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Dive into the research topics where Eneida Franco Vêncio is active.

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Featured researches published by Eneida Franco Vêncio.


Oral Surgery Oral Medicine Oral Pathology Oral Radiology and Endodontology | 2009

Peripheral dentinogenic ghost cell tumor: a case report and review of the literature

Germano Angarani Candido; Karolline Alves Viana; Satiro Watanabe; Eneida Franco Vêncio

Dentinogenic ghost cell tumor (DGCT) is a rare neoplasm, representing 1.9% to 2.1% of all odontogenic tumors. Few cases of DGCT have been reported and only 11 show no bone involvement. A rare case of peripheral DGCT is reported, located in the anterior mandible of a 45-year-old man. The patient presented a slow painless growth in the canine region of an edentulous mandible. Radiographically, no bone involvement was registered. The lesion was enucleated and microscopically characterized by islands of epithelial cells showing ameloblastomalike features in fibrous tissue. Dysplasic dentin and ghost cells were frequently observed. Areas showing a connection between tumor cells and the overlying mucosa were also identified. Immunohistochemical analysis demonstrated positivity for pan-cytokeratin, cytokeratin-14, and 2 neural markers. Denditric cells (Langerhans cells and melanocytes) were identified inside tumoral islands. A rare case of peripheral DGCT is reported, with immunohistochemical analysis and a review of the English literature.


BMC Medical Genomics | 2011

Lineage relationship of prostate cancer cell types based on gene expression

Laura E. Pascal; Ricardo Zn Vêncio; Robert L. Vessella; Carol B. Ware; Eneida Franco Vêncio; Gareth Denyer; Alvin Y. Liu

BackgroundProstate tumor heterogeneity is a major factor in disease management. Heterogeneity could be due to multiple cancer cell types with distinct gene expression. Of clinical importance is the so-called cancer stem cell type. Cell type-specific transcriptomes are used to examine lineage relationship among cancer cell types and their expression similarity to normal cell types including stem/progenitor cells.MethodsTranscriptomes were determined by Affymetrix DNA array analysis for the following cell types. Putative prostate progenitor cell populations were characterized and isolated by expression of the membrane transporter ABCG2. Stem cells were represented by embryonic stem and embryonal carcinoma cells. The cancer cell types were Gleason pattern 3 (glandular histomorphology) and pattern 4 (aglandular) sorted from primary tumors, cultured prostate cancer cell lines originally established from metastatic lesions, xenografts LuCaP 35 (adenocarcinoma phenotype) and LuCaP 49 (neuroendocrine/small cell carcinoma) grown in mice. No detectable gene expression differences were detected among serial passages of the LuCaP xenografts.ResultsBased on transcriptomes, the different cancer cell types could be clustered into a luminal-like grouping and a non-luminal-like (also not basal-like) grouping. The non-luminal-like types showed expression more similar to that of stem/progenitor cells than the luminal-like types. However, none showed expression of stem cell genes known to maintain stemness.ConclusionsNon-luminal-like types are all representatives of aggressive disease, and this could be attributed to the similarity in overall gene expression to stem and progenitor cell types.


Journal of Cellular Physiology | 2011

Embryonal carcinoma cell induction of miRNA and mRNA changes in co-cultured prostate stromal fibromuscular cells

Eneida Franco Vêncio; Laura E. Pascal; Laura S. Page; Gareth Denyer; Amy J. Wang; Hannele Ruohola-Baker; Shile Zhang; Kai Wang; David J. Galas; Alvin Y. Liu

The prostate stromal mesenchyme controls organ‐specific development. In cancer, the stromal compartment shows altered gene expression compared to non‐cancer. The lineage relationship between cancer‐associated stromal cells and normal tissue stromal cells is not known. Nor is the cause underlying the expression difference. Previously, the embryonal carcinoma (EC) cell line, NCCIT, was used by us to study the stromal induction property. In the current study, stromal cells from non‐cancer (NP) and cancer (CP) were isolated from tissue specimens and co‐cultured with NCCIT cells in a trans‐well format to preclude heterotypic cell contact. After 3 days, the stromal cells were analyzed by gene arrays for microRNA (miRNA) and mRNA expression. In co‐culture, NCCIT cells were found to alter the miRNA and mRNA expression of NP stromal cells to one like that of CP stromal cells. In contrast, NCCIT had no significant effect on the gene expression of CP stromal cells. We conclude that the gene expression changes in stromal cells can be induced by diffusible factors synthesized by EC cells, and suggest that cancer‐associated stromal cells represent a more primitive or less differentiated stromal cell type. J. Cell. Physiol. 226: 1479–1488, 2011.


