may be a regulator of vertebrate tissue development. To dissect the function of Crim1 in normal mammalian development, two vertebrate models were used, zebrafish and mice. The results show that in zebrafish, crim1 is expressed early in development from the 16-cell stage through to 30 hours post fertilisation (Chapter 3). At 24 hours post fertilisation crim1 is expressed in the intermediate cell mass (icm), the site of haemangioblast development. Haemangioblasts are precursor cells that contribute to the formation of the blood and endothelial cell lineages. Injection of crim1 antisense oligonucleotides into zebrafish embryos (crim1 morphants) lead to an expansion of the icm and defects in the trunk, tail, somites and vasculature. The injection of crim1 antisense oligonucleotides into transgenic fli:GFP zebrafish revealed defects in the intersegmental, dorsal longitudinal anastomotic and parachordal vessels. Although crim1 is expressed during haemagiogensis the primary defect in the crim1 morphant zebrafish appears to be vascular. Further experiments used a ‘knock-in’ mouse, Crim1KST264, in which a loss of functional Crim1 leads to defects in limb (syndactyly), skeleton, eye, vascular, kidney and placental development. Analysis of the kidney phenotype in the embryonic Crim1KST264 homozygotes showed that a loss of Crim1 affects ERK1/2 and phosphorylated-Smad1/5/8 protein expression, although has no direct effect on BMP or TGFβ protein expression (Chapter 4). Analysis of the adult Crim1 outbred kidneys revealed they have albuminuria and leaky vasculature. The complex phenotype presented by the Crim1KST264 homozygote kidneys suggests Crim1 may be regulating multiple growth factor pathways. As Crim1 was shown to be expressed in the placenta, we characterised the role of Crim1 in placental development using the Crim1KST264 mouse (Chapter 5). Crim1KST264 homozygote placentas and embryos are smaller than their wild-type littermates. Our investigations revealed that Crim1 is expressed in trophoblast giant cells and in spongiotrophoblasts. A loss of Crim1 causes a developmental defect in that the junctional zone (region of the placenta containing spongiotrophoblasts and glycogen cells) is expanded, although this phenotype does not appear to be due to a defect in proliferation or apoptosis. Further analysis of E15.5 Crim1KST264 homozygote placentas revealed there was a reduction in the number of labyrinth trophoblast gaint cells. Thus, by using zebrafish and mouse as two model organisms of vertebrate development, this thesis has showed that Crim1 is clearly important for normal embryonic development. To dissect the complex phenotype presented by the Crim1KST264 mouse, further studies of Crim1 and its interaction with other growth factor pathways is needed to elucidate how and to what extent they interact with Crim1 to determine its biological effect on vertebrate tissue.

Les nématodes à galles du genre Meloidogyne sont des parasites obligatoires des plantes. Lors de l’interaction compatible, ils induisent la formation de cellules nourricières hypertrophiées et plurinucléées leur permettant d’assurer croissance et reproduction. L'étude des mécanismes moléculaires impliqués dans la formation de ces cellules géantes a permis d’identifier une protéine associée aux microtubules, MAP65-3, essentielle à la formation de ces cellules géantes et au développement du nématode. Un des partenaires protéiques de MAP65-3 est un homologue de BUB3, membre du « Mitotic Checkpoint Complex » (MCC). Le MCC est un point de contrôle de la mitose assurant la fidélité de la ségrégation des chromosomes. Au cours de ma thèse, j'ai caractérisé chez la plante modèle Arabidopsis thaliana les homologues du MCC: BUB3.1, MAD2 et la famille multigénique composée de BUBR1, BRK1 et BUB1.2. J’ai démontré les interactions in planta entre les membres du complexe, certaines interactions ayant lieu au niveau des noyaux, voire au niveau des centromères. J’ai réalisé l’analyse fonctionnelle de ces gènes et montré qu’ils étaient exprimés dans les tissus enrichis en cellules en division comme MAP65-3. L’étude de la localisation subcellulaire des protéines a révélé une localisation cytoplasmique pour BUB3.1, BUB1.2 et MAD2, nucléaire