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
Carregando...
Citações na Scopus
25
Tipo de produção
article
Data de publicação
2014
Título da Revista
ISSN da Revista
Título do Volume
Editora
CIG MEDIA GROUP, LP
Autores
HERRERA, Ana Cristina S.
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
Citação
CLINICAL BREAST CANCER, v.14, n.6, p.451-459, 2014
Resumo
This 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.
Palavras-chave
Breast cancer, Lipid peroxidation, Oxidative stress, Tumor resection
Referências
- Chuang CH, 2010, MUTAGENESIS, V25, P71, DOI 10.1093/mutage/gep047
- Daniel WW., 1999, BIOSTATISTICS FDN AN
- De Rossi T, 2009, APPL CANC RES, V29, P150
- De Boniface J, 2012, INT J CANCER, V131, P129, DOI 10.1002/ijc.26355
- Franco R, 2008, CANCER LETT, V266, P6, DOI 10.1016/j.canlet.2008.02.026
- Gago-Dominguez M, 2005, CANCER EPIDEM BIOMAR, V14, P2829, DOI 10.1158/1055-9965.EPI-05-0015
- Gago-Dominguez M, 2007, BREAST CANCER RES, V9, DOI 10.1186/bcr1628
- Gast MCW, 2011, J CANCER RES CLIN, V137, P1773, DOI 10.1007/s00432-011-1055-4
- Ge YL, 2009, INT IMMUNOPHARMACOL, V9, P389, DOI 10.1016/j.intimp.2008.11.020
- Halliwell B, 2007, BIOCHEM J, V401, P1, DOI 10.1042/BJ20061131
- Halliwell B., 2007, FREE RADICALS BIOL M
- Halliwell B, 1993, DNA FREE RADICALS
- HIETANEN E, 1994, EUR J CLIN NUTR, V48, P575
- Jing Y, 2011, TOXICOL SCI, V125, P10
- Kim JH, 2011, APOPTOSIS, V16, P696, DOI 10.1007/s10495-011-0605-1
- Lei L, 2011, ANAT REC, V294, P941, DOI 10.1002/ar.21399
- Lozovoy MAB, 2011, LUPUS, V20, P1250, DOI 10.1177/0961203311411350
- Madian AG, 2010, J PROTEOME RES, V9, P3766, DOI 10.1021/pr1002609
- Madian AG, 2011, J PROTEOME RES, V10, P3959, DOI 10.1021/pr200140x
- Madian AG, 2011, ANAL CHEM, V83, P9328, DOI 10.1021/ac201856g
- Manello F, 2007, INT J CANCER, V120, P1971
- Mannello F, 2013, BMC CANCER, V13, DOI 10.1186/1471-2407-13-344
- Mannello F, 2013, J INORG BIOCHEM, V128, P250, DOI 10.1016/j.jinorgbio.2013.07.003
- Mannello F, 2010, CLIN BREAST CANCER, V10, P238, DOI 10.3816/CBC.2010.n.032
- Mannello F, 2007, INT J CANCER, V120, P1971, DOI 10.1002/ijc.22522
- Mannello F, 2009, EXPERT REV PROTEOMIC, V6, P43, DOI 10.1586/14789450.6.1.43
- Menard S, 2003, LANCET, V362, P1503, DOI 10.1016/S0140-6736(03)14708-3
- Menard S, 2002, CLIN CANCER RES, V8, P520
- Nikki E., 2009, FREE RADICAL BIO MED, V47, P469
- Panis C, 2012, CANCER IMMUNOL IMMUN, V61, P481, DOI 10.1007/s00262-011-1117-0
- Panis C, 2012, BREAST CANCER RES TR, V133, P881, DOI 10.1007/s10549-011-1851-1
- Panis C, 2012, BREAST CANCER RES TR, V133, P89, DOI 10.1007/s10549-011-1693-x
- Prasad S, 2011, CANCER RES, V71, P538, DOI 10.1158/0008-5472.CAN-10-3121
- Selmeci L, 2006, FREE RADICAL RES, V40, P952, DOI 10.1080/10715760600818789
- Sidiqui RA, 2008, CHEM PHYS LIPIDS, V153, P47
- Sonmez B, 2011, J BUON, V16, P227
- Stoll BA, 2002, BRIT J NUTR, V87, P193, DOI [10.1079/BJNBJN2001512, 10.1079/BJN2002512]
- Victorino VJ, 2013, AGE, V35, P1411, DOI 10.1007/s11357-012-9431-9
- Victorino VJ, 2014, TUMOR BIOL, V35, P3025, DOI 10.1007/s13277-013-1391-x
- Villasenor A, 2014, CANCER EPIDEM BIOMAR, V23, P189, DOI 10.1158/1055-9965.EPI-13-0852
- Widschwendter M, 2002, ONCOGENE, V21, P5462, DOI 10.1038/sj.onc.1205606
- Wink DA, 1998, CARCINOGENESIS, V19, P711, DOI 10.1093/carcin/19.5.711
- ZAMBURLINI A, 1995, ANAL BIOCHEM, V232, P107, DOI 10.1006/abio.1995.9953