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MeSH Review

Carcinoma, Intraductal, Noninfiltrating

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Disease relevance of Carcinoma, Intraductal, Noninfiltrating

  • We previously showed that a p53 mutation present in invasive breast cancer was found in all surrounding areas of ductal carcinoma in situ (DCIS) but not in areas of hyperplasia or normal breast epithelium [1].
  • Our finding that p53 mutations can occur before the development of invasive breast cancer, particularly in DCIS of high histologic grade, has potentially important implications for prevention and treatment [1].
  • These results demonstrate for the first time that specific TN isoforms are expressed in invasive breast carcinomas and that these isoforms are identified in a subset of DCIS and suggest that detection of TN16 and/or TN14/16 may be used as a predictor for invasion [2].
  • We determined, by serial analysis of gene expression (SAGE) analysis of normal and DCIS (ductal carcinoma in situ) mammary epithelial cells, that psoriasin and several other genes implicated in psoriasis are aberrantly expressed in high-grade, comedo DCIS [3].
  • Furthermore, maspin was expressed in 23 of 24 tumor specimens obtained from pancreatic cancer patients as well as all high-grade precancerous lesions (PanIN3 and intraductal carcinoma extension) [4].

Psychiatry related information on Carcinoma, Intraductal, Noninfiltrating

  • The role of tamoxifen is currently under study, and although approved by the FDA for "risk reduction," its use in patients with DCIS is uncertain [5].

High impact information on Carcinoma, Intraductal, Noninfiltrating

  • In DCIS lesions, increased levels of HIF-1 alpha were statistically significantly associated with increased microvessel density [6].
  • In the present investigation, we studied patients with DCIS, but without invasive breast cancer, to determine the spectrum of DCIS types that can harbor a p53 mutation [1].
  • METHODS: Formalin-fixed, paraffin-embedded tissues from 94 patients with DCIS were evaluated histologically for the predominant cellular architectural pattern, degree of necrosis, and nuclear grade [1].
  • The frequency of p53 missense mutations was statistically significantly different among the three overall histologic grade categories (zero [0%] of 49 with low-grade DCIS, one [4.35%] of 23 with intermediate-grade DCIS, and nine [40.9%] of 22 with high-grade DCIS; df = 2 and P<.0001) [1].
  • Estrogen treatment of the xenograft-bearing mice had no effect on the high level of cell proliferation observed in estrogen receptor-negative, comedo DCIS specimens (two-sided P = .89) [7].

Chemical compound and disease context of Carcinoma, Intraductal, Noninfiltrating


Biological context of Carcinoma, Intraductal, Noninfiltrating

  • RESULTS: DCIS from 10 of 94 patients were found to contain p53 missense mutations [1].
  • We reported earlier that 100% of female ACI (August/Copenhagen/Irish) rats treated with essentially physiological serum levels of 17beta-estradiol lead to mammary gland tumors with histopathologic, cellular, molecular, and ploidy changes remarkably similar to those seen in human DCIS and invasive sporadic ductal BC [14].
  • Mechanisms other than gene amplification may be responsible for increased cyclin D1 protein in DCIS, especially in low grade DCIS [15].
  • A significant fraction of untreated DCIS will evolve into invasive cancer. ras homologue I (ARHI) is an imprinted tumor suppressor gene that is expressed in normal breast epithelial cells but absent or down-regulated in breast cancer cells [16].
  • Increased expression of IAP, (leading to reduced apoptosis) may explain the effect of COX-2 in increasing recurrence of DCIS after surgical treatment [17].

Anatomical context of Carcinoma, Intraductal, Noninfiltrating


Gene context of Carcinoma, Intraductal, Noninfiltrating


Analytical, diagnostic and therapeutic context of Carcinoma, Intraductal, Noninfiltrating

  • We did a double-blind randomised controlled trial to find out whether lumpectomy, radiation therapy, and tamoxifen was of more benefit than lumpectomy and radiation therapy alone for DCIS [28].
  • Archival primary breast carcinomas (n = 57), adjacent DCIS (n = 14) and DCIS alone (n = 2) were analyzed for COX-2 and HER2 expression by immunohistochemistry using specific monoclonal antibodies [29].
  • Using the PCR, we examined DNA extracts from microdissected stromal and epithelial tissues of 11 breast samples containing DCIS, including five cases associated with IDC [18].
  • In contrast, treatment of mice bearing ER+ DCIS xenografts with 17beta-estradiol raised both the AI (1.03% versus 0.40%, P = 0.03) and LI (11.0% versus 5.1%, P = 0.007) compared with controls [30].
  • By Southern blot analysis, cyclin D1 gene amplification was detected in 10 per cent (3/32) of DCIS cases [31].