pour BUBR1 et centromérique pour BRK1. Nous avons pu également montrer que lorsque des défauts d’attachement des microtubules du fuseau mitotique sont provoqués, BUB3.1, BUBR1 et MAD2 se relocalisent au niveau des kinétochores. L’étude de la famille BUB1/BUBR1 a révélé que l’inactivation des gènes correspondants induisait une sensibilité accrue à un traitement chimique déstabilisant les réseaux de microtubules. L’étude de la mitose chez ces mutants a révélé que BUBR1 est essentielle à la réalisation d’une mitose sans erreur chez Arabidopsis. Ce travail a ainsi permis de caractériser pour la première fois le MCC chez A. thaliana. / Root-knot nematodes from the genus Meloidogyne are obligate biotrophic plant parasites. During a compatible interaction, they induce the redifferentiation of root cells into multinucleated and hypertrophied feeding cells to ensure their growth and reproduction. The study of molecular and cellular mechanisms underlying giant cell ontogenesis has led to the identification of a Microtubule-Associated Protein, MAP65-3, essential for giant cell ontogenesis and nematode development. One of the MAP65-3 interacting partners is a BUB3 homologue, member of the Mitotic Checkpoint Complex (MCC). The MCC is a surveillance mechanism ensuring that chromosomes undergoing mitosis do not segregate until they are properly attached to the microtubules of the mitotic spindle. During my thesis, I have characterized the Arabidopsis thaliana orthologs of the MCC, BUB3.1, MAD2 and the multigenic family composed of BUBR1, BRK1 et BUB1.2. I have demonstrated that MAP65-3 and all the MCC members interact together in planta, some interactions taking place within the nuclei or at the centromeres. As MAP65-3, all these genes are expressed in dividing cells. The study of the subcellular localization of the protein showed a cytoplasmic localization for BUB3.1, BUB1.2 and MAD2, nuclear for BUBR1 and centromeric for BRK1. Thus, the MCC proteins did not relocalize to the kinetochore during a normal mitosis in planta. BUB3.1, BUBR1 and MAD2 localize to the unattached kinetochores following defects in spindle assembly as observed in cells treated with microtubule poisons. The functional analysis of BUB1/BUBR1 multigenic family showed that the knock-out mutants were more sensitive to microtubule-destabilizing drugs. Furthermore, analysis of mitosis revealed that BUBR1 is essential for an error-free mitosis in Arabidopsis. This work represents the first characterization of the MCC in A. thaliana.

Orientador: Jose Ricardo Albergaria Barbosa / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba / Made available in DSpace on 2018-08-08T02:07:16Z (GMT). No. of bitstreams: 1 Luna_AnibalHenriqueBarbosa_D.pdf: 1133521 bytes, checksum: 0b56f9a0d7a3c458d4ca3675a6467a94 (MD5) Previous issue date: 2006 / Resumo: O granuloma central de células gigantes (GCCG) é uma lesão benigna que acomete tanto a maxila como a mandíbula, representando menos de 7% de todos os tumores benignos dos maxilares. A sua etiologia é incerta, sendo implicados fatores genéticos. O GCCG pode manifestar-se como lesões de grandes dimensões com características de agressividade ¿ como crescimento rápido, reabsorções radiculares ou parestesia e tendência à recidiva, ou como lesões pequenas, uniloculares, sem aspectos de agressividade. A modalidade de tratamento mais empregada é a curetagem, associada ou não a ostectomia periférica. No entanto são relatadas outras modalidades de tratamento, como a administração de corticosteróides, calcitonina ou a-interferon. Os índices de recidiva podem ser altos, variando de 0% a 49%. A ocorrência de recidiva parece depender do comportamento clínico da lesão, da localização anatômica e da modalidade de tratamento instituída. O presente estudo retrospectivo analisou o tratamento de GCCG no período de janeiro de 1996 a julho de 2006 atendidos pela Área de Cirurgia Buco-Maxilo-Facial da FOP ¿ Unicamp, correlacionando seus aspectos clínicos. Foram analisados 14 casos (9M; 5F) com uma média de idade de 18,5 (variando de 5 ¿ 59) anos, sendo a maxila o osso mais acometido. Do total, 5 casos foram tratados cirurgicamente por meio de curetagem associada a ostectomia periférica, e 9 foram