medigraphic.com
Instituto de Seguridad y Servicios Sociales de los Trabajadores del Estado

2010, Número 4

<< Anterior Siguiente >>

Rev Esp Med Quir 2010; 15 (4)


Cáncer de mama triple negativo, estado actual

Olaya GEJ

Idioma: Español
Referencias bibliográficas: 81
Paginas: 228-236
Archivo PDF: 91.56 Kb.


RESUMEN

El cáncer de mama es el más frecuente en las mujeres, se han hecho múltiples esfuerzos para clasificarlo con base en su perfil genético y el perfil de tinción de inmunohistoquímica. El cáncer de mama triple negativo se define por su falta de expresión a receptores de estrógeno, receptores de progesterona y receptor del factor de crecimiento epidérmico humano 2. Representa 15% de todos los cánceres de mama y son más frecuentes en mujeres premenopáusicas afroamericanas. Tiene distintas características moleculares, histológicas y clínicas, que incluyen particularmente el mal pronóstico a pesar de su alta sensibilidad a la quimioterapia estándar. Se ha asociado con el llamado cáncer de mama basal-like por todas las similitudes que guardan entre sí; sin embargo, no son sinónimos, por lo que siguen haciéndose esfuerzos para poder diferenciarlos con técnicas rutinarias de patología. Además de revisar dichas características, nos enfocamos en su tratamiento actual y en las terapias blanco posibles de acuerdo con los defectos moleculares propios de este subgrupo, incluidas las implicaciones de la disfunción del BRCA1.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Glass AG, Lacey JV Jr, Carreon JD, et al. Breast cancer incidence, 1980–2006: combined roles of menopausal hormone therapy, screening mammography, and estrogen receptor status. J Natl Cancer Inst 2007;99:1152-1161.

  2. Sorlie T, Perou CM, Tibshirani R, et al. Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proc Natl Acad Sci USA 2001;98:10869-10874.

  3. Seal MD, CHia SK. What is the difference between triplenegative and basal breast cancers? Cancer J 2010;16:12-16.

  4. Perou CM, Sorlie T, Eisen MB, et al. Molecular portraits of human breast tumours. Nature 2000;406:747.

  5. Rakha EA, Ellis IO. Triple-negative/basal-like breast cancer: review. Pathology 2009;41:40-47.

  6. Parker JS, Mullins M, Cheang MCU, et al. Supervised risk predictor of breast cancer based on intrinsic subtypes. J Clin Oncol 2009;27:1160-1167.

  7. Gluzi O, Gottschalk N, Pusztai L, Harbeck N. Triple-negative breast cancer-current status and future directions. Review. Ann Oncol 2009;20:1913-1927.

  8. Millikan RC, Newman B, Tse C-K, et al. Epidemiology of basal-like breast cancer. Breast Cancer Res Treat 2008;109:123-139.

  9. Carey LA, Perou CM, Livasy CA, et al. Race, breast cancer subtypes, and survival in the Carolina breast cancer study. JAMA 2006;295:2492-2502.

  10. Fan C, Oh DS, Wessels L, et al. Concordance among geneexpression-based predictors for breast cancer. N Engl J Med 2006;355:560-569.

  11. Nielsen TO, Hsu FD, Jensen K, et al. Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma. Clin Cancer Res 2004;10:5367-5374.

  12. Rouzier R, Perou CM, Symmans WF, et al. Breast cancer molecular subtypes respond differently to preoperative chemotherapy. Clin Cancer Res 2005;11:5678-5685.

  13. Calza S, Hall P, Auer G, et al. Intrinsic molecular signature of breast cancer in a population-based cohort of 412 patients. Breast Cancer Res 2006;8:R34.

  14. Slamon DJ, Leyland-Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that over expresses HER2. N Engl J Med 2001;344:783-792.

  15. Rakha E, El-Sayed M, Green A, et al. Prognostic markers in triple-negative breast cancer. Cancer 2007;109:25-32.

  16. Tischkowitz M, Brunet J-S, Begin L, et al. Use of immunohistochemical markers can refine prognosis in triple negative breast cancer. BMC Cancer 2007;7:134.

  17. Tan D, Marchio’ C, Jones R, et al. Triple negative breast cancer: molecular profiling and prognostic impact in adjuvant anthracycline-treated patients. Breast Cancer Res Treat 2008;111:27-44.

  18. Rakha EA, Elsheikh SE, Aleskandarany MA, et al. Triplenegative breast cancer: distinguishing between basal and nonbasal subtypes. Clin Cancer Res 2009;15:2302.

