Abstract:
A case of about-80-year-old-female is herein presented. She felt palpable mass in her right breast of about 10mm-in-diameter before 1 year for our exams. In this time, she felt the mass is larger and larger. Hence, she came to our hospital for further examinations and treatments. Ultrasonography (US) demonstrated 31x22x24mm-in-size of heterogenous-low-echoic mass of right inner quadrants. The mass showed blood signal and irregular border in US. Hence, malignancy was suggested and breast core needle biopsy (CNB) was done. The pathological-biopsy-diagnosis was “invasive breast carcinoma”. Then, total mastectomy was done. The operated specimen revealed the consisted cells showed collection (aggregation) of DCIS (ductal carcinoma in situ) lesions and partially observed invasion like as “carcinoma arising from sclerosing papilloma”. Collected and aggregated DCISs exhibited mass-like lesion of prominent intraductal papillary lesion with non-comedo necrosis mainly “solid -paillary DCIS feature”. The composed cells revealed large and abundant eosinophilic cytoplasm with contained granules with AR and GCDFP15 both positive compatible with pure-apocrine-carcinoma (pAC). The composed cells exhibited the nuclei were round with conspicuous nucleoli with high nuclear atypia. Intrinsic subtype was “Triple negative” (ER:0, PgR:0, HER2:0). In immunohistochemically (IHC), partial invaded cells revealed CK5/6 positive with negative nests and stromal type was SMA as well as D2-40 positive heterogenous feature of cancer associated fibroblasts (CAFs) were heterogenous positive. However, expansile-invasion-like cells exhibited no CK5/6 positive and stayed in fibrous capsule. This phenomen might reflect the previous report of Rakha EA, at al. of hypothesizing theory of “breast expansile growth”. Our results suggests their theory in a part. We think our case is only case report however, would be worthy for understanding and enlightning the “DCIS to invasion mechanism”.Further, D2-40 showed intraductal fibrovascular-core (FVC) positive with contained pAC cells with partial destruction of FVC. Besides, silver staining demonstrated intraductal FVC infarctions as well as distraction of FVC by pAC cells. These features might reflect infarction of FVC and leading to failure its function and it might cause intraductal “heterogenous necrosis” not “comedo-necrosis” in this case. This might reflect comparatively long-term clinical-status as well as good prognostic factor. It is well known heterogenous necrosis is worse prognostic factor in all “invasive carcinomas”, however, our case suggests in the conditions of not non-comedo but “heterogenous necrosis in intraductal lesions”, it might be considered the one of the sign of comparatively well prognostic factor. We would like to thoroughly discuss this special phenomenon and its mechanism by reference of related articles including WHO 5th and hypothesizing its unique “breast expansile invasion” pattern by our pathological new knowledge. Furthermore, we would like to discuss the “DCIS to Invasion Mechanism” of its difficulty and challenging theme by our unique case.