  1. p53 missense mutations in microdissected high-grade ductal carcinoma in situ of the breast. Done, S.J., Eskandarian, S., Bull, S., Redston, M., Andrulis, I.L. J. Natl. Cancer Inst. (2001) [Pubmed]
  2. Changes in tenascin-C isoform expression in invasive and preinvasive breast disease. Adams, M., Jones, J.L., Walker, R.A., Pringle, J.H., Bell, S.C. Cancer Res. (2002) [Pubmed]
  3. Psoriasin expression in mammary epithelial cells in vitro and in vivo. Enerbäck, C., Porter, D.A., Seth, P., Sgroi, D., Gaudet, J., Weremowicz, S., Morton, C.C., Schnitt, S., Pitts, R.L., Stampl, J., Barnhart, K., Polyak, K. Cancer Res. (2002) [Pubmed]
  4. Expression of the tumor suppressor gene Maspin in human pancreatic cancers. Maass, N., Hojo, T., Ueding, M., Lüttges, J., Klöppel, G., Jonat, W., Nagasaki, K. Clin. Cancer Res. (2001) [Pubmed]
  5. The current treatment of ductal carcinoma in situ. Schwartz, G.F. The breast journal. (2001) [Pubmed]
  6. Levels of hypoxia-inducible factor-1 alpha during breast carcinogenesis. Bos, R., Zhong, H., Hanrahan, C.F., Mommers, E.C., Semenza, G.L., Pinedo, H.M., Abeloff, M.D., Simons, J.W., van Diest, P.J., van der Wall, E. J. Natl. Cancer Inst. (2001) [Pubmed]
  7. Assessment of hormone dependence of comedo ductal carcinoma in situ of the breast. Holland, P.A., Knox, W.F., Potten, C.S., Howell, A., Anderson, E., Baildam, A.D., Bundred, N.J. J. Natl. Cancer Inst. (1997) [Pubmed]
  8. Effect of epidermal growth factor receptor tyrosine kinase inhibition on epithelial proliferation in normal and premalignant breast. Chan, K.C., Knox, W.F., Gee, J.M., Morris, J., Nicholson, R.I., Potten, C.S., Bundred, N.J. Cancer Res. (2002) [Pubmed]
  9. Deregulated estrogen receptor alpha expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma in situ. Frech, M.S., Halama, E.D., Tilli, M.T., Singh, B., Gunther, E.J., Chodosh, L.A., Flaws, J.A., Furth, P.A. Cancer Res. (2005) [Pubmed]
  10. The morphologic effects of synthetic reproductive steroids on the mammary gland of rhesus monkeys. Mestranol, ethynerone, mestranol-ethynerone, chloroethynyl norgestrel-mestranol, and anagestone acetate-mestranol combinations. Tavassoli, F.A., Casey, H.W., Norris, H.J. Am. J. Pathol. (1988) [Pubmed]
  11. Intratumoral concentration of sex steroids and expression of sex steroid-producing enzymes in ductal carcinoma in situ of human breast. Shibuya, R., Suzuki, T., Miki, Y., Yoshida, K., Moriya, T., Ono, K., Akahira, J., Ishida, T., Hirakawa, H., Evans, D.B., Sasano, H. Endocr. Relat. Cancer (2008) [Pubmed]
  12. Integrated genomic and transcriptomic analysis of ductal carcinoma in situ of the breast. Vincent-Salomon, A., Lucchesi, C., Gruel, N., Raynal, V., Pierron, G., Goudefroye, R., Reyal, F., Radvanyi, F., Salmon, R., Thiery, J.P., Sastre-Garau, X., Sigal-Zafrani, B., Fourquet, A., Delattre, O. Clin. Cancer Res. (2008) [Pubmed]
  13. Cyclooxygenase-2 inhibition does not improve the reduction in ductal carcinoma in situ proliferation with aromatase inhibitor therapy: results of the ERISAC randomized placebo-controlled trial. Bundred, N.J., Cramer, A., Morris, J., Renshaw, L., Cheung, K.L., Flint, P., Johnson, R., Young, O., Landberg, G., Grassby, S., Turner, L., Baildam, A., Barr, L., Dixon, J.M. Clin. Cancer Res. (2010) [Pubmed]
  14. Estrogen mediates Aurora-A overexpression, centrosome amplification, chromosomal instability, and breast cancer in female ACI rats. Li, J.J., Weroha, S.J., Lingle, W.L., Papa, D., Salisbury, J.L., Li, S.A. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  15. Amplification of CCND1 and expression of its protein product, cyclin D1, in ductal carcinoma in situ of the breast. Simpson, J.F., Quan, D.E., O'Malley, F., Odom-Maryon, T., Clarke, P.E. Am. J. Pathol. (1997) [Pubmed]
