Detection of clonal T cells in lichen planus.
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Biomedical subjects
Publications and source records attributed to P I Schiller.
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In situ polymerase chain reaction (PCR) and PCR in situ hybridization are new diagnostic tools in dermatopathology. These techniques can combine the sensitivity of PCR with the advantage of in situ hybridization to localize specific cellular structures. With optical control of the PCR reaction product in these techniques, false-positive results due to contamination can be minimized. Several working protocols have been established which allow detection of DNA and RNA sequences in a rapid and reproducible manner. Two different methods have been established to detect the amplification product, the indirect PCR in situ hybridization (PCRisHyb), and the direct in situ PCR (isPCR). An easy and reproducible method for PCRisHyb and isPCR in formalin-fixed and paraffin-embedded tissue is described and the two techniques are compared. Using both isPCR and PCRisHyb, the amplification product can be visualized with an optimal morphological preservation of the tissue. Indirect PCRisHyb showed a slightly higher specificity whereas direct isPCR was the quicker, easier and less expensive method.
The product of the p16/INK4a/CDKN2/MTS1 tumor-suppressor gene acts as a negative cell cycle regulator by inhibiting G1 cyclin-dependent kinases that phosphorylate the retinoblastoma protein. p16 is inactivated in a wide range of human malignancies, including familial melanoma. However, its expression and function in sporadic melanoma has not been extensively investigated. We studied p16 expression in 62 archival melanomas and 30 archival nevi and lentigines by immunohistochemistry. Eighteen of 26 (69%) superficial spreading melanomas, 17 of 28 (61%) nodular melanomas, all of three lentigo maligna melanomas, and all of five melanoma metastases were found to harbor less than 10% p16-positive tumor cells. In contrast, only six of 24 (25%) nevi had less than 10% positive cells. No correlation between tumor thickness and loss of p16 expression was found. Using DNA from micro-dissected tumor and matched normal tissues, five of seven (71%) p16-negative melanoma cases had 9p21 loss of heterozygosity (LOH), and one of these 9p21 LOH cases had promoter region hypermethylation of the remaining p16 allele. These data demonstrate that partial or complete loss of p16 expression is prevalent in sporadic melanoma and is frequently associated with 9p21 LOH.
Nuchal fibroma is a fibrolipoma-like soft tissue mass, located on the back and neck of middle-aged men. Clinically it presents as adiffuse indurated subcutaneous swelling and, sometimes painful and inflamed. Since the first descriptions, by Enzinger and Weiss and Lister et al. both in 1988, under the name "collagenosis nuchae", only 15 additional cases have been reported. Nonetheless, the lesion is comparatively common. We report another case of nuchal fibroma emphasizing the distinctive clinical and histopathological features of this lesion and its differential diagnosis.
Angioedema is a rare but potentially life-threatening adverse effect of angiotensin-converting enzyme inhibitors (ACEI) which usually occurs within the first weeks of therapy. We report three patients in whom ACEI-induced angioedema began with a late onset of 12-33 months, and who had an irregular, unpredictable course under ACEI therapy. In two patients, other drugs or trauma appeared to trigger some of the episodes. After withdrawal of the ACEI, the trigger drugs were well tolerated in provocation tests and upon re-exposure. To avoid putting some patients unnecessarily at risk for long periods, one should consider this irregular pattern of ACEI-induced angioedema and regularly monitor patients for this adverse effect.
Angiokeratomas are vascular lesions which are defined histologically as one or more dilated blood vessel(s) lying directly subepidermal and showing an epidermal proliferative reaction. At the center of pathogenesis there is a capillary ectasia in the papillary dermis. The epidermal changes in all forms of angiokeratoma are secondary. The different entities causing vessel ectasia lead to the many clinical variants of angiokeratoma. Current classification distinguishes between widespread forms (angiokeratoma corporis diffusum), which is usually associated with an inborn error of metabolism, and localized forms, which include solitary angiokeratoma, Fordyce's angiokeratoma, angiokeratoma circumscriptum naeviforme and angiokeratoma of Mibelli.