Expressão de c-myc em lesões mamárias associadas a microcalcificações detectadas por mamografia de rotina
Palavras-chave:
Proteínas proto-oncogênicas c-myc, Expressão gênica, Mamografia, Neoplasias mamárias, Biópsia por agulhaResumo
CONTEXTO E OBJETIVO: Alterações nos genes reguladores da proliferação celular foram descritas em lesões pré-malignas. Os objetivos foram avaliar a expressão da proteína c-myc em biópsias de lesões mamárias não-palpáveis associadas a microcalcificações detectadas em mamografias de rastreamento e comparar estes resultados com as variáveis histopatológicas, clínicas e epidemiológicas. DESENHO E LOCAL: Estudo retrospectivo, em um hospital universitário em São Paulo. MÉTODOS: Setenta e nove pacientes do sexo feminino submetidas a mamografia de rotina de 1998 a 2004 foram estudadas. As lesões classificadas pelo sistema BI-RADS (Breast Imaging Reporting and Data) como 4 e 5 sofreram biópsias percutâneas com agulha grossa. Do ponto de vista anatomopatológico, foram estudadas 98 lesões. Os blocos com representação adequada para estudo imunoistoquímico com a técnica da estreptoavidina-biotina-peroxidase com o anticorpo monoclonal de camundongo c-myc foram incluídos. RESULTADOS: Das 98 lesões, 29 (29,6%), continham neoplasia maligna; 40 (40,8%) tiveram reação de imunoistoquímica positiva para o c-myc. Quando divididos os grupos em lesões sem atipia versus lesões atípicas mais lesões malignas, encontramos o c-myc positivo em 31,03% das 58 lesões sem atipias e 55% das 40 lesões atípicas e malignas (P = 0,018). Quando agrupamos as lesões atípicas com o carcinoma ductal in situ (CDIS) versus as lesões benignas sem atipias, observamos a presença do c-myc em 51,61% das 31 lesões atípicas e 31,03% das lesões benignas sem atipias (P = 0,057). CONCLUSÃO: A proteína c-myc está mais frequentemente expressa em lesões atípicas e malignas do que em lesões benignas sem atipia. A expressão do c-myc está correlacionada com a presença de atipia (P = 0,018).
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Harris JR, Morrow ME, Lippman ME, Morrow M, Hellman S, editors. Diseases of the breast. Philadelphia: Lippincott-Raven; 1996.
Sickles EA. Breast imaging: from 1965 to the present. Radiology. 2000;215(1):1-16.
Kopans DB. Breast imaging. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1998.
Fondrinier E, Lorimier G, Guerin-Boblet V, Bertrand AF, Mayras C, Dauver N. Breast microcalci- fications: multivariate analysis of radiologic and clinical factors for carcinoma. World J Surg. 2002;26(3):290-6.
Ellis IO, Galea M, Broughton N, Locker A, Blamey RW, Elston CW. Pathological prognostic factors in breast cancer. II. Histological type. Relationship with survival in a large study with long-term follow-up. Histopathology. 1992;20(6):479-89.
Holland R, Peterse JL, Millis RR, et al. Ductal carcinoma in situ: a proposal for a new classi- fication. Semin Diagn Pathol. 1994;11(3):167-80.
Bobrow LG, Happerfield LC, Gregory WM, Springall RD, Millis RR. The classification of duc- tal carcinoma in situ and its association with biological markers. Semin Diagn Pathol. 1994;11(3):199-207.
Brenner RJ. Lesions entirely removed during stereotactic biopsy: preoperative localization on the basis of mammographic landmarks and feasibility of freehand technique--initial experience. Radiology. 2000;214(2):585-90.
Liberman L. Centennial dissertation. Percutaneous imaging-guided core breast biopsy: state of the art at the millennium. AJR Am J Roentgenol. 2000;174(5):1191-9.
Tibiletti MG, Sessa F, Bernasconi B, et al. A large 6q deletion is a common cytogenetic alte- ration in fibroadenomas, pre-malignant lesions, and carcinomas of the breast. Clin Cancer Res. 2000;6(4):1422-31.
Liao DJ, Dickson RB. c-Myc in breast cancer. Endocr Relat Cancer. 2000;7(3):143-64.
Nusse R, Varmus HE. Many tumors induced by the mouse mammary tumor virus contain a provirus integrated in the same region of the host genome. Cell. 1982;31(1):99-109.
Brown AM. Wnt signaling in breast cancer: have we come full circle? Breast Cancer Res. 2001;3(6):351-5.
Polakis P. Wnt signaling and cancer. Genes Dev. 2000;14(15):1837-51.
Amati B, Alevizopoulos K, Vlach J. Myc and the cell cycle. Front Biosci. 1998;3:d250-68.
