Navegando por Palavras-chave "vegf"

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    Análise do tempo de sobrevida de doentes com adenocarcinoma colorretal esporádico pela utilização de um painel de biomarcadores de carcinogênese constituído por vegf, egfr, ki-67, p53 e bcl-2
    (Universidade Federal de São Paulo (UNIFESP), 2014-12-17) Luderer, Loreley Andrade [UNIFESP]; Matos, Delcio Matos [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objective: To evaluate the prognostic power of survival of a carcinogenesis biomarkers panel formed by p53, VEGF, Bcl-2, Ki-67, and EGFR in subjects with sporadic colorectal adenocarcinoma subjected to radical surgical treatment. Methods: 114 post-surgical subjects with colorectal adenocarcinoma were studied and followed for 3 to 5 years at Fundação Pio XII – Hospital de Câncer de Barretos. The study was conducted in paraffin-embedded tumor tissue whose slides were stained using the hematoxylin-eosin technique. The tissue microarray slides, as well as the immunohistochemical staining, were examined by two pathologists, blinded to the evaluations. The statistical analyses were conducted using mean, median, minimum, maximum, and number of valid observations for the descriptive analysis of the numeric variable, global survival. The comparison of the expression of EGFR, VEGF, Ki-67, p53, and Bcl-2 biomarkers was conducted through the Chi-square test or, when required, Fisher’s exact test. The Cox regression model was used for global survival analysis with a panel of markers and for uni and multivariate global survival analyses. Results: Isolated expression correlation results of the markers with the variables: age, differentiation degree, venous invasion, perineural invasion, TNM (I+II) x (III+IV), and survival showed statistically significant differences in the EGFR expression with venous invasion, TNM classification, and global survival; the expression of the VEGF marker has showed significant correlation with the perineural invasion; the Ki-67 marker, with age, venous invasion, and TNM; expression of p53 was significantly related with age, venous invasion, TNM, and global survival; the Bcl-2 marker did not show significant correlation with any of the variables analyzed. The survival analysis, using the markers panel, has significantly showed lesser time of survival in surgical species with 60% or more overexpression. Conclusion: Overexpression of the selected tumor markers panel is related with lesser time of survival in those suffering from sporadic colorectal adenocarcinoma subjected to radical surgical treatment.
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    Estudo histológico da cicatrização da parede abdominal em camundongos com a neoplasia de ehrlich por método imuno-histoquímico
    (Universidade Federal de São Paulo (UNIFESP), 2014-08-27) Salgado, Flavio Luiz Lima [UNIFESP]; Lopes Filho, Gaspar de Jesus Lopes Filho [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objective: To evaluate the histological changes in laparotomy scars of healthy BALB/c mice with an Ehrlich tumor in its various forms of presentation using immunohistochemical techniques. Methods: Studies were conducted on 54 mice divided into 3 groups of 18 animals. One group was the control, the second presented the Ehrlich ascites tumors, and the third group had the subcutaneous form. Seven days after inoculation of the tumor, all 54 mice were submitted to laparotomy. All of the animals in the experiment were operated on again on the seventh day after surgery, with resection of the scar and subsequent euthanasia of the animal. The scars were sent for histological assessment using immunohistochemical techniques to evaluate Cox-2 (cyclooxygenase 2), VEGF (vascular endothelial growth factor) and FGF (fibroblast growth factor); and were analyzed semi-quantitatively on the laparotomy scar and the abdominal wall farthest from the site of the operation. Results: Assessing the weight of the animals, the correct inoculation of the tumor and weight gain in the group with ascites tumors was observed. The histological studies showed that groups with the tumor showed a statistically significant higher presence of Cox-2 compared to the control. In the Cox-2 study of the abdominal wall location, this was the site in which the ascites group showed the most significant difference. The VEGF did not present any significant differences between the 3 groups, regardless of the site studied. The FGF showed a significant increase in animals with the tumor. Conclusion: In mice with different forms of presentation of the Ehrlich tumor, there was a statistically significant predominance of immunoreactivity of Cox-2 and FGF in the surgical scars compared to the group of healthy animals. VEGF showed no significant difference. This finding suggests more inflammation and fibroblast proliferation in animals from the groups with tumors.
