Ductal Carcinoma In Situ of Breast: From Molecular Etiology to Therapeutic Management

Author:

Hophan Shelby Lynn1,Odnokoz Olena2ORCID,Liu Huiping3,Luo Yuan4ORCID,Khan Seema5,Gradishar William6,Zhou Zhuan7,Badve Sunil8,Torres Mylin A9,Wan Yong29ORCID

Affiliation:

1. Department of Obstetrics and Gynecology, Department of Pharmacology, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

2. Department of Pharmacology and Chemical Biology, Winship Cancer Center, Emory University School of Medicine, Atlanta, GA 30322, USA

3. Department of Pharmacology, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

4. Department of Preventive Medicine, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

5. Department of Surgery, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

6. Department of Medicine, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

7. Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA

8. Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322, USA

9. Department of Hematology and Oncology, Winship Cancer Center, Emory University School of Medicine, Atlanta, GA 30322, USA

Abstract

AbstractDuctal carcinoma in situ (DCIS) makes up a majority of noninvasive breast cancer cases. DCIS is a neoplastic proliferation of epithelial cells within the ductal structure of the breast. Currently, there is little known about the progression of DCIS to invasive ductal carcinoma (IDC), or the molecular etiology behind each DCIS lesion or grade. The DCIS lesions can be heterogeneous in morphology, genetics, cellular biology, and clinical behavior, posing challenges to our understanding of the molecular mechanisms by which approximately half of all DCIS lesions progress to an invasive status. New strategies that pinpoint molecular mechanisms are necessary to overcome this gap in understanding, which is a barrier to more targeted therapy. In this review, we will discuss the etiological factors associated with DCIS, as well as the complexity of each nuclear grade lesion. Moreover, we will discuss the possible molecular features that lead to progression of DCIS to IDC. We will highlight current therapeutic management and areas for improvement.

Funder

National Institutes of Health

Publisher

The Endocrine Society

Subject

Endocrinology

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