  16. Loss of the expression of the tumor suppressor gene ARHI is associated with progression of breast cancer. Wang, L., Hoque, A., Luo, R.Z., Yuan, J., Lu, Z., Nishimoto, A., Liu, J., Sahin, A.A., Lippman, S.M., Bast, R.C., Yu, Y. Clin. Cancer Res. (2003) [Pubmed]
  17. Survivin expression in in situ and invasive breast cancer relates to COX-2 expression and DCIS recurrence. Barnes, N., Haywood, P., Flint, P., Knox, W.F., Bundred, N.J. Br. J. Cancer (2006) [Pubmed]
  18. Concurrent and independent genetic alterations in the stromal and epithelial cells of mammary carcinoma: implications for tumorigenesis. Moinfar, F., Man, Y.G., Arnould, L., Bratthauer, G.L., Ratschek, M., Tavassoli, F.A. Cancer Res. (2000) [Pubmed]
  19. Receptor for urokinase is present in tumor-associated macrophages in ductal breast carcinoma. Pyke, C., Graem, N., Ralfkiaer, E., Rønne, E., Høyer-Hansen, G., Brünner, N., Danø, K. Cancer Res. (1993) [Pubmed]
  20. The clinical significance of cytokeratin-positive cells in lymph nodes at the time of mastectomy from patients with ductal carcinoma-in-situ. Tamhane, R., Dahlstrom, J.E., McCallum, D.D., Buckingham, J.M. Ann. Surg. Oncol. (2002) [Pubmed]
  21. Myoepithelial cell staining patterns of papillary breast lesions: from intraductal papillomas to invasive papillary carcinomas. Hill, C.B., Yeh, I.T. Am. J. Clin. Pathol. (2005) [Pubmed]
  22. Variant of intraductal carcinoma (with scant mucin production) is of main pancreatic duct origin: a clinicopathological study of four patients. Suda, K., Hirai, S., Matsumoto, Y., Mogaki, M., Oyama, T., Mitsui, T., Fujibayashi, M., Kumazawa, K., Kajiwara, T. Am. J. Gastroenterol. (1996) [Pubmed]
  23. Endometase/matrilysin-2 in human breast ductal carcinoma in situ and its inhibition by tissue inhibitors of metalloproteinases-2 and -4: a putative role in the initiation of breast cancer invasion. Zhao, Y.G., Xiao, A.Z., Park, H.I., Newcomer, R.G., Yan, M., Man, Y.G., Heffelfinger, S.C., Sang, Q.X. Cancer Res. (2004) [Pubmed]
  24. Expression of the hypoxia-inducible and tumor-associated carbonic anhydrases in ductal carcinoma in situ of the breast. Wykoff, C.C., Beasley, N., Watson, P.H., Campo, L., Chia, S.K., English, R., Pastorek, J., Sly, W.S., Ratcliffe, P., Harris, A.L. Am. J. Pathol. (2001) [Pubmed]
  25. Expression levels of estrogen receptor-alpha, estrogen receptor-beta, coactivators, and corepressors in breast cancer. Kurebayashi, J., Otsuki, T., Kunisue, H., Tanaka, K., Yamamoto, S., Sonoo, H. Clin. Cancer Res. (2000) [Pubmed]
  26. Microsatellite instability in ductal carcinoma in situ of the breast. Walsh, T., Chappell, S.A., Shaw, J.A., Walker, R.A. J. Pathol. (1998) [Pubmed]
  27. BRCA mutations in women with ductal carcinoma in situ. Smith, K.L., Adank, M., Kauff, N., Lafaro, K., Boyd, J., Lee, J.B., Hudis, C., Offit, K., Robson, M. Clin. Cancer Res. (2007) [Pubmed]
  28. Tamoxifen in treatment of intraductal breast cancer: National Surgical Adjuvant Breast and Bowel Project B-24 randomised controlled trial. Fisher, B., Dignam, J., Wolmark, N., Wickerham, D.L., Fisher, E.R., Mamounas, E., Smith, R., Begovic, M., Dimitrov, N.V., Margolese, R.G., Kardinal, C.G., Kavanah, M.T., Fehrenbacher, L., Oishi, R.H. Lancet (1999) [Pubmed]
  29. Cyclooxygenase-2 expression in human breast cancers and adjacent ductal carcinoma in situ. Half, E., Tang, X.M., Gwyn, K., Sahin, A., Wathen, K., Sinicrope, F.A. Cancer Res. (2002) [Pubmed]
  30. Effects of a pure antiestrogen on apoptosis and proliferation within human breast ductal carcinoma in situ. Gandhi, A., Holland, P.A., Knox, W.F., Potten, C.S., Bundred, N.J. Cancer Res. (2000) [Pubmed]
  31. Cyclin D1 gene amplification and overexpression are present in ductal carcinoma in situ of the breast. Vos, C.B., Ter Haar, N.T., Peterse, J.L., Cornelisse, C.J., van de Vijver, M.J. J. Pathol. (1999) [Pubmed]
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