  19. Korsching E, Packeisen J, Agelopoulos K, et al. Cytogenetic alterations and cytokeratin expression patterns in breast cancer: integrating a new model of breast differentiation into cytogenetic pathways of breast carcinogenesis. Lab Invest 2002;82:1525.

  20. Parker JS, Mullins M, Cheang MC, et al. Supervised risk predictor of breast cancer based on intrinsic subtypes. J Clin Oncol. 2009;27:1160-1167.

  21. Nielsen TO, Hsu FD, Jensen K, et al. Immunohistochemical and clinical characterization of the basal-like subtype of invasive breast carcinoma. Clin Cancer Res. 2004;10:5367-5374.

  22. Fulford L, Easton D, Reis-Filho J, et al. Specific morphological features predictive for the basal phenotype in grade 3 invasive ductal carcinoma of breast. Histopathology 2006;49:22-34.

  23. Lakhani SR, Reis-Filho JS, Fulford L, et al. Prediction of BRCA1 status in patients with breast cancer using estrogen receptor and basal phenotype. Clin Cancer Res 2005;11:5175-5180.

  24. Reis-Filho J, Milanezi F, Steele D, et al. Metaplastic breast carcinomas are basal-like tumours. Histopathology 2006;49:10-21.

  25. Jacquemier J, Padovani L, Rabayrol L, et al. Typical medullary breast carcinomas have a basal/myoepithelial phenotype. J Pathol 2005;207:260-268.

  26. Livasy CA, Karaca G, Nanda R, et al. Phenotypic evaluation of the basal-like subtype of invasive breast carcinoma. Mod Pathol 2005;19:264.

  27. Tsuda H, Takarabe T, Hasegawa T, et al. Myoepithelial differentiation in highgrade invasive ductal carcinomas with large central acellular zones. Hum Pathol 1999;30:1134-1139.

  28. Tsuda H, Takarabe T, Hasegawa F, et al. Large, central acellular zones indicating myoepithelial tumor differentiation in high-grade invasive ductal carcinomas as markers of predisposition to lung and brain metastases. Am J Surg Pathol 2000;24:197-202.

  29. Lin NU, Vanderplas A, Hughes ME, et al. Clinicopathological features and sites of recurrence according to breast cancer subtype in the National Comprehensive Cancer Network (NCCN). J Clin Oncol 2009;27:(Abstr 543).

  30. Abd El-Rehim DM, Ball G, Pinder SE, et al. High-throughput protein expression analysis using tissue microarray technology of a large well-characterized series identifies biologically distinct classes of breast cancer confirming recent cDNA expression analyses. Int J Cancer 2005;116:340-50.

  31. Abd El-Rehim DM, Pinder SE, Apish CE, et al. Expression of luminal and basal cytokeratins in human breast carcinoma. J Pathol 2004;203:661-671.

  32. Foulkes WD, Brunet JS, Stefansson IM, et al. The prognostic implication of the basal-like (cyclin E high/p27 low/p53+/glomeruloid-microvascular-proliferation+) phenotype of BRCA1- related breast cancer. Cancer Res 2004;64:830-835.

  33. van de Rijn M, Perou CM, Tibshirani R, et al. Expression of cytokeratins 17 and 5 identifies a group of breast carcinomas with poor clinical outcome. Am J Pathol 2002;161:1991-1996.

  34. Sorlie T, Tibshirani R, Parker J, et al. Repeated observation of breast tumor subtypes in independent gene expression data sets. Proc Natl Acad Sci USA 2003;100:8418-8423.

  35. Stark A, Kapke A, Schultz D, et al. Advanced stages and poorly differentiated carcinoma only in white women: findings from a prospective cohort study of African-American and White-American women. Breast Cancer Res Treat 2008;107:405-414.

  36. Kwan ML, Kushi LH, Weltzien E, et al. Epidemiology of breast cancer subtypes in two prospective cohort studies of breast cancer survivors. Breast Cancer Res 2009;11:R31.

  37. Millikan RC, Newman B, Tse CK, et al. Epidemiology of basal-like breast cancer. Breast Cancer Res Treat 2008;109:123-139.

  38. Bauer KR, Brown M, Cress RD, et al. Descriptive analysis of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a populationbased study from the California cancer Registry. Cancer 2007;109:1721-1728.

