Syringocystadenocarcinoma Papilliferum In Situ: Case Report with Immunohistochemical Observations

Abstract

A 23-year-old man was operated for a skin tumor in the right axilla. Histological examination revealed findings consistent with a syringocystadenoma papilliferum. However, most of the papillary structures showed a disorganized proliferation of atypical cells without invasive growth, that is, a syringocystadenocarcinoma papilliferum in situ. Immunohistochemistry disclosed a different staining profile between the basal cells of the papillary structures and those of the columnar and atypical cells which reacted similarly. However, the atypical cells showed a stronger and more extensive expression of S-100 protein and CD56 than the columnar epithelium and a few of them also reacted with CEA. Ki-67 staining highlighted the increased proliferative activity of the atypical cells. The best antibody for depicting the basal cells was p63. In the present case immunohistochemistry was of little help to support the diagnosis of malignant transformation since the differences between the atypical and regular columnar cells were small and of a quantitative character only.

Syringocystadenocarcinoma Papilliferum: A case report of a rare skin adnexal tumour

“…SCACP differs from SCAAP and SCAAP IN SITU by infiltration of tumour cells into deep dermis or subcutaneous fat. SCACP and SCAAP IN SITU differ from SCAAP by cytological features of tumour cells characterized by higher nuclear cytoplasmic ratio, nuclear irregularity, coarse chromatin and increased mitotic activity [1,3,6]. Though there is no definitive immunohistochemical profile for a SCACP, the strong expression of CK7, CEA and GCFDP-15 supports the apocrine differentiation of the neoplasm [1].…”

Cysts, Sebum, Papillae-Syringocystadenoma papilliferum

“…Syringocystadenoma papilliferum is concurrent with apocrine hidrocystoma and emerges from multi-potent, undifferentiated cells which sequentially differentiate towards the dual cellular genealogy. Syringocystadenoma papilliferum is probably the sole neoplasm which triggers the differentiation of primeval cells into an apocrine hidrocystoma [3,4]. Syringocystadenoma papilliferum delineates sebaceous induction, a phenomenon which is usually cogitated in lesions such as dermatofibroma and melanocytic nevi.Sebaceous induction elucidated in Syringocystadenoma papilliferum is essentially defined as the occurrence of two or more rudimentary sebaceous glands enveloping extraneous zones of the cutaneous lesion in the absence of a normal hair follicle.…”

“…Although the aetiology is obscure, mechanics of sebaceous induction involves pleuri-potent cells composing immature sebaceous articulations at a specific anatomic site, growth factors secreted by contingent lesions such as a dermatofibroma, apocrine hidrocystoma or Syringocystadenoma papilliferum, a cogent alteration of micro-environment, ectopic hedgehog signalling and declining mobilization of β catenin [4,5]. Undifferentiated, peripherally arranged sebocytes are intensely immune reactive to epidermal growth factor receptor (EGFR) and the pertinent molecule (EGFR) with specific ligands are implicated in the differentiation of sebocytes and efficient lipogenesis.…”

“…Immune histochemical elucidation is inadequate in expressing malignant transformation as staining of normal columnar or atypical epithelium is essentially quantitative and divergent. Eccrine origin of the tumefaction is contemplated on account of elucidated eccrine specific immune marker IKH4 [3,4].…”

“…Sebaceous hyperplasia is commonly elucidated at puberty. Miniature lobules of sebaceous glands and glandular articulations are continuous with or directly extend to the superficial epidermis or a characteristic adherence to infundibular region of hair follicles is exemplified [2,4]. Syringocystadenoma papilliferum arising in the female genitalia mandates a distinction from hidradenoma papilliferum which represents a benign, asymptomatic tumefaction of apocrine sweat glands.…”