Melanoma has a wide spectrum of histologic features which mimic epithelial, hematologic, mesenchymal, and neural tumors. Immunohistochemistry has been the primary tool to distinguish melanomas from these other tumors; it has also been studied for use as an adjunct to distinguish benign and malignant melanocytic tumors and to elucidate prognosis. Furthermore, there has been extensive effort to find a suitable marker to differentiate spindle cell and desmoplastic melanoma from other tumors. We have reviewed the literature investigating melanocytic differentiation markers, proliferation markers, immunomodulatory markers, signaling molecules, and nerve growth factors and receptors. Despite the proliferation of immunohistochemical markers, S‐100 remains the most sensitive marker for melanocytic lesions, while markers such as HMB‐45, MART‐1/Melan‐A, tyrosinase, and MITF demonstrate relatively good specificity but not as good sensitivity as S‐100. No marker has proven useful in distinguishing spindle cell and desmoplastic melanomas from other tumors. Ki67 remains the most useful adjunct in distinguishing benign from malignant melanocytic tumors. None of the markers reviewed has been shown conclusively to have prognostic value for melanocytic neoplasms.

There is increasing evidence for the efficacy of lymphatic mapping and sentinel lymph node biopsy in predicting prognosis, reducing the morbidity traditionally associated with regional lymph node dissection and increasing survival in subgroups of patients with cutaneous melanoma. Further study is needed to determine the role of the immune system in the spread of nodal metastases and the role of immunomodulatory therapy to prevent or possibly even reverse nodal metastases.

A generalized absence of enteroendocrine cells characterizes 2 diarrheal/malabsorptive diseases, namely, enteroendocrine cell dysgenesis and autoimmune polyglandular syndrome 1. However, it is not routine for pathologists to examine mucosal biopsies for enteroendocrine cells in cases of chronic diarrheal illness. Our primary aim was to prospectively examine colonic mucosa for loss of enteroendocrine cells using chromogranin A immunohistochemistry for diagnostic purposes. Our secondary aim was to investigate enterochromaffin cells as a subset of enteroendocrine cells, using serotonin (5HT) immunohistochemistry; we hypothesized that other causes of diarrhea due to loss of enteroendocrine cell subsets are missed by evaluating enteroendocrine cells alone. Our approach was limited to patients with chronic unexplained diarrhea partly selected by referring physicians who considered the patients problematic. Seven problematic patients with reduced enteroendocrine or enterochromaffin cells were collected over a 9-month period and placed in group A. Three group A patients demonstrated reduced enteroendocrine cells relative to controls, and they were later diagnosed as having enteroendocrine cell dysgenesis (n = 1) and autoimmune polyglandular syndrome 1 (n = 2). Four group A patients had reduced enterochromaffin cells but normal enteroendocrine cells. These 4 patients had conditions such as congenital diarrhea, mild graft-versus-host disease, acquired childhood chronic diarrhea, and diarrhea post lung transplant. The reduced enterochromaffin cells in the graft-versus-host disease patient inspired a third aim, that is, to investigate whether a loss of enterochromaffin cells would be a generalized defect seen in patients with mild colonic graft-versus-host disease (group B). However, no loss of enterochromaffin cells was detected in group B. Two methods of enumerating endocrine cells were used and demonstrated 67% agreement.

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Congenital self‐healing reticulohistiocytosis of Hashimoto and Pritzker (CSHR) is a rare, benign form of Langerhans Cell Histiocytosis (LCH) that presents at birth and involutes by 6 months of age. We present an atypical case of CSHR with the first onset at 7 months of age, treated with surgical excision.

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