  39. Young SR, Pilarski RT, Donenberg T, et al. The prevalence of BRCA1 mutations among young women with triple-negative breast cancer. BMC Cancer 2009;9:86.

  40. Morris G, Naidu S, Topham A, et al. Differences in breast carcinoma characteristics in newly diagnosed African-American and Caucasian patients: A single-institution compilation compared with the National Cancer Institute's Surveillance, Epidemiology, and End Results database. Cancer 2007;110:876-884.

  41. Sotiriou C, Neo SY, McShane LM, et al. Breast cancer classification and prognosis based on gene expression profiles from a population-based study. Proc Natl Acad Sci USA 2003;100:10393-10398.

  42. Callahan R, Campbell G. Mutations in human breast cancer: an overview. J Natl Cancer Inst 1989;81:1780-1786.

  43. Wang ZC, Lin M, Wei LJ, et al. Loss of heterozygosity and its correlation with expression profiles in subclasses of invasive breast cancers. Cancer Res 2004;64:64-71.

  44. Turner N, Tutt A, Ashworth A. Hallmarks of ‘BRCAness’ in sporadic cancers. Nat Rev Cancer 2004;4:814-819.

  45. Kennedy RD, Quinn JE, Mullan PB, et al. The role of BRCA1 in the cellular response to chemotherapy. J Natl Cancer Inst 2004;96:1659-1668.

  46. Turner N, Tutt A, Ashworth A. Targeting the DNA repair defect of BRCA tumours. Curr Opin Pharmacol 2005;5:388-393.

  47. Tirkkonen M, Johannsson O, Agnarsson BA, et al. Distinct somatic genetic changes associated with tumor progression in carriers of BRCA1 and BRCA2 germ-line mutations. Cancer Res 1997;57:1222-1227.

  48. Wessels LF, van Welsem T, Hart AA, et al. Molecular classification of breast carcinomas by comparative genomic hybridization: a specific somatic genetic profile for BRCA1 tumors. Cancer Res 2002;62:7110-7117.

  49. Jones C, Nonni AV, Fulford L, et al. CGH analysis of ductal carcinoma of the breast with basaloid/myoepithelial cell differentiation. Br J Cancer 2001;85:422-427.

  50. Wang ZC, Lin M, Wei LJ, et al. Loss of heterozygosity and its correlation with expression profiles in subclasses of invasive breast cancers. Cancer Res 2004;64:64-71.

  51. Crook T, Crossland S, Crompton MR, Osin P, Gusterson BA. P53 mutations in BRCA1-associated familial breast cancer. Lancet 1997;350:638-639.

  52. Futreal PA, Liu Q, Shattuck-Eidens D, et al. BRCA1 mutations in primary breast and ovarian carcinomas. Science 1994;266:120-122.

  53. Turner NC, Reis-Filho JS, Russell AM, et al. BRCA1 dysfunction in sporadic basal-like breast cancer. Oncogene 2007;26:2126-2132.

  54. Rodriguez-Pinilla SM, Sarrio D, Honrado E, et al. Prognostic significance of basal-like phenotype and fascin expression in no denegative invasive breast carcinomas. Clin Cancer Res 2006;12:1533-1539.

  55. Dent RTM, Pritchard KI, Hanna WM, et al. Triple-negative breast cancer: Clinical features and patterns of recurrence. Clin Cancer Res 2007;13:4429-4434.

  56. Osbourne CR, Kannan L, Ashfaq R, et al. Clinical and pathological characterization of basal-like breast cancer. Breast Cancer Res Treat 2005;94(Suppl. 1):S118.

  57. Smid M, Wang Y, Zhang Y, et al. Subtypes of breast cancer show preferential site of relapse. Cancer Res 2008;68:3108-3114.

  58. Guarneri V, Broglio K, Kau SW, et al. Prognostic value of pathologic complete response after primary chemotherapy in relation to hormone receptor status and other factors. J Clin Oncol 2006; 24:1037-1044.

  59. Urruticoechea A, Smith IE, Dowsett M. Proliferation marker Ki-67 in early breast cancer. J Clin Oncol 2005; 23:7212-7220.

  60. Geisler S, Lonning PE, Aas T, et al. Influence of TP53 gene alterations and c-erbB-2 expression on the response to treatment with doxorubicin in locally advanced breast cancer. Cancer Research 2001;61:2505-2012.

  61. Lanni JS, Lowe SW, Licitra EJ, et al. p53-independent apoptosis induced by paclitaxel through an indirect mechanism. Proc Natl Acad Sci USA 1997;94:9679-9683.

