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The critical rationale for breast cancer screening is that early detection and resultant treatment improve the disease outcome.(1,2) Early detection often enables breast‐conserving surgery and less harmful treatment. A large multicenter trial by the American College of Radiology Imaging Network (ACRIN) Protocol 6666 has shown that the addition of a single screening ultrasound (US) to mammography increased the detection of small and node‐negative cancers from 7.6 to 11.9 per 1000 women with elevated risk for breast cancer.(3,4) A randomized controlled trial on effectiveness of US screening in women aged 40–49 years is underway in Japan.(5) Ultrasound has been proposed as a supplemental screening test in women with dense breast tissues and in high‐risk women who cannot undergo MRI for any reason.(1) Although mammography remains the gold standard in breast imaging, high mammographic density may make breast cancer more difficult to detect and thus can increase the risk of cancer development in women screened by mammography alone.(3,6–14)
New individualized therapy approaches use specific molecular signatures, biomarkers, and clinicopathological features of tumors and patients.(15–19) Adjuvant systemic therapy is planned based on patient age, tumor size, histological grade, lymph node metastasis, hormonal receptor status, and human epidermal growth factor receptor 2 (HER2) status.(20) Comprehensive molecular analysis has revealed that breast cancer is not a single disease, but that it shows heterogeneous morphology and expression of various molecular markers.(16,18,21–27) Currently, gene expression studies have resulted in the identification of five molecularly distinct subtypes of breast cancer.(18,22,23) To date, these subtypes are luminal A and B, which are hormone receptor‐positive, the HER2 subtype, the basal‐like subtype, and an unclassified group. Molecular markers specific for breast cancer include estrogen receptor (ER), progesterone receptor (PR), c‐erbB2 (HER2), Ki‐67, p53, bcl‐2, basal cytokeratins, and E‐cadherin.(18,21) Clinical differences between ER‐negative and ER‐positive cancers have been long recognized.(17,22–27) Most patients with ER‐negative cancers do not benefit from antihormonal therapy, and many of these cancers are unaffected by conventional cytotoxic chemotherapy.(15,17) Triple‐negative cancer, defined as a tumor that is negative for ER, PR, and HER2, has a relatively poor prognosis.(