• Journal of the Korean Society of Radiology
• /
• v.81 no.6
• /
• pp.1504-1510
• /
• 2020

In this case report, we present the radiologic and pathologic findings of atypical ductal hyperplasia (ADH) in the male breast. It is well known that a high-risk lesion such as ADH is a precursor of breast cancer in females. However, the clinical significance of these lesions in the male breast is still uncertain because male breasts mainly consist of ducts without lobule formation, unlike the female breast. To our knowledge, imaging findings of ADH in the male breast have not been reported previously, except for a few studies on the pathologic findings of these lesions. Through this paper, we would like to present the possible imaging features of this high-risk lesion in the male breast and review the related literature.

• Korean Journal of Radiology
• /
• v.21 no.11
• /
• pp.1220-1229
• /
• 2020

Objective: Stereotactic vacuum-assisted breast biopsy (VABB) is considered a reliable alternative to surgical biopsy for suspicious calcifications. In most cases, the management of flat epithelial atypia (FEA) and atypical ductal hyperplasia (ADH) after VABB with residual calcifications requires surgical excision. This study aimed to evaluate the impact of pathology of non-calcified specimens on the underestimation of malignancy. Materials and Methods: We retrospectively reviewed 1147 consecutive cases of stereotactic VABB of suspicious calcifications without mass from January 2010 to December 2016 and identified 46 (4.0%) FEA and 52 (4.5%) ADH cases that were surgically excised for the retrieval of residual calcifications. Mammographic features and pathology of the calcified and non-calcified specimens were reviewed. Results: Seventeen specimens (17.3%) were upgraded to malignancy. Mammographic features associated with the underestimation of malignancy were calcification extent (> 34.5 mm: odds ratio = 6.059, p = 0.026). According to the pathology of calcified versus non-calcified specimens, four risk groups were identified: Group A (ADH vs. high-risk lesions), Group B (ADH vs. non-high-risk lesions), Group C (FEA vs. high-risk lesions), and Group D (FEA vs. non-high-risk lesions). The lowest underestimation rate was observed in Group D (Group A vs. Group B vs. Group C vs. Group D: 35.0% vs. 20.0% vs. 15.0% vs. 3.6%, p = 0.041, respectively). Conclusion: Considering that the calcification extent and pathology of non-calcified specimens may be beneficial in determining the likelihood of malignancy underestimation, excision after FEA or ADH diagnosis by VABB is required, except for the diagnoses of FEA coexisting without atypia lesions in non-calcified specimens.

• BMB Reports
• /
• v.51 no.11
• /
• pp.584-589
• /
• 2018

Secondary prevention via earlier detection would afford the greatest chance for a cure in premalignant lesions. We investigated the exomic profiles of non-malignant and malignant changes in head and neck squamous cell carcinoma (HNSCC) and the genomic blueprint of human papillomavirus (HPV)-driven carcinogenesis in oropharyngeal squamous cell carcinoma (OPSCC). Whole-exome (WES) and whole-genome (WGS) sequencing were performed on peripheral blood and adjacent non-tumor and tumor specimens obtained from eight Korean HNSCC patients from 2013 to 2015. Next-generation sequencing yielded an average coverage of $94.3{\times}$ for WES and $35.3{\times}$ for WGS. In comparative genomic analysis of non-tumor and tumor tissue pairs, we were unable to identify common cancer-associated early mutations and copy number alterations (CNA) except in one pair. Interestingly, in this case, we observed that non-tumor tonsillar crypts adjacent to HPV-positive OPSCC appeared normal under a microscope; however, this tissue also showed weak p16 expression. WGS revealed the infection and integration of high-risk type HPV16 in this tissue as well as in the matched tumor. Furthermore, WES identified shared and tumor-specific genomic alterations for this pair. Clonal analysis enabled us to infer the process by which this transitional crypt epithelium (TrCE) evolved into a tumor; this evolution was accompanied by the subsequent accumulation of genomic alterations, including an ERBB3 mutation and large-scale CNAs, such as 3q27-qter amplification and 9p deletion. We suggest that HPV16-driven OPSCC carcinogenesis is a stepwise evolutionary process that is consistent with a multistep carcinogenesis model. Our results highlight the carcinogenic changes driven by HPV16 infection and provide a basis for the secondary prevention of OPSCC.