tratados clinicamente. A administração intralesional de corticosteróides foi iniciada nestes casos, sendo o tratamento com calcitonina instituído na ausência de uma resposta clínica satisfatória. O tempo médio de tratamento com corticosteróides foi de 3,84 (±3,87) meses, sendo que em dois casos foi instituída a administração de calcitonina. O tempo médio de tratamento com calcitonina foi de 18,8 (±7,94) meses, sendo que em um caso não foi observada boa evolução clínica. Nenhum caso de recidiva foi observado após um acompanhamento de 38,22 (variando de 3 ¿ 174) meses / Abstract: The central giant cell granuloma is a benign lesion of the jaws, accounting for less than 7% of all benign lesions of the jaws. Its origin is unknown, but it has been suggested that genetic factors may be implicated. The central giant cell granuloma demonstrates a variable clinical behavior, ranging from slowly growing painless swelling to rapidly expanding aggressive tumors, characterized by pain, local destruction of bone, root displacement or resorption and a significantly high recurrence rate. Surgical treatment represented by curettage with peripheral ostectomy or not is the most widely used procedure. However, other treatment options such as intralesional corticosteroids, daily calcitonin administration or a-interferon are advocated. The recurrence rate may be high (ranging form 0% to 49%), and it seems to depend on the clinical behavior, the treatment employed, and anatomic site envolved. The aim of this study was to report the results of long-term follow up of the management of central giant cell granulomas. A retrospective analysis was conducted from January 1996 to July 2006, analyzing all cases of the Oral and Maxillofacial Area, Piracicaba Dental School. The sample was represented by 14 patients (9 M; 5 F) with a mean age of 18.5 (ranging from 5 ¿ 59) years, and the maxilla was involved in most of the cases. Regarding the treatment modality, 5 cases were treated by curettage with peripheral ostectomy, and a medical treatment was instituted in the others. In these cases, intralesional injections with corticosteroids were initiated, and the treatment with calcitonin was employed only if proper resolution was not achieved. The mean time of treatment with corticosteroids was 3.84 (±3.87) months, but in two cases calcitonin daily administration was initiated. The mean time of treatment with calcitonin was 18.8 (±7.94) months, but in one case calcitonin did not seem to be effective. No case of recurrence was observed after a mean follow-up of 38.22 (ranging from 3 ¿ 174) months / Doutorado / Cirurgia e Traumatologia Buco-Maxilo-Faciais / Doutor em Clínica Odontológica

Introduction: Below knee amputation is the safest treatment for aggressive benign and malignant bone tumours of the distal tibia yielding good oncological and functional results. However, in selected patients where limb salvage is feasible and amputation unacceptable to the patient, limb salvage using a distal tibial replacement (DTR) can be considered. This study aims to present the oncological and functional results of the use of this treatment method in our unit. Patients & Methods: A retrospective folder review was performed for all 10 patients who received a modular distal tibial replacement between 01/01/2005 and 31/01/2019 for a primary bone tumour either benign aggressive or malignant. Six were female and the mean age was 31 (1275) years. There were five patients with giant cell tumour of bone, four with osteosarcoma and one with a low-grade chondrosarcoma. The patients with osteosarcoma had neo-adjuvant chemotherapy before surgery. Function was assessed by the Musculoskeletal Tumor Society (MSTS) score. Results: There were six females and four males, with a mean age of 31 (12-75) years. Two patients had local recurrence treated with a BKA and one other patient died of metastases three years postoperatively. At a mean follow-up of three years, the remaining eight patients had a mean MSTS score of 83% (67–93%). There were no radiological signs of loosening, and no revision surgeries. Conclusion: Endoprosthetic replacement of the distal tibia for primary bone tumours can be a safe treatment option in very selected cases.

