CARCINO-SARCOMA 256 DE WALKER: DISSEMINACAO METASTATICA EM DUAS LINHAGENS DO TUMOR

Walker's 256 carcinoma changes its behaviour as a consequence of various factors. In this paper the authors compare the evolution of 2 lines of the tumor: WM 16 (muscular) and Christ Hospital (ascitic) both inoculated intramuscularly. Animals receiving line WM 16 had a severe rapidly progressive evolution dying around day 14 after inoculation with diffuse metastases to lymph nodes (65% of animals), kidneys (53%), spleen (50%), lungs (46.5%), liver (45%), bone marrow (44.8%), in 56% of the animals there were circulating tumoral cells. Animals receiving the Christ Hospital line survived up to 40 days, metastases were limited to lungs (48.7%) and lymph nodes (31.7%) and only in 2 of 45 animals circulating tumoral cells were observed.

Cytohistological and immunohistochemical features of a mammary invasive pleomorphic lobular carcinoma in a dog

This case report describes a case of a mammary invasive pleomorphic lobular carcinoma in a female dog. Cytology revealed small cohesive clusters of cells and many scattered single large round cells with eccentric nuclei. Histologically, the neoplasm presented plasmacytoid cells with multiple, often bizarre nuclei and an invasive pattern with cells occasionally arranged in Indian files. Vascular invasion was consistently present. Tumour cells also revealed loss of E-cadherin immunoexpression and positive immunoreactivity for HER2/c-erbB2, oestrogen receptor alpha, cytokeratin 19, and Ki67 (52 %), and the tumour was characterised as a mammary invasive pleomorphic lobular carcinoma. This is an interesting case since this is a rare condition that is not widely recognised in dogs. © 2012 Springer-Verlag London Limited.

Visceral mast cell tumor and mastocythemia in a dog

Mast cell tumor manifests as a localized proliferation of mast cells in the skin, or less frequently as a systemic disorder, which may be accompanied by the presence of neoplastic mast cells in the peripheral blood (mastocythemia). In some cases, the neoplastic circulating mast cells originate in the bone marrow, designated as mast cell leukemia, rarely observed in dogs, or the cells may arise from visceral mast cell tumors, characterizing systemic mastocytosis. The aim of this report was to describe a case of a six-year-old female German shepherd dog presenting with history of anorexia, hematemesis and diarrhea. The blood work revealed intense mastocythemia (43%), with degranulated mast cells, and anisocytosis. At necropsy, white nodular lesions in the thymic region and an infiltrative mass in mesenteric and abdominal lymph nodes were observed. Those lymph nodes were enlarged and off-white. Histopathological examination revealed neoplastic mast cells in the liver, spleen, lymph nodes, kidneys, lungs, gastric and enteric mucosae, and adrenal glands. The clinical, hematological and histopathological findings were compatible with mastocythemia, associated with a moderately differentiated visceral mast cell tumor.

Lentinula edodes (Shiitake) modulates chemically induced mutagenesis by enhancing pitting

This study was undertaken to understand how Lentinula edodes modulates in vivo mutagenesis induced by alkylating agents in bone marrow and peripheral blood as described in our previous article. Male Swiss mice were pretreated for 15 consecutive days with aqueous extracts prepared from L. edodes, after which, the number of circulating blood cells, normal erythroid bone marrow cell cycling, and phagocytosis of micronucleated reticulocyte (MNRET) and activation of spleen macrophages were assessed. The results indicate that the antimutagenicity seen in bone marrow and peripheral blood is exerted by distinct compounds with different actions. The antimutagenic effect in bone marrow is exerted by compounds subject to degradation at deep-freeze storage temperature of -20 C. On the other hand, compounds responsible for antimutagenicity in peripheral blood are not subject to degradation at -20 C. The results also indicate that the antimutagenic action in peripheral blood leading to the reduction of circulating MNRET occurs in the spleen primarily through a phagocytic activity due to higher macrophage numbers and probably not due to the enhanced activation state of individual cells. © Mary Ann Liebert, Inc.

Mielopatia infiltrativa por tumores não-hematológicos

Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

Investigação das propriedades citotóxicas e imunológicas de complexos de paládio(II) in vitro utilizando o modelo experimental de Ehrlich

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Investigação dos efeitos tóxicos do biossurfactante ramnolipídio e suas implicações quando usado na biorremediação de águas contaminadas por petróleo

Pós-graduação em Ciências Biológicas (Biologia Celular e Molecular) - IBRC

Prevalência e associação da infecção por Helicobacter pylori e do vírus de Epstein-Barr em adenocarcinoma gástrico, em uma população do norte do Brasil