Packham G, Cleveland JL. c-Myc and apoptosis. Biochim Biophys Acta. 1995;1242(1): 11-28.
Hoffman B, Liebermann DA. The proto-oncogene c-myc and apoptosis. Oncogene. 1998;17(25):3351-7.
Dang CV. c-Myc target genes involved in cell growth, apoptosis, and metabolism. Mol Cell Biol. 1999;19(1):1-11.
Elend M, Eilers M. Cell growth: downstream of Myc - to grow or to cycle? Curr Biol. 1999;9(24):R936-8.
Prendergast GC. Mechanisms of apoptosis by c-Myc. Oncogene. 1999;18(19):2967-87.
Cory S, Vaux DL, Strasser A, Harris AW, Adams JM. Insights from Bcl-2 and Myc: malignancy involves abrogation of apoptosis as well as sustained proliferation. Cancer Res. 1999;59(7 Suppl):1685s-1692s.
Lowe SW, Lin AW. Apoptosis in cancer. Carcinogenesis. 2000;21(3):485-95.
Nesbit CE, Tersak JM, Prochownik EV. MYC oncogenes and human neoplastic disease. Onco- gene. 1999;18(19):3004-16.
American College of Radiology (ACR). BI-RADS® — Mammography. 4th ed. Reston: Ameri- can College of Radiology; 2003. Available from: http://www.acr.org/SecondaryMainMe- nuCategories/quality_safety/BIRADSAtlas/BIRADSAtlasexcerptedtext/BIRADSMammogra- phyFourthEdition.aspx. Accessed in 2009 (Mar 17).
Lakhani SR. The transition from hyperplasia to invasive carcinoma of the breast. J Pathol. 1999;187(3):272-8.
Page DL, Steel CM, Dixon JM. ABC of breast diseases. Carcinoma in situ and patients at high risk of breast cancer. BMJ. 1995;310(6971):39-42.
Cole MD. Activation of the c-myc oncogene. Basic Life Sci. 1986;38:399-406.
Ghoussoub RA, Dillon DA, D’Aquila T, Rimm EB, Fearon ER, Rimm DL. Expression of c- met is a strong independent prognostic factor in breast carcinoma. Cancer. 1998;82(8): 1513-20.
Stratton MR, Collins N, Lakhani SR, Sloane JP. Loss of heterozygosity in ductal carcinoma in situ of the breast. J Pathol. 1995;175(2):195-201.
Gupta SK, Douglas-Jones AG, Fenn N, Morgan JM, Mansel RE. The clinical behavior of breast carcinoma is probably determined at the preinvasive stage (ductal carcinoma in situ). Can- cer. 1997;80(9):1740-5.
Evan GI, Littlewood TD. The role of c-myc in cell growth. Curr Opin Genet Dev. 1993;3(1): 44-9.
Heikkila R, Schwab G, Wickstrom E, et al. A c-myc antisense oligodeoxynucleotide inhibits entry into S phase but not progress from G0 to G1. Nature. 1987;328(6129):445-9.
Deming SL, Nass SJ, Dickson RB, Trock BJ. C-myc amplification in breast cancer: a meta- analysis of its occurrence and prognostic relevance. Br J Cancer. 2000;83(12):1688-95.
Ioachim E, Charchanti A, Briasoulis E, et al. Immunohistochemical expression of extra- cellular matrix components tenascin, fibronectin, collagen type IV and laminin in breast cancer: their prognostic value and role in tumour invasion and progression. Eur J Cancer. 2002;38(18):2362-70.
Mai S. Overexpression of c-myc precedes amplification of the gene encoding dihydrofolate reductase. Gene. 1994;148(2):253-60.
Schmitt FC, Reis-Filho JS. c-myc, not her-2/neu, can predict the prognosis of breast cancer patients: how novel, how accurate, and how significant? Breast Cancer Res. 2003;5(4): 188-91.
Le Roy X, Escot C, Brouillet JP, et al. Decrease of c-erbB-2 and c-myc RNA levels in tamoxi- fen-treated breast cancer. Oncogene. 1991;6(3):431-7.
Berns EM, Klijn JG, van Putten WL, van Staveren IL, Portengen H, Foekens JA. c-myc amplifi- cation is a better prognostic factor than HER2/neu amplification in primary breast cancer. Cancer Res. 1992;52(5):1107-13.
Riva C, Lavieille JP, Reyt E, Brambilla E, Lunardi J, Brambilla C. Differential c-myc, c-jun, c-raf and p53 expression in squamous cell carcinoma of the head and neck: implication in drug and radioresistance. Eur J Cancer B Oral Oncol. 1995;31B(6):384-91.
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