VANESSA JACOB VICTORINO
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
6 resultados
Resultados de Busca
Agora exibindo 1 - 6 de 6
article 29 Citação(ões) na Scopus Oxidative Stress, Redox Signaling and Cancer Chemoresistance: Putting Together the Pieces of the Puzzle(2014) VICTORINO, Vanessa Jacob; PIZZATTI, Luciana; MICHELLETTI, Pamela; PANIS, CarolinaChemotherapy continues to be the main treatment option for cancer. Although systemic chemotherapy can efficiently eradicate cancer cells, a significant proportion of patients carry tumors that present a chemoresistant phenotype, resulting in disease progression, cancer relapse, and reduced survival. It has also become clear that the effect of most chemotherapeutic drugs is associated with their capacity to generate reactive species (RS) that bind to specific structures within the cancer cell and promote cell death. Due to repeated exposure to chemotherapeutic agents, the redox homeostasis of cancer cells is continuously disturbed, which can result in changes to the cell's ability to cope with excessive RS levels through the production of protective molecules. It is thought that the imbalance resulting from this process-oxidative stress-is toxic to cancer cells. Paradoxically, the metabolites produced during oxidative stress can favor the survival of some cancer subpopulations, which present specific gene signatures that confer a chemoresistant phenotype on these clones. Despite the huge amount of information generated by currently available technologies, we cannot predict whether this resistance will arise during chemotherapy and we still do not fully understand the mechanism by which it arises. In this review, we discuss the main findings regarding the role of oxidative stress signaling in cancer chemotherapy and the key redox molecules and pathways that lead to the development of chemoresistance.conferenceObject Increase of splenic lymphocyte apoptosis in septic encephalopathy(2014) JEREMIAS, Isabela; VICTORINO, Vanessa; LIMA, Thais; SORIANO, Francisco- Clinical insights from adiponectin analysis in breast cancer patients reveal its anti-inflammatory properties in non-obese women(2014) PANIS, C.; HERRERA, A. C. S. A.; ARANOME, A. M. F.; VICTORINO, V. J.; MICHELLETI, P. L.; MORIMOTO, H. K.; CECCHINI, A. L.; SIMAO, A. N. C.; CECCHINI, R.Adiponectin is a cytokine reported as a determinant of poor prognosis in women with breast cancer. However, because data regarding its role in breast cancer have been obtained primarily from studies employing overweight or obese women, the adiponectin profile in non-obese women is poorly understood. In this study, we determined adiponectin levels in plasma from non-obese women with breast cancer and investigated a possible correlation with systemic inflammatory status. We determined the plasma adiponectin levels as well as biochemical and oxidative stress parameters in 80 women. Our results revealed that plasma adiponectin levels were affected by chemotherapy, estrogen receptor status, and disease progression. Adiponectin was positively correlated with antioxidant levels, without affecting either the metastatic behavior of disease or patient outcome. These findings highlight adiponectin as a novel player in the endocrine signaling that modulates the oxidative inflammatory response in human breast cancer, and contribute to the understanding of the role of adiponectin in pathological conditions in non-obese women.
- Impact of Tumor Removal on the Systemic Oxidative Profile of Patients With Breast Cancer Discloses Lipid Peroxidation at Diagnosis as a Putative Marker of Disease Recurrence(2014) HERRERA, Ana Cristina S.; VICTORINO, Vanessa J.; CAMPOS, Fernanda C.; VERENITACH, Beatriz D.; LEMOS, Lauana T.; ARANOME, Adrian M. F.; OLIVEIRA, Sayonara R.; CECCHINI, Alessandra L.; SIMAO, Andrea Name C.; ABDELHAY, Eliana; PANIS, Carolina; CECCHINI, RubensThis study highlights the systemic oxidative changes that occur in women with invasive breast cancer at diagnosis that are indicative of disease recurrence in a 5-year follow-up, before the primary tumor removal. Background: Recent studies have suggested a regulatory role for some of the metabolites derived from oxidative stress in breast cancer. In this way, cancer-induced oxidative changes could modify the breast environment and potentially trigger systemic responses that may affect disease prognosis and recurrence. In this study, we investigated the systemic oxidative profile of women with early breast cancer bearing the primary tumor and after tumor withdrawal, and its long-term implications. Patients and Methods: Plasma samples were collected at diagnosis, and the systemic oxidative profile was determined by evaluating the lipid peroxidation, total antioxidant capacity of plasma (TRAP), malondialdehyde (MDA), protein carbonylation, and hydroperoxides. Nitric oxide, vascular endothelial growth factor (VEGF), and tumor necrosis factor alpha (TNF-alpha) levels were further measured. We also evaluated the impact of the oxidative profiling at diagnosis on disease recurrence in a 5-year follow-up. Results: Enhanced oxidative stress was detected in patients bearing the primary tumors, characterized by high lipid peroxidation, TRAP consumption, high carbonyl content, and elevated VEGF and TNF-a levels. After tumor removal, the systemic oxidative status presented attenuation in lipid peroxidation, MDA, VEGF, and TNF-a. The 5-year recurrence analysis indicated that all patients who recidivated presented high levels of lipid peroxidation measured by chemiluminescence at diagnosis. Conclusions: Our data suggest that the presence of the primary tumor is indicative of the systemic pro-oxidant status of breast cancer and demonstrates a role for lipid peroxidation in disease recurrence, highlighting the need for a metabolic follow-up of patients with cancer at diagnosis before tumor removal.