As neoplasias gástricas são a segunda maior causa de morte por câncer e apesar das descobertas sobre a fisiopatologia das células tumorais, o câncer é considerado como, no melhor das hipóteses, minimamente controlado pela medicina moderna. O carcinoma gástrico é uma das poucas neoplasias malignas nas quais os agentes infecciosos tem um importante papel etiológico. O objetivo do presente trabalho foi pesquisar a prevalência e o grau de associação da infecção por Helicobacter pylori e do vírus de Epstein-Barr em adenocarcinoma gástrico, em uma população do norte do Brasil. Foram analisadas 125 amostras de adenocarcinoma gástrico que foram submetidas à técnica de PCR para detecção de H. pylori e da cepa cagA de H. pylori, à técnica de hibridização in situ para detecção do EBV e à análise histopatológica para determinação de características clínico-patológicas e epidemiológicas. Observou-se o maior acometimento de pacientes do sexo masculino (68%) e de faixa etária acima de 50 anos (78%). A prevalência encontrada para H. pylori foi de 88%, e foi considerada alta quando comparada a estudos anteriores na região norte. A prevalência encontrada para o EBV foi de 9,6%. Os pacientes positivos para H. pylori-cagA+ apresentaram um risco relativo aumentado para adenocarcinoma do tipo intestinal. A frequência para os estádios III e IV foi de 82,4%, evidenciando que o diagnóstico desta neoplasia é geralmente realizado tardiamente. Os casos positivos para urease apresentaram um fator de risco relativo (OR=4,231) maior que quatro vezes, para H. pylori-cagA+, que é a cepa mais virulenta de H. pylori. Não houve significância estatística para a associação entre H. pylori e EBV na população estudada, porém os casos positivos para EBV apresentaram 100% de positividade para H. pylori, sugerindo uma possível atuação sinérgica destes agentes na carcinogênese gástrica.

Segurança oncológica no uso de células tronco de origem adiposa e lipofilling na reconstrução mamária após câncer

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Perfil imunofenotípico e nível de citocinas plásmáticas em portadores de hepatite C crônica com diferentes graus de comprometimento hepático

Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

Peripheral Blood Mononuclear Phagocytes From Patients With Chronic Periodontitis Are Primed for Osteoclast Formation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Propriedades oncolíticas do vírus da cinomose canina: expressão da proteína 8 (TNFAIP8) em células de carcinoma mamário: Juliana Albarracin Garcia. -

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Angiotensin II Facilitates Breast Cancer Cell Migration and Metastasis

Breast cancer metastasis is a leading cause of death by malignancy in women worldwide. Efforts are being made to further characterize the rate-limiting steps of cancer metastasis, i.e. extravasation of circulating tumor cells and colonization of secondary organs. In this study, we investigated whether angiotensin II, a major vasoactive peptide both produced locally and released in the bloodstream, may trigger activating signals that contribute to cancer cell extravasation and metastasis. We used an experimental in vivo model of cancer metastasis in which bioluminescent breast tumor cells (D3H2LN) were injected intra-cardiacally into nude mice in order to recapitulate the late and essential steps of metastatic dissemination. Real-time intravital imaging studies revealed that angiotensin II accelerates the formation of metastatic foci at secondary sites. Pre-treatment of cancer cells with the peptide increases the number of mice with metastases, as well as the number and size of metastases per mouse. In vitro, angiotensin II contributes to each sequential step of cancer metastasis by promoting cancer cell adhesion to endothelial cells, trans-endothelial migration and tumor cell migration across extracellular matrix. At the molecular level, a total of 102 genes differentially expressed following angiotensin II pretreatment were identified by comparative DNA microarray. Angiotensin II regulates two groups of connected genes related to its precursor angiotensinogen. Among those, up-regulated MMP2/MMP9 and ICAM1 stand at the crossroad of a network of genes involved in cell adhesion, migration and invasion. Our data suggest that targeting angiotensin II production or action may represent a valuable therapeutic option to prevent metastatic progression of invasive breast tumors.

Expression of PAFR as Part of a Prosurvival Response to Chemotherapy: A Novel Target for Combination Therapy in Melanoma

Melanoma cells express the platelet-activating factor receptor (PAFR) and, thus, respond to PAF, a bioactive lipid produced by both tumour cells and those in the tumour microenvironment such as macrophages. Here, we show that treatment of a human melanoma SKmel37 cell line with cisplatin led to increased expression of PAFR and its accumulation. In the presence of exogenous PAF, melanoma cells were significantly more resistant to cisplatin-induced cell death. Inhibition of PAFR-dependent signalling pathways by a PAFR antagonist (WEB2086) showed chemosensitisation of melanoma cells in vitro. Nude mice were inoculated with SKmel37 cells and treated with cisplatin and WEB2086. Animals treated with both agents showed significantly decreased tumour growth compared to the control group and groups treated with only one agent. PAFR accumulation and signalling are part of a prosurvival program of melanoma cells, therefore constituting a promising target for combination therapy for melanomas.