Cancer Biomarkers | 2011

Stromal-epithelial interactions in early neoplasia

Alvin Y. Liu; Laura E. Pascal; Ricardo Z. N. Vêncio; Eneida Franco Vêncio

In prostate tumors, both the epithelial and stromal mesenchyme compartments show gene expression changes from their respective normal counterpart. In fact, there are more such changes in the stroma than the epithelium. These include down-regulated expression of genes involved in smooth muscle cell differentiation and those differentially expressed between prostate and bladder, i.e., organ-restricted. In development, the stromal cell type mediates tissue formation from differentiation of stem or progenitor cells. Diseases like cancer may arise as a result of defective stromal signaling. Stromal signaling can be demonstrated by co-culture of stromal cells and embryonal carcinoma NCCIT cells used as a stem cell substitute. In co-culture, stromal cells induce NCCIT cells through diffusible molecules to lose stem cell gene expression, gain expression of prostate genes, alter cytomorphology, and lower proliferation. This NCCIT response is varied as co-cultured bladder stromal cells induce a different gene expression. At the same time, NCCIT factors also affect gene expression of co-cultured stromal cells. NCCIT induces normal prostate tissue (NP) stromal cells to become more like cancer-associated (CP) stromal cells in both mRNA and microRNA expression. In contrast, NCCIT shows minimal effect on CP stromal cells. CP stromal cells may represent a less differentiated state in the prostate stromal cell lineage.


Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology | 2015

Multifocal red bands of the marginal gingiva.

Brunno Santos de Freitas Silva; Simone Sousa Silva Sant’ana; Satiro Watanabe; Eneida Franco Vêncio; Virgílio Moreira Roriz; Fernanda Paula Yamamoto-Silva

Multifocal red bands of the marginal gingiva Brunno Santos de Freitas Silva, DDS, MSc, PhD, Simone Sousa Silva Sant’Ana, DDS, MSc, Satiro Watanabe, DDS, MSc, Eneida Franco Vencio, DDS, MSc, PhD, Virgilio Moreira Roriz, DDS, MSc, PhD, and Fernanda Paula Yamamoto-Silva, DDS, PhD University of Anapolis, Anapolis, Goias, Brazil; Federal University of Goias, Goiânia, Goias, Brazil (Oral Surg Oral Med Oral Pathol Oral Radiol 2015;119:3-7)


Pathology Research and Practice | 2009

Pulmonary atherosclerosis associated with an atrial septal defect in old age: case report of an elderly autopsied patient.

Douglas Montielle Silva Nascimento; Lucas Nunes; Flávia Aparecida de Oliveira; Eneida Franco Vêncio; Vicente de Paula Antunes Teixeira; Marlene Antônia dos Reis

In the literature, there are few studies on atherosclerosis in the pulmonary artery in human beings, especially in aging. The aim of the study was to report the anatomic pathological aspects of an old patient who had severe pulmonary atherosclerosis associated with an atrial septal defect (ASD). The patient had marked atherosclerosis in the pulmonary trunk and its branches, probably caused by a series of hemodynamic and endothelial changes, subsequent to the ASD. The left to right shunt could have caused an increase in the blood flow and pulmonary hypertension, intensified by the vascular alterations in the region. This hypertension probably became intense to the point of reversing the direction of the shunt, from the right to the left, characterizing a probable Eisenmenger syndrome, responsible for the patients dyspnea and cyanosis. Our study demonstrates a condition that is especially infrequent because of the patients age of 64 years and, thus, adds to the literature.


Journal of Oral and Maxillofacial Surgery | 2010

Slow-growing palatal mass: a challenging differential diagnosis.

