Prognostic significance of CD24 and claudin-7 immunoexpression in ductal invasive breast cancer

Carregando...
Imagem de Miniatura
Citações na Scopus
44
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPANDIDOS PUBL LTD
Autores
BERNARDI, M. A.
LOGULLO, A. F.
NONOGAKI, S.
BLUMKE, C.
SOARES, F. A.
Citação
ONCOLOGY REPORTS, v.27, n.1, p.28-38, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
This study aimed to identify the CD24 and CD44 immunophenotypes within invasive ductal breast carcinoma (I DC) subgroups defined by immunohistochesmistry markers and to determine its influence on prognosis as well as its association with the expression of Ki-67, cytokeratins (CK5 and CK 18) and claudin-7. Immunohistochemical expression of CD44 and CD24 alone or in combination was investigated in 95 IDC cases arranged in a tissue microarray (TMA). The association with subgroups defined as luminal A and B; HER2 rich and triple negative, or with the other markers and prognosis was analyzed. CD44(+)/CD24(-) and CD44(-)/CD24(+) were respectively present in 8.4% and 16.8% of the tumors, a lack of both proteins was detected in 6.3%, while CD441(-)/CD24(+) was observed in 45.3% of the tumors. Although there was no significant correlation between subgroups and different phenotypes, the CD44(+)/CD24(-) phenotype was more common in the basal subgroups but absent in HER2 tumors, whereas luminal tumors are enriched in CD44(-)/CD24(+) and CD44(+)/CD24(+) cells. The frequency of CD44(+)/CD24(-) or CD44(-)/CD24(+) was not associated with clinical characteristics or biological markers. There was also no significant association of these phenotypes with the event free (DFS) and overall survival (OS). Single CD44(+) was evident in 57.9% of the tumors and was marginally associated to grading and not to any other tumor characteristics as well as OS and DFS. CD24(+) was positive in 74.7% of the tumors, showing a significant association with estrogen receptor, progesterone receptor and Ki-67 and a marginal association with CKI8 and claudin-7. Expression of claudin-7 and Ki-67 did not associate with the cancer subgroups, while a positive association between CK18 and the luminal subgroups was found (P=0.03). CK5, CK18 and Ki-67 expression had no influence in OS or DFS. Single CD24(+) (P=0.07) and claudin-7 positivity (P=0.05) were associated with reduced time of recurrence, suggesting a contribution of these markers to aggressiveness of breast cancer.
Palavras-chave
cancer stem cell, CD24, CD44, claudin-7, prognosis, breast cancer subgroups
Referências
  1. Abraham BK, 2005, CLIN CANCER RES, V11, P1154
  2. Al-Hajj M, 2003, P NATL ACAD SCI USA, V100, P3983, DOI 10.1073/pnas.0530291100
  3. Allred DC, 1998, MODERN PATHOL, V11, P155
  4. Baumann P, 2005, CANCER RES, V65, P10783, DOI 10.1158/0008-5472.CAN-05-0619
  5. Carey LA, 2006, JAMA-J AM MED ASSOC, V295, P2492, DOI 10.1001/jama.295.21.2492
  6. Cheang MCU, 2009, J NATL CANCER I, V101, P736, DOI 10.1093/jnci/djp082
  7. Diaz LK, 2005, CLIN CANCER RES, V11, P3309, DOI 10.1158/1078-0432.CCR-04-2184
  8. Dontu G, 2003, CELL PROLIFERAT, V36, P59, DOI 10.1046/j.1365-2184.36.s.1.6.x
  9. Giatromanolaki A, 2011, MED ONCOL, V28, P745, DOI 10.1007/s12032-010-9530-3
  10. Hill RP, 2006, CANCER RES, V66, P1891, DOI 10.1158/0008-5472.CAN-05-3450
  11. Honeth G, 2008, BREAST CANCER RES, V10, DOI 10.1186/bcr2108
  12. Hwang-Verslues WW, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0008377
  13. Kim HJ, 2007, CANCER LETT, V258, P98, DOI 10.1016/j.canlet.2007.08.025
  14. Kim HJ, 2011, BREAST, V20, P78, DOI 10.1016/j.breast.2010.08.001
  15. Klingbeil P, 2010, BREAST CANCER RES TR, V120, P95, DOI 10.1007/s10549-009-0380-7
  16. Kristiansen G, 2003, CLIN CANCER RES, V9, P4906
  17. Lanigan F, 2009, INT J CANCER, V124, P2088, DOI 10.1002/ijc.24159
  18. Lim SC, 2005, PATHOL RES PRACT, V201, P479, DOI 10.1016/j.prp.2005.05.004
  19. Meyer MJ, 2009, BREAST CANCER RES, V11, DOI 10.1186/bcr2449
  20. Myal Y, 2010, J BIOMED BIOTECHNOL, DOI 10.1155/2010/956897
  21. Mylona E, 2008, HUM PATHOL, V39, P1096, DOI 10.1016/j.humpath.2007.12.003
  22. Pal SK, 2011, BREAST CANCER RES TR, V125, P627, DOI 10.1007/s10549-010-1293-1
  23. Pandit TS, 2009, INT J ONCOL, V35, P297, DOI 10.3892/ijo_00000340
  24. Park SY, 2010, CLIN CANCER RES, V16, P876, DOI 10.1158/1078-0432.CCR-09-1532
  25. Perou CM, 2000, NATURE, V406, P747, DOI 10.1038/35021093
  26. Prat A, 2010, BREAST CANCER RES, V12, DOI 10.1186/bcr2635
  27. Prat A, 2011, MOL ONCOL, V5, P5, DOI 10.1016/j.molonc.2010.11.003
  28. Sheridan C, 2006, BREAST CANCER RES, V8, DOI 10.1186/bcr1610
  29. Shipitsin M, 2007, CANCER CELL, V11, P259, DOI 10.1016/j.ccr.2007.01.013
  30. Smalley M, 2003, NAT REV CANCER, V3, P832, DOI 10.1038/nrc1212
  31. Szasz AM, 2011, CLIN EXP METASTAS, V28, P55, DOI 10.1007/s10585-010-9357-5
  32. Weigelt B, 2010, J PATHOL, V220, P263, DOI 10.1002/path.2648
  33. Weigelt B, 2009, MODERN PATHOL, V22, P1401, DOI 10.1038/modpathol.2009.112
  34. Yang XR, 2007, CANCER EPIDEM BIOMAR, V16, P439, DOI 10.1158/1055-9965.EPI-06-0806