<p>Giant cell tumour of bone (GCT) is an aggressive primary bone tumour with an unclear etiology that presents with significant local osteolysis due in part to the accumulation of multinucleated osteoclast-like giant cells. However, it is the neoplastic spindle-like stromal cells within GCT that largely direct the pathogenesis of the tumour. I hypothesize that parathyroid hormone-related protein (PTHrP) is a key mediator within GCT that promotes the characteristic osteolytic phenotype by stimulating both bone resorption and giant cell formation. The work presented in this thesis collectively demonstrates that the stromal cells express PTHrP and its receptor, the parathyroid hormone type 1 receptor (PTH1R), and that PTHrP acts in an autocrine/paracrine manner within the tumour to stimulate expression of factors that promote bone resorption. Data are presented that demonstrate that PTHrP stimulates stromal cell expression of the receptor activator of nuclear factor-κB ligand (RANKL), a known essential regulator of osteoclastogenesis, which results in increased formation of multinucleated cells from murine monocytes. Moreover, the GCT stromal cells express matrix metalloproteinase (MMP)-1 and MMP-13. These results suggest that the stromal cells may participate directly in bone resorption through the degradation of type I collagen, the promotion of osteoclast activity, or through a combination of these elements. PTHrP also regulates the expression of MMP-13 by the stromal cells. Experiments with CD40 ligand show that local factors present within the tumour can influence PTHrP expression by the stromal cells and potentiate its catabolic effects by stimulation of RANKL and MMP-13 expression. Together, this thesis presents evidence that suggests PTHrP is an important factor in the pathophysiology of GCT by its actions on promoting catabolism within the tumour. The role of PTHrP in normal physiology and the mechanisms of action presented here suggest that research into the effects of PTHrP within GCT may provide invaluable information that enhances our understanding of the biology of this particularly aggressive bone tumour.</p> / Doctor of Philosophy (PhD)

Made available in DSpace on 2014-12-17T15:32:18Z (GMT). No. of bitstreams: 1 FelipeRM.pdf: 2960586 bytes, checksum: f36dd0983baaaf9fe7c3bb48e095490e (MD5) Previous issue date: 2010-02-12 / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico / Central giant cell lesion (CGCL) and peripheral giant cell lesion (PGCL) of the jaws have a distinct clinical behavior, although they share histopathologic features. It is still unclear whether these clinical differences are supported by a distinct pattern of immunoexpression of markers for multinucleated giant cells (GC) and mononuclear cells (MC). The purpose of this study was to compare the immunohistochemical expression of VEGF, MMP-9 in CG and MC and measure the vascularization by vWF to check whether there are differences in expression of these biomarkers between CGCL and PGCL. Paraffin wax blocks of 20 cases of LCCG and 20 LPCG were retrieved. MMP-9 immunoreactivity was greater in the CM of PGCL compared to VEGF (p<0.05). VEGF expression was greater in the CM of CGCL compared to PGCL (p<0.05) and it was greater in the overall expression of CGCL compared to PGCL (p<0.05). Vascularity was quantified by microvascular counting (MVC). MVC was greater in the PGCL compared CGCL (p<0.05). MMP-9 showed a greater tendency of expression in CGCL, though was not significant (p>0.05). We tested correlation between the proteins studied in each group and found a significant negative correlation between VEGF and vWF in CGCL (p<0.05). These results suggest that there are differences in the expression of VEGF in CM and overall expression between the lesions, although no statistically significant difference in the overall expression of the MMP-9. Then, there was a trend in increased expression of MMP-9 and VEGF in CGCL, possibly by the involvement of both proteins in osteoclastogenesis. Additionally, the results of this study indicate a higher degree of vascularization in PGCL compared to CGCL, fact that can be directly linked to the reactive nature of the PGCL, where the inflammatory process with its rich angiogenesis contributes significantly to these findings. / Les?es centrais (LCCG) e perif?ricas de c?lulas gigantes (LPCG) dos maxilares possuem um comportamento cl?nico distinto, embora compartilhem caracter?sticas histopatol?gicas semelhantes. Ainda ? obscuro se essas diferen?as cl?nicas s?o apoiadas por um padr?o distinto de imunoexpress? o de marcadores para c?lulas gigantes multinucleadas (CG) e mononucleadas (CM). O escopo do presente trabalho foi realizar um estudo imuno-histoqu?mico comparativo, analisando quantitativamente c?lulas gigantes multinucleadas e mononucleadas imunorreativas ? MMP-9 e ao VEGF e mensurar a vasculariza??o atrav?s do FvW para verificar se h? ou n?o diferen?as de express?o desses biomarcadores entre as LCCG e LPCG. Foram selecionados 20 casos de LCCG e 20 de LPCG emblocados em parafina. Constatou-se diferen?a significativa (p<0.05) em rela??o ? imunorreatividade na CM para MMP-9 e VEGF nas LPCG, sendo a MMP-9 mais expressa. O VEGF foi mais expresso nas CM das LCCG em rela??o ?s LPCG (p<0.05), assim como sua express?o global (p<0.05). A MMP-9 apresentou uma tend?ncia maior de express?o nas LCCG, embora n?o significativa estatisticamente (p>0.05). Na mensura??o dos vasos atrav?s da contagem microvascular (MVC), verificou-se maior MVC nas LPCG do que nas LCCG (p<0.05). Testou-se correla??o entre as prote?nas estudadas em cada grupo de les?es e constatou-se uma correla??o negativa significativa entre VEGF e FvW nas LCCG (p<0.05). Diante dos achados deste estudo, observa-se que h? diferen?a na express?o do VEGF nas CM, bem como na express?o global entre as les?es. Observou-se uma tend?ncia na maior express?o da MMP-9 nas LCCG, embora n?o significativa estatisticamente. Dessa forma, sugere-se que a maior express?o de ambas as prote?nas nas LCCG esteja mais relacionada possivelmente com a osteoclastog?nese. Adicionalmente, os resultados do presente estudo apontam um maior grau de vasculariza??o nas LPCG quando comparadas com as LCCG, fato este que pode estar relacionado diretamente com a natureza reacional das primeiras, em que o processo inflamat?rio com sua rica angiog?nese contribui sobremaneira para estes achados.