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    Fator de crescimento vascular endotelial na neovascularização corneana de camundongos
    (Universidade Federal de São Paulo (UNIFESP), 2014-09-30) Oliveira, Hailton Barreiros de [UNIFESP]; Siqueira, Wallace Chamon Alves de Siqueira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Angiogenesis is defined as the formation of new vessels from existing vessels. It is a complex multistep process that includes proliferative migration and differentiation of endothelial cells, degradation of extracelluar matrix, microtubule formation, and sprouting of new capillary branches. Angiogenic factors such as basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have been used as angiogenic inducers. bFGF is the prototype member of 13 structurally related heparin-binding growth factors and it is known as a mitogen for several types of cells, including vascular endothelial cells and fibroblasts. Miquerol and collaborators have produced mice that express VEGF-LacZ. This was possible by inserting a gene identifier (reporter) 3i non-transcribed region of the endogenous VEGF gene. Thus, it was possible to produce VEGF mRNA containing the LacZ indentifier (reporter). The balance between angiogenic and antiangiogenic factors is responsible for the regulation of angiogenesis. Studies show the effects of a specific inhibitor of VEGF. VEGF TrapR1R2, which is a fusion protein of human Fc domain to the second domain and the third domain receptor R1 receptor R2 . This protein is able to sequester VEGF, antagonize and therefore prevent the formation of blood vessels. The objectives of this study are: demonstrate that mice cornea produces VEGF when stimulated by bFGF and to demonstrate that intraperitoneal administration of VEGF TrapR1R2 inhibits VEGF production and angiogenesis. Control pellets or pellets containing 80 ng bFGF were surgically implanted into wild-type C57BL/6 and VEGF-LacZ mouse corneas. The corneas were photographed, harvested, and the percentage of corneal NV was calculated. The corneas were evaluated for the expression of VEGF and neovascularization using Confocal Microscopy. VEGF-LacZ mice received tail vein injections of an endothelial-specific lectin after pellet implantation to determine the temporal and spatial relationship between VEGF expression and corneal NV using confocal microscopy. Western blot was used to analyze the presence of VEGF in corneas of mice that received wild implantation of pellets containing bFGF. Neovascularization was assessed on corneas that received the implant pellet containing bFGF after administration of intraperitoneal injections of VEGF TrapR1R2 or control IgG-Fc protein. NV of the corneal stroma began on day 4 and was sustained through day 21 following bFGF pellet implantation. Progression of vascular endothelial cells correlated with increased VEGF-LacZ expression. Western Blot analysis showed increased VEGF expression in the corneal NV zone. Following bFGF pellet implantation, the area of corneal NV in untreated controls was 1.05±0.12 mm² and 1.53±0.27 mm² at days 4 and 7, respectively. This was significantly greater than that of mice treated with VEGF TrapR1R2 (0.24±0.11 mm² and 0.35±0.16 mm² at days 4 and 7, respectively; p<0.05). The avascular cornea depends on a balance between various endogenous angiogenic factors (including VEGF , bFGF) and anti - angiogenic factors , when this balance is broken for some reason , corneal neovascularization occurs. This study suggests that the mice cornea produces VEGF when stimulated with bFGF. VEGF proteins are of great importance in corneal neovascularization, as function stimulating factors such as vascular endothelial cells. However, the specific mechanism of regulation of VEGF production by stimulation of bFGF has not yet been fully elucidated. It has been shown that injection of VEGF TrapR1R2 blocks the formation of blood vessels in the corneas of mice subjected to suturing. Using different technique to induce neovascularization, we demonstrate that VEGF TrapR1R2 blocks neovascularization in corneas that had implantation of sediments containing bFGF. More experiments are needed to dissect the role of bFGF in the production of VEGF and blocking using VEGF TrapR1R2. Probably, this mechanism contributes to the prevention of corneal neovascularization. The cornea of mice expressed VEGF after stimulation by bFGF. Systemic administration of VEGF TrapR1R2 blocks the vascularization of the mice cornea triggered by implanting pellets containing bFGF. Systemic administration of VEGF TrapR1R2 may have potential therapeutic applications in the management of corneal NV.