TY - JOUR
T1 - Ductal Carcinoma In Situ of Breast
T2 - From Molecular Etiology to Therapeutic Management
AU - Hophan, Shelby Lynn
AU - Odnokoz, Olena
AU - Liu, Huiping
AU - Luo, Yuan
AU - Khan, Seema
AU - Gradishar, William
AU - Zhou, Zhuan
AU - Badve, Sunil
AU - Torres, Mylin A.
AU - Wan, Yong
N1 - Publisher Copyright:
© 2022 The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: [email protected].
PY - 2022/4/1
Y1 - 2022/4/1
N2 - Ductal 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.
AB - Ductal 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.
KW - breast cancer
KW - ductal carcinoma in situ
KW - invasive breast cancer
KW - invasive ductal carcinoma
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U2 - 10.1210/endocr/bqac027
DO - 10.1210/endocr/bqac027
M3 - Review article
C2 - 35245349
AN - SCOPUS:85128159951
SN - 0013-7227
VL - 163
JO - Endocrinology (United States)
JF - Endocrinology (United States)
IS - 4
M1 - bqac027
ER -