VANESSA JACOB VICTORINO
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
Agora exibindo 1 - 4 de 4
- 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.
- Early downregulation of acute phase proteins after doxorubicin exposition in patients with breast cancer(2016) PANIS, Carolina; PIZZATTI, Luciana; BUFALO, Aedra Carla; HERRERA, Ana Cristina; VICTORINO, Vanessa Jacob; CECCHINI, Rubens; ABDELHAY, ElianaChemotherapy remains the first-choice option for adjuvant therapy in breast cancer. Here, we investigated the impact of the first chemotherapic cycle of doxorubicin on the plasmatic-proteomic profiling of women diagnosed with breast cancer (n = 87). Blood samples were obtained from the same patient before and after doxorubicin infusion (1 h, 60 mg/m(2)) and processed for label-free LC-MS proteomic screening. A total of 80 proteins were downregulated after chemotherapy. In silico analysis revealed that the main biological process enrolled was inflammation and canonical pathways involving acute phase proteins. TNF-alpha, IL-1 beta, IL-12, TGF-beta 1, clusterin, and gelsolin were chosen as relevant for further validation. All selected targets presented reduced plasmatic levels after treatment. Our results indicate that doxorubicin downregulated acute phase proteins immediately after its infusion. Since such proteins are cancer promoting, its downregulation could support the effectiveness of doxorubicin along treatment.