Signet-ring Change Research Articles

Diagnosing seminoma: practicalities and problems

Classical seminoma is the most commonly encountered testicular neoplasm. Most clinically localised seminomas are now managed by surveillance, though adjuvant chemo or radiotherapy can be given. The diagnosis of seminoma can be relatively straightforward, but may present unforseen challenges leading to inappropriate treatment or serious misdiagnosis in a number of ways. 1) Thorough macroscopy. Seminomas require rigorous blocking. This is because tiny amounts of non-seminoma may be missed, leading to potential under-treatment. Inflammatory lesions and granulomatous lesions may also harbour small foci of seminoma and should be treated with suspicion. 2) Unusual histological patterns. Some seminomas show unusual features. They may show frequent syncytiotrophoblastic cells leading to misdiagnosis as choriocarcinoma. A minority show tubular elements or even signet ring change. 3) Mimicks. Solid type yolk sac tumour may mimic seminoma as well as a number of other entities, especially some malignant sex cord stromal tumours. The former should be considered for adjuvant treatment, while the latter may require a prophylactic retroperitoneal lymph node dissection. Spermatocytic seminoma, especially when monomorphic may be mistaken for seminoma. Close morphological inspection allied to to judicious use of immunochemistry and knowledge of clinical details including serology is essential for the accurate diagnosis of seminoma.

Non-neoplastic endometrial signet-ring cell change

Background Non-neoplastic signet-ring cell change in the endometrium appears to be a degenerative phenomenon associated with abnormal bleeding and exogenous hormone use. It more often occurs from the fourth decade onwards. Understanding this change can aid in distinguishing this condition from potential malignant mimicks. Case report We report four cases of endometrial curettings displaying florid non-neoplastic endometrial signet-ring cell change from women in their fourth and fifth decades with menorrhagia and/or post-menopausal bleeding. All women were on exogenous hormone therapy. All biopsies showed inactive endometrium, with prominent stromal pseudo-decidualisation. The decidual cells showed prominent cytoplasmic vacuolation and were negative for mucin (PAS-D, Alcian blue, mucicarmine), pancytokeratins (AE1/AE3) and histiocytic markers (CD68, MAC387). Electron microscopy showed the vacuoles devoid of organelles. Follow-up curettings showed no neoplastic change. Discussion Non-neoplastic signet-ring change should be recognised and reported where present. The change was first described as an idiopathic postmenopausal decidual reaction. It was recognised as a potential mimick of metastatic carcinoma. The incidence of non-neoplastic endometrial signet-ring cell change is not known. Further study is required to understand this change, and may provide insight to an individual’s response to a specific exogenous hormone regime. A panel of histochemical and immunohistochemical methods should be applied to differentiate this change from various signet-ring cell neoplasms. Conclusions Non-neoplastic endometrial signet-ring cell change is a benign condition. It is important to differentiate this change from a primary or secondary signet-ring cell neoplasm.