Amyloid is a form of abnormal protein aggregation within the living body. Massive deposits can lead to organ failure. There is also increasing evidence that smaller pre-amyloid aggregates exert direct toxic effects to cells. To date 25 different proteins are known to occur as amyloid deposition in human tissues, although not all of these conditions are known to be associated with clinical diseases. This thesis deals with the very common form of amyloid localized to the arterial media. The fibril protein called ‘medin’ was identified in 1999. Medin is a 50 amino acid residue internal fragment of the precursor protein lactadherin. Lactadherin, first found in human milk, is expressed in various tissues such as breast epithelium (including carcinomas), macrophages and aorta. The function of the protein is not known but it has several functional domains. There is an EFG like domain, including an RGD-sequence, in the N-terminal part of the molecule. The C-terminal part consists of C1 and C2 coagulation factor V and VIII like domains. Medin is from within the C2 domain. This region is suggested to be involved in phosphatidyl serine binding, important in phagocytosis of apoptotic cells. Medin amyloid was originally described from studies of the aorta. It is shown here that deposits are more widely spread and can be found in many large arteries, particularly within the upper part of the body. The prevalence of medin amyloid increases with age and deposits are found, to a certain degree, in virtually everyone above the age of 60 years. The amyloid is not only found extracellularly but intracellular deposits may also occur. Amyloid is usually associated with elastic lamina or lamellae which often show signs of fragmentation. Given the localization of amyloid to elastic structures of the arterial media, three different vascular diseases were studied: temporal (giant cell) arteritis, thoracic aortic aneurysm and thoracic aortic dissection. Medin amyloid was found in temporal arteries with and without inflammation. In inflamed arteries, amyloid was mainly located along the broken internal elastic lamina. Medin was also demonstrated within giant cells. It is suggested that medin may be an antigen triggering autoimmune giant cell arteritis. In the study of thoracic aortic aneurysms and dissections, we found significant less medin amyloid in diseased aortic tissues compared with a control material. On the other hand, immunoreactive medin, probably in the state of oligomeric aggregates, was regularly found in association with aneurysms and dissections but not in the control material. It is suggested that medin oligomers exert toxic effects on smooth muscle cells which may lead to weakening of the arterial wall with aneurysm or dissection as a consequence.

Made available in DSpace on 2014-06-11T19:27:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-02-26Bitstream added on 2014-06-13T20:36:41Z : No. of bitstreams: 1 dune_acc_me_jabo.pdf: 415734 bytes, checksum: 508642fb7787a9fec7ba22d33d842496 (MD5) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / O tumor ósseo de células gigantes apresenta 3 diferentes tipos celulares, sendo duas estromais: fibroblastos neoplásicos e células mononucleares; e o terceiro tipo, células gigantes. Propôs-se que este tumor é de linhagem monócito-macrofágica e acredita-se que as células gigantes se formam por fusão de células mononucleares. Aparentemente os fibroblastos neoplásicos que expressam o fator transformador de crescimento TGFbeta1 estão envolvidos no recrutamento das células gigantes para o tumor. Com o intuito de compreender melhor a histogênese, o envolvimento do estrógeno e a expressão de receptores TGFbeta1, foi realizado este estudo em casos deste tumor em gatos domésticos. Para tanto foi utilizado o método imuno-enzimático Streptoavidina-biotina utilizando-se o anticorpo primário anti-vimentina, clone 3B4 (Dako A/s, Denmark); o anticorpo marcador de macrófago, MAC387 (Dako A/s, Denmark); o anticorpo para receptores de estrógeno, clone 15D (Dako A/s, Denmark) e o anticorpo marcador para TGFBeta1 (Santa Cruz Biotechnology). Os resultados foram analisados pela porcentagem e desvio