Breast cancerDuctal carcinoma in situ: a review of recent advancesTang, Pinga; Hajdu, Steven Ib; Lyman, Gary HcAuthor Information aDepartment of Pathology and Laboratory Medicine and Department of Medicine bNew York University School of Medicine, New York, USA cThe James P. Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York, USA Correspondence to Ping Tang MD PhD, Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Box 626, Rochester, NY 14642, USA Tel: +1 585 275 6640; fax: +1 585 273 3637; e-mail: email@example.com Current Opinion in Obstetrics and Gynecology: February 2007 - Volume 19 - Issue 1 - p 63-67 doi: 10.1097/GCO.0b013e3280114a3a Buy Metrics Abstract Purpose of review This review summarizes recent findings on ductal carcinoma in situ of the breast and their impact on prognosis and management of the disease. Recent findings Great advances have been made in our understanding of ductal carcinoma in situ. Nuclear grading is probably the most important pathological factor that affects clinical outcome and correlates with distinct genetic pathways. Identifying key molecules in each pathway may provide better markers for prognostic, predictive and therapeutic purposes. Not all cases of ductal carcinoma in situ will progress to invasive ductal carcinoma, and identifying this subgroup of patients should lead to a reduction of overtreatment. Progenitor cell theory at the cellular level and sick lobe theory at the architectural level may help provide a better understanding of ductal carcinoma in situ from a different perspective and facilitate the development of individualized therapy. Prevention of local recurrence is the primary goal for treatment. Debate continues, however, on the use of radiotherapy, hormonal therapy, and sentinel lymph node biopsy. A panel of molecular markers may be needed for accurately predicting clinical outcome for the disease. Summary Understanding the carcinogenesis of ductal carcinoma in situ at the molecular level may lead to an optimal individualized therapy with minimal over or undertreatment. © 2007 Lippincott Williams & Wilkins, Inc.