@article{oai:shiga-med.repo.nii.ac.jp:00003349,
 author = {北村, 美奈 and 仲山, 貴永 and 向所, 賢一 and 森, 毅 and 梅田, 朋子 and 森谷, 鈴子 and 九嶋, 亮治 and 谷, 眞至 and 杉原, 洋行 and KITAMURA, Mina and NAKAYAMA, Takahisa and MUKAISHO, Ken-ichi and MORI, Tsuyoshi and UMEDA, Tomoko and Moritani, Suzuko and KUSHIMA, Ryoji and TANI, Masaji and SUGIHARA, Hiroyuki},
 issue = {2-3},
 journal = {Pathobiology},
 month = {Oct},
 note = {BACKGROUND:Ductal carcinoma in situ (DCIS) of the breast is heterogeneous in terms of the risk of progression to invasive ductal carcinoma (IDC). To treat DCIS appropriately for its progression risk, we classified individual DCIS by its profile of genomic changes into 2 groups and correlated them with clinicopathological progression factors.

METHODS:We used surgically resected, formalin-fixed, paraffin-embedded tissues of 22 DCIS and 30 IDC lesions. We performed immunohistochemical intrinsic subtyping, array-based comparative genomic hybridization, and unsupervised clustering.

RESULTS:The samples were divided into 2 major clusters, A and B. Cluster A showed a greater number of gene and chromosome copy number alterations, a larger IDC/DCIS ratio, a higher frequency of nonluminal subtype, a lower frequency of luminal subtype, and a higher nuclear grade, when compared with cluster B. However, there was no difference in the frequencies of lymph node metastasis between clusters A and B. We identified 9 breast-cancer-related genes, including TP53 and GATA3, that highly contributed to the discrimination of A and B clusters.

CONCLUSION:Classification of breast tumors into rapidly progressive cluster A and the other (cluster B) may contributeto select the treatment appropriate for their progression risk.},
 pages = {92--101},
 title = {Progression Potential of Ductal Carcinoma in situ Assessed by Genomic Copy Number Profiling.},
 volume = {86},
 year = {2018}
}