padrão de células marcadas para cada anticorpo e permitiram concluir que: o TOCG de gatos domésticos, assim como em humanos, tem origem mesenquimal e expressa receptores de estrógeno e de TGF 1 e as células gigantes do tumor não reagem com o clone 387, marcador de células de linhagem mielomonocítica. / Giant cell tumor of bone are composed of 3 different cell types: round mononuclear stromal cells, spindle-shaped mononuclear stromal cells, and giant cells. Some authors assert giant cell could arise by fusion of mononuclear cell mielomonocytic. Aparently neoplasic fibroblast that expression TGF is involved in the recruitment of giant cells from tumor. For better understand of histogenesis, the involved of receptors estrogen and of expression of TGF receptors, achieved this study in this cases tumor in domestics cats. By using the immune-enzymatic Streptoavidin- biotin using the primary antibody anti-vimentin, clone VIM 3B4 (Dako A/s, Denmark); antibody myeloid/histocyte clone MAC 387 (Dako A/s, Denmark); antibody estrogen receptor clone 1D5 (Dako A/s, Denmark) and the antibody TGFb1 (Santa Cruz Biotechnology). The results analyzed for percent and standara deviation of marks cells for each antibody and permissive to come to a conclusion: the GCT of bone in domestic cats, like humans, has mesenchymal origin and has expression of estrogen receptors and of TGFbeta, and giants cells this tumor not react with the clone 387, mark the cells myeloidmonocyte lineage.

Orientador: Mirela Tinucci Costa / Banca: Gisele Fabrino Machado / Banca: Gervásio Henrique Bechara / Resumo: O tumor ósseo de células gigantes apresenta 3 diferentes tipos celulares, sendo duas estromais: fibroblastos neoplásicos e células mononucleares; e o terceiro tipo, células gigantes. Propôs-se que este tumor é de linhagem monócito-macrofágica e acredita-se que as células gigantes se formam por fusão de células mononucleares. Aparentemente os fibroblastos neoplásicos que expressam o fator transformador de crescimento TGF"beta"1 estão envolvidos no recrutamento das células gigantes para o tumor. Com o intuito de compreender melhor a histogênese, o envolvimento do estrógeno e a expressão de receptores TGF"beta"1, foi realizado este estudo em casos deste tumor em gatos domésticos. Para tanto foi utilizado o método imuno-enzimático Streptoavidina-biotina utilizando-se o anticorpo primário anti-vimentina, clone 3B4 (Dako A/s, Denmark); o anticorpo marcador de macrófago, MAC387 (Dako A/s, Denmark); o anticorpo para receptores de estrógeno, clone 15D (Dako A/s, Denmark) e o anticorpo marcador para TGF"Beta"1 (Santa Cruz Biotechnology). Os resultados foram analisados pela porcentagem e desvio padrão de células marcadas para cada anticorpo e permitiram concluir que: o TOCG de gatos domésticos, assim como em humanos, tem origem mesenquimal e expressa receptores de estrógeno e de TGF 1 e as células gigantes do tumor não reagem com o clone 387, marcador de células de linhagem mielomonocítica. / Abstract: Giant cell tumor of bone are composed of 3 different cell types: round mononuclear stromal cells, spindle-shaped mononuclear stromal cells, and giant cells. Some authors assert giant cell could arise by fusion of mononuclear cell mielomonocytic. Aparently neoplasic fibroblast that expression TGF is involved in the recruitment of giant cells from tumor. For better understand of histogenesis, the involved of receptors estrogen and of expression of TGF receptors, achieved this study in this cases tumor in domestics cats. By using the immune-enzymatic Streptoavidin- biotin using the primary antibody anti-vimentin, clone VIM 3B4 (Dako A/s, Denmark); antibody myeloid/histocyte clone MAC 387 (Dako A/s, Denmark); antibody estrogen receptor clone 1D5 (Dako A/s, Denmark) and the antibody TGFb1 (Santa Cruz Biotechnology). The results analyzed for percent and standara deviation of marks cells for each antibody and permissive to come to a conclusion: the GCT of bone in domestic cats, like humans, has mesenchymal origin and has expression of estrogen receptors and of TGF"beta", and giants cells this tumor not react with the clone 387, mark the cells myeloidmonocyte lineage. / Mestre