  62. Kandioler-Eckersberger D, Ludwig C, Rudas M, et al. TP53 mutation and p53 overexpression for prediction of response to neoadjuvant treatment in breast cancer patients. Clin Cancer Res 2000;6:50-56.

  63. Moynahan ME, Cui TY, Jasin M. Homology-directed DNA repair, mitomycin-c resistance, and chromosome stability is restored with correction of a Brca1 mutation. Cancer Res 2001;61:4842-4850.

  64. Bhattacharyya A, Ear US, Koller BH, et al. The breast cancer susceptibility gene BRCA1 is required for subnuclear assembly of Rad51 and survival following treatment with the DNA cross-linking agent cisplatin. J Biol Chem 2000;275:23899-23903.

  65. Quinn JE, Kennedy RD, Mullan PB, et al. BRCA1 functions as a differential modulator of chemotherapy-induced apoptosis. Cancer Res 2003;63:6221-6228.

  66. Chappuis PO, Goffi n J, Wong N, et al. A significant response to neoadjuvant chemotherapy in BRCA1/2 related breast cancer. J Med Genet 2002; 39:608-610.

  67. Delaloge S. BRCA1-linked breast cancer (BC) is highly more chemosensitive than its BRCA2-linked or sporadic counterparts (abstract). Ann Oncology 2002;13(Suppl 5):34.

  68. Decatris MP, Sundar S, O’Byrne KJ. Platinum-based chemotherapy in metastatic breast cancer: the Leicester (UK) experience. Clin Oncol (R Coll Radiol) 2005;17:249–257.

  69. Gluz O, Nitz UA, Harbeck N, et al. Triple-negative high-risk breast cancer derives particular benefit from dose intensification of adjuvant chemotherapy: results of WSG AM-01 trial. Ann Oncol 2008;19:861-870.

  70. Cunningham D, Humblet Y, Siena S, et al. Cetuximab monotherapy and cetuximab plus irinotecan in irinotecanrefractory metastatic colorectal cancer. N Engl J Med 2004;351:337-345.

  71. Mendelsohn J, Baselga J. Epidermal growth factor receptor targeting in cancer. Semin Oncol 2006;33:369-385.

  72. Corkery B, Crown J, Clynes M, et al. Epidermal growth factor receptor as a potential therapeutic target in triple-negative breast cancer. Ann Oncol 2009;20:862-867.

  73. Sartor C, Zhou H, Perou C, et al. Basal-like breast tumorderived cell lines are growth inhibited and radiosensitized by epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors. Breast Cancer Res Treat 2004;88:(Abstr 311).

  74. Sarrio D, Rodriguez-Pinilla SM, Hardisson D, et al. Epithelial- mesenchymal transition in breast cancer relates to the basal-like phenotype. Cancer Res 2008;68:989-997.

  75. Farmer H, McCabe N, Lord CJ, et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature 2005;434:917.

  76. Finn RS, Lau A, Kalous O, et al. Pre-clinical activity of the PARP inhibitor AZD2281 in human breast cancer cell lines and in combination with DNA damaging agents. Cancer Res 2009;69:Abstr 1038.

  77. Huang F, Reeves K, Han X, et al. Identification of candidate molecular markers predicting sensitivity in solid tumors to dasatinib: rationale for patient selection. Cancer Res 2007;67:2226–2238.

  78. Finn R, Dering J, Ginther C, et al. Dasatinib, an orally active small molecule inhibitor of both the src and abl kinases, selectively inhibits growth of basaltype/‘‘triple-negative’’ breast cancer cell lines growing in vitro. Breast Cancer Res Treat 2007;105:319.

  79. Linderholm BK, Klintman M, Grabau D, et al. Significantly higher expression of vascular endothelial growth factor (VEGF) and shorter survival after recurrences in premenopausal node negative patients with triple negative breast cancer. Cancer Res 2009;69:(Abstr 1077).

  80. Ryden L, Ferno M, Stal O, et al. Vascular endothelial growth factor receptor 2 is a significant negative prognostic biomarker in triple-negative breast cancer: results from a controlled randomised trial of premenopausal breast cancer. Cancer Res 2009;69:(Abstr 1087).

  81. Hebbar M, Wacrenier AS, Desauw C, et al. Lack of usefulness of epidermal growth factor receptor expression determination for cetuximab therapy in patients with colorectal cancer. Anticancer Drugs 2006;17:855-857.




2020     |     www.medigraphic.com