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Ovarian serous neoplasms are thought to arise from the fallopian tube or from the ovarian surface epithelium. The possibility of a third pathway-involving the mesenchymal-epithelial transition and mimicking the formation of the Müllerian duct-arose from observations gathered from our routine cases. The purpose of this study is to determine the association of precursors in the ovarian stroma with different types of ovarian serous neoplasms. Three hundred neoplasms, benign (25), borderline (63), and malignant ovarian serous neoplasms (40 low-grade serous carcinomas [LGSCas] and 172 high-grade serous carcinomas [HGSCas]), were reviewed. Clinicopathologic features analyzed included patient's age, tumor size, stage, histologic pattern, and possible precursors in the ovarian parenchyma (endosalpingiosis, inverted macropapillae, polyploid giant cancer cells, and simple cysts). All benign and borderline cases showed continuity with benign serous cysts or endosalpingiosis. In LGSCas, continuity with serous cysts was found in 29 (72%) of 40 cases, and inverted macropapillae were found in 12 (30%) of 40 cases. In untreated HGSCas, there was continuity with simple cysts in 42% of cases. In addition, these HGSCas contained polyploid giant cancer cells in 20% of cases. There were no different features in the ovaries in cases with or without serous tubal intraepithelial carcinoma. Our study shows that in a subset of cases, ovarian serous neoplasms and the Müllerian duct develop in similar fashion, originating from epithelial cells derived from the mesothelium, or occur de novo from structures derived from mesenchymal-epithelial transition.

Merkel cell carcinoma (MCC) is an aggressive, highly metastatic, cutaneous neuroendocrine malignancy with poor prognosis. Here, we describe a MCC excision specimen with a rare case of tumor-associated amyloid deposition in the absence of residual tumor cells. A 72-year-old man presented with a lesion of 5-6 months' duration on his left elbow, clinically thought to be a ganglion cyst. The biopsy specimen revealed a Stage IIA MCC with classic histomorphologic and immunophenotypic findings, with tumor extending to the tissue edges. The patient underwent wide local excision with negative margins and a negative sentinel lymph node biopsy. Although the patient did not receive any presurgical chemotherapy, immunotherapy, or targeted therapy, the re-excision specimen showed only amphophilic, feathery deposits that were salmon-pink with Congo red stain and further confirmed as amyloid by electron microscopy; there were no residual carcinoma cells. Amyloid deposition in MCC has been described in rare case reports. Our case was extraordinary in that there was only amyloid deposition and an associated granulomatous reaction, without identifiable MCC cells. This case demonstrates that amyloid deposition may be evidence of a prior MCC at the site of a prior procedure and may warrant careful evaluation for residual MCC.

Context.— The tissue diagnosis of amyloidosis is traditionally suggested by hematoxylin-eosin stain and confirmed by Congo red stain, both examined by routine light microscopy. Both false-positive and false-negative congophilia are well documented, limiting the sensitivity and specificity of the Congo red stain for the diagnosis of amyloidosis. Examination of Congo red–stained tissue by Texas Red–filtered fluorescence microscopy (TRFM) is known to enhance the amyloid-specific congophilia, thus increasing the diagnostic sensitivity. Objective.— To determine whether TRFM can mitigate the false positivity and thus improve the diagnostic specificity of the Congo red stain. Design.— Ninety-two tissue samples were categorized into 3 groups. Group I included 15 samples with tissue deposition of amyloid. Group II consisted of 63 samples in which amorphous eosinophilic structures reminiscent of amyloid were seen on hematoxylin-eosin–stained tissue sections. Group III included 14 samples in which amyloid and amyloid-like tissue were seen side by side. The final diagnosis of presence or absence of amyloidosis in each case was established by clinicopathologic correlation. The congophilic areas in each case were identified by light microscopy. The same areas were then examined by TRFM. Results.— TRFM enhanced congophilia, confirming the diagnosis of amyloidosis in all cases of group I. Enhancement was not seen in 52 of the 63 cases in group II. For group III cases, TRFM enhanced the amyloid-specific congophilia, but not the nonspecific congophilia, in all cases. Conclusions.— TRFM increases the diagnostic yield and specificity of Congo red–stained tissue sections for detection of amyloid.