Karlla Dias Siqueira Marques; Flávia Reis Andrade; Luciano Alberto de Castro; Eneida Franco Vêncio; Elismauro Francisco Mendonça; Rejane Faria Ribeiro-Rotta; Tarcília Aparecida Silva; Aline Carvalho Batista

A 41-year-old Brazilian man was referred to the Oral edicine Center of Goiás State, School of Dentistry, Federal niversity of Goiás (Goiânia, Brazil) for evaluation of a ainless swelling of 3 years’ duration on the hard palate (Fig ). The patient had previously undergone 2 incisional biopies without conclusive diagnosis and was otherwise ealthy. No significant medical history and no other sympoms were reported. Family history was likewise unremarkble. Intraoral examination revealed a submucosal mass on he right side of the hard palate, extending from the preolar to the tuberosity region (Fig 1). On palpation, the ass was asymptomatic and resilient. Conventional radioraphs showed an osteolytic lesion in the premolar area xtending to the tuberosity and tooth resorption in the right econd molar. Computed tomography and magnetic resoance (MR) imaging showed a neoplasm extending from he premolars to the tuberosity region on the right side of he maxilla and the resorption of the ipsilateral maxillary inus floor (Fig 2). This mass was fairly well circumscribed, xcept at its medial margin with the soft palate. It appeared s a well-defined low signal mass on T1-weighted image, as igh contrast enhancement on T1-weighted postcontrast mage, and heterogeneous high signal on T2-weighted imge (Fig 2). There was no significant lymphadenopathy ccording to imaging features and clinical examination.


Tumor Biology | 2017

Expression of hypoxia-induced factor-1 alpha in early-stage and in metastatic oral squamous cell carcinoma

Maisa Ribeiro; Sarah R. Teixeira; Monarko Nunes De Azevedo; Ailton C Fraga; Antônio Pm Gontijo; Eneida Franco Vêncio

To investigate hypoxia-induced factor-1 alpha expression in distinct oral squamous cell carcinoma subtypes and topographies and correlate with clinicopathological data. Hypoxia-induced factor-1 alpha expression was assessed by immunohistochemistry in 93 cases of OSCC. Clinical and histopathological data were reviewed from medical records. Hypoxia-induced factor-1 alpha status was distinct according to tumor location, subtype and topography affect. In superficial oral squamous cell carcinomas, most tumor cells overexpressed hypoxia-induced factor-1 alpha, whereas hypoxia-induced factor-1 alpha was restricted to the intratumoral region in conventional squamous cell carcinomas. All basaloid squamous cell carcinomas exhibited downregulation of hypoxia-induced factor-1 alpha. Interestingly, metastatic lymph nodes (91.7%, p = 0.001) and the intratumoral regions of corresponding primary tumors (58.3%, p = 0.142) showed hypoxia-induced factor-1 alpha-positive tumor cells. Overall survival was poor in patients with metastatic lymph nodes. Hypoxia-induced factor-1 alpha has distinct expression patterns in different oral squamous cell carcinoma subtypes and topographies, suggesting that low oxygen tension promotes the growth pattern of superficial and conventional squamous cell carcinoma, but not basaloid squamous cell carcinoma. Indeed, a hypoxic environment may facilitate regional metastasis, making it a useful diagnostic and prognostic marker in primary tumors.


Current Urology Reports | 2015

Reprogramming of Prostate Cancer Cells - Technical Challenges

Gisely T. Borges; Eneida Franco Vêncio; Ricardo Z. N. Vêncio; Robert L. Vessella; Carol B. Ware; Alvin Y. Liu

Prostate cancer progression is characterized by tumor dedifferentiation. Cancer cells of less differentiated tumors have a gene expression/transcriptome more similar to that of stem cells. In dedifferentiation, cancer cells may follow a specific program of gene expression changes to a stem-like state. In order to treat cancer effectively, the stem-like cancer cells and cancer differentiation pathway need to be identified and studied. Due to the very low abundance of stem-like cancer cells, their isolation from fresh human tumors is technically challenging. Induced pluripotent stem cell technology can reprogram differentiated cells into stem-like, and this may be a tool to generate sufficient stem-like cancer cells.


Head and Neck Pathology | 2009

Salivary Gland Tumor: A Review of 599 Cases in a Brazilian Population

Flávia Aparecida de Oliveira; Eliza Carla Barroso Duarte; Cláudia Teixeira Taveira; Aline Abreu Máximo; Érica Carvalho de Aquino; Rita de Cássia Alencar; Eneida Franco Vêncio

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Alvin Y. Liu

University of Washington

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Carol B. Ware

University of Washington

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Nádia Lago Costa

Universidade Federal de Goiás

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Satiro Watanabe

Universidade Federal de Goiás

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