article 45 Citação(ões) na Scopus Mapping Oxidative Changes in Breast Cancer: Understanding the Basic to Reach the Clinics(2014) MENCALHA, Andre; VICTORINO, Vanessa Jacob; CECCHINI, Rubens; PANIS, CarolinaSince long, oxidative stress-driven modifications in breast cancer were faced as detrimental cellular events that cause obligatory cell damage. Recent studies show that the products generated during redox reactions are able to modulate pivotal processes regarding breast cancer survival, proposing a new way of looking at the events linked to oxidative stress. Therefore, it is necessary to understand the basis of oxidative stress generation in breast cancer by reviewing the two most important events that perpetuate the malignant transformation: mitochondrial dysfunction and DNA damage/misguided repair. In this context, the present review addresses the main events related with redox events reported in breast cancer studies, highlighting the impact of the oxidative environment on DNA damage and the role of the mitochondria as a determinant of oxidative modifications. In addition, we further discuss the main stand-out findings concerning the modulatory role of the metabolites derived from redox stresses, with a special focus on the oxidative changes detected in the breast cancer microenvironment and its systemic impact.- Systemic toxicity induced by paclitaxel in vivo is associated with the solvent cremophor EL through oxidative stress-driven mechanisms(2014) CAMPOS, Fernanda C.; VICTORINO, Vanessa J.; MARTINS-PINGE, Marli Cardoso; CECCHINI, Alessandra L.; PANIS, Carolina; CECCHINI, RubensThe toxic effects of paclitaxel (PTX) and its solubilizing agent cremophor EL (CREL) have been well established in vitro; however, the in vivo mechanisms underlying this toxicity remain unclear. Thus, the aim of this study was to analyze the in vivo toxicity induced by infusion of PTX and CREL and to investigate the involvement of oxidative stress as a potential mechanism for this toxicity. We treated male Wistar rats with PTX and/or CREL for 1 h using human-equivalent doses (PTX + CREL/ethanol + NaCl 175 mg/m(2) or CREL + ethanol + NaCl) and sacrificed immediately or 24 h after these drug infusions to systemic biochemical evaluations. Hidrosoluble vitamin E (vitE, Trolox) was added as a control in some groups. The oxidative profile was determined by measuring erythrocyte and plasma lipid peroxidation, superoxide dismutase and catalase activities, reduced glutathione (GSH) levels, red blood cell (RBC) counts, hemoglobin profile, plasma total radical-trapping antioxidant parameter (TRAP), plasma lipid peroxidation, nitric oxide levels and malondialdehyde levels. Our findings showed that CREL infusion triggered immediate high plasma lipid peroxidation and augmented TRAP, while PTX caused immediate TRAP consumption and metahemoglobin formation. Pronounced oxidative effects were detected 24 h after infusion, when CREL treatment enhanced RBC counts and plasma lipid peroxidation, increased catalase activity, and decreased TRAP levels. On the other hand, after 24 h, PTX-infused rats showed reduced catalase activity and reduced metahemoglobin levels. These data indicate the existence of a continuous oxidative stress generation during CREL-PTX treatment and highlight CREL as primarily responsible for the in vivo oxidative damage to RBCs.