Medical Oncology

, Volume 29, Issue 3, pp 1536–1542 | Cite as

Coexisting ductal carcinoma in situ independently predicts lower tumor aggressiveness in node-positive luminal breast cancer

  • H. Wong
  • S. Lau
  • R. Leung
  • J. Chiu
  • P. Cheung
  • T. T. Wong
  • R. Liang
  • R. J. Epstein
  • T. YauEmail author
Original Paper


Primary breast invasive ductal carcinoma coexisting with ductal carcinoma in situ (IDC-DCIS) is characterized by lower proliferation rate and metastatic propensity than size-matched pure IDC. IDC-DCIS is also more often ER-positive, PR-positive and/or HER2-positive. This analysis aims to clarify whether the presence of coexisting DCIS in IDC affects tumor aggressiveness in various biological subtypes of breast cancer, respectively. Tumor data obtained from 1,355 consecutive female patients undergoing upfront surgery for primary breast cancer were analyzed retrospectively; 196 patients with pure DCIS were excluded. Based on evidence that immunohistochemistry (IHC) provides a reasonable approximation of molecular phenotypes, the tumor samples were divided into 4 groups: (1) luminal A (ER and/or PR-positive, HER2-negative, Ki67 ≤ 12), (2) luminal B (ER and/or PR-positive, HER2-negative, Ki67 > 12), (3) HER2 (HER2-positive) and (4) basal-like (triple-negative) disease. Ki67 expression and nodal involvement of IDC with or without DCIS in these groups were compared. The number of patients with luminal A, luminal B, HER2 and basal-like breast cancer were 396, 265, 258 and 117, respectively. Ki-67 was lower in IDC-DCIS than in size-adjusted pure IDC of both luminal A and luminal B subtypes (P = 0.15 and <0.005, respectively). In HER2 or basal-like tumors, there were no significant difference between pure IDC and IDC-DCIS. The presence of coexisting DCIS in IDC predicts lower biological aggressiveness in luminal cancers but not in the conventionally more aggressive HER2-positive and triple-negative subtypes.


Ductal carcinoma in situ (DCIS) Invasive ductal carcinoma (IDC) Ki67 Luminal breast cancer 


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • H. Wong
    • 1
  • S. Lau
    • 2
  • R. Leung
    • 1
  • J. Chiu
    • 1
  • P. Cheung
    • 2
  • T. T. Wong
    • 2
  • R. Liang
    • 2
  • R. J. Epstein
    • 3
  • T. Yau
    • 1
    • 4
    Email author
  1. 1.Division of Hematology and Oncology, Department of MedicineThe University of Hong KongPokfulam, Hong KongChina
  2. 2.Comprehensive Oncology CentreHong Kong Sanatorium HospitalHong KongChina
  3. 3.Department of OncologySt. Vincent’s HospitalSydneyAustralia
  4. 4.Department of SurgeryThe University of Hong KongHong KongChina

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