Human pathology · 2026
Histomorphologic analysis and clinical correlation of atypical apocrine lesions in breast pathology.
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Podany Peter, Zhan Haiying, Colón-Cartagena Lorraine, Ai Di, Du Jing, Krishnamurti Uma, Liang Yuanxin
Аннотация
INTRODUCTION: Apocrine change is common in breast pathology, yet atypical apocrine lesions remain poorly defined and diagnostically challenging. This study aimed to clarify the terminology of atypical apocrine proliferations and assess their clinical significance by correlating histologic features with clinical outcomes.
METHODS: We retrospectively analyzed 59 specimens initially diagnosed as atypical apocrine adenosis (AAA) or atypical apocrine hyperplasia (AAH), including apocrine atypical ductal hyperplasia, from 2014 to 2024. Cases with coexisting in situ or invasive ductal carcinoma were excluded. Histologic features and clinical follow-up data were reviewed.
RESULTS: No significant differences were observed between AAA and AAH with respect to patient age, lesional size, most architectural patterns, lobular involvement, nuclear features, necrosis, calcifications, or carcinoma upstaging on subsequent excision. Cribriform architecture was significantly more frequent in AAH than AAA (63% vs. 33%, p = 0.047). Lesions upstaged to in situ or invasive ductal carcinoma demonstrated a significantly larger extent of atypia on biopsy (1.3 cm vs. 0.8 cm, p = 0.043), higher frequencies of marked nuclear enlargement (≥3-fold compared with background epithelium; 92% vs. 54%, p = 0.027), nuclear irregularity (54% vs. 17%, p = 0.028), and necrosis (23% vs. 0%, p = 0.037). Lesional extent, nuclear irregularity, and necrosis were independently associated with carcinoma upstaging (p < 0.05).
CONCLUSIONS: Cribriform architecture supports classification as AAH, though AAA and AAH show no significant clinical differences. Marked nuclear enlargement, nuclear irregularity, and necrosis in larger atypical apocrine lesions are strongly associated with carcinoma upstaging and should prompt consideration of apocrine DCIS.
METHODS: We retrospectively analyzed 59 specimens initially diagnosed as atypical apocrine adenosis (AAA) or atypical apocrine hyperplasia (AAH), including apocrine atypical ductal hyperplasia, from 2014 to 2024. Cases with coexisting in situ or invasive ductal carcinoma were excluded. Histologic features and clinical follow-up data were reviewed.
RESULTS: No significant differences were observed between AAA and AAH with respect to patient age, lesional size, most architectural patterns, lobular involvement, nuclear features, necrosis, calcifications, or carcinoma upstaging on subsequent excision. Cribriform architecture was significantly more frequent in AAH than AAA (63% vs. 33%, p = 0.047). Lesions upstaged to in situ or invasive ductal carcinoma demonstrated a significantly larger extent of atypia on biopsy (1.3 cm vs. 0.8 cm, p = 0.043), higher frequencies of marked nuclear enlargement (≥3-fold compared with background epithelium; 92% vs. 54%, p = 0.027), nuclear irregularity (54% vs. 17%, p = 0.028), and necrosis (23% vs. 0%, p = 0.037). Lesional extent, nuclear irregularity, and necrosis were independently associated with carcinoma upstaging (p < 0.05).
CONCLUSIONS: Cribriform architecture supports classification as AAH, though AAA and AAH show no significant clinical differences. Marked nuclear enlargement, nuclear irregularity, and necrosis in larger atypical apocrine lesions are strongly associated with carcinoma upstaging and should prompt consideration of apocrine DCIS.