Cutaneous Lichen Planus (cutaneous + lichen_planu)

Distribution by Scientific Domains


Selected Abstracts


Cutaneous lichen planus and squamous cell carcinoma

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 1 2003
GK Patel
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Multilineage progression of genetically unstable tumor subclones in cutaneous T-cell lymphoma

EXPERIMENTAL DERMATOLOGY, Issue 8 2004
Albert Rübben
Abstract:, Molecular analysis of solid malignant tumors has suggested multilineage progression of genetically unstable subclones during early stages of tumorigenesis as a common mechanism of tumor cell evolution. We have investigated whether multilineage progression is a feature of cutaneous T-cell lymphoma (CTCL). To identify individual tumor cell subclones, we determined the pattern of mutations within microsatellite DNA obtained from multiple histomorphologically confined tumor cell nests of mycosis fungoides (MF) and lymphomatoid papulosis (LyP) lesions. Tumor cells were isolated by laser microdissection, and allelotypes were determined at microsatellite markers D6S260, D9S162, D9S171, D10S215, TP53.PCR15, and D18S65. Nine cases of MF and one patient with anaplastic large cell lymphoma (ALCL) originating from LyP were analyzed at 277 different microdissected areas obtained from 31 individual lesions. Three specimens of cutaneous lichen planus microdissected at 26 areas served as the control tissue. Microsatellite instability in microdissected tissue [MSI(md-tissue)] was detected in tumor tissues of all CTCL patients. One hundred and fifty-seven of 469 analyzed polymerase chain reaction (PCR) amplifications contained mutated microsatellite alleles (34%). In lichen planus, MSI(md-tissue) was seen in only four of 76 PCR products (5%) (P < 0.0001). The distribution of allelotypes in tumor cells from different disease stages was consistent with multilineage progression in five MF cases, as well as in the LyP/ALCL patient. Our results suggest that CTCL may evolve by multilineage progression and that tumor subclones in MF can be detected in early disease stages by mutation analysis of microsatellite DNA obtained from multiple microdissected areas. [source]


Hepatitis C virus infection and oral lichen planus: a report from the Netherlands

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 6 2000
E. H. Meij
Abstract: The reported frequency of anti-hepatitis C virus (HCV) antibodies in groups of cutaneous lichen planus (CLP) and/or oral lichen planus (OLP) patients varies from about 4% to 65%. Most of these studies have been performed in countries with a high overall prevalence of HCV infection in the general population, such as the southern European countries and Japan. Limited data are available from areas with a low prevalence of HCV infection. Therefore, we investigated the prevalence of HCV infection in a series of 55 patients with OLP in the Netherlands, which apparently has a low prevalence of HCV infection. None of the 55 patients revealed serological evidence of antibodies to HCV. The present data suggest that HCV infection in OLP patients in the Netherlands is probably not very common. A larger study group with a sex- and age-matched control group is required to advise against routine serological examination for HCV infection in Dutch OLP patients. [source]


Giant keratoacanthoma arising in hypertrophic lichen planus

AUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 4 2003
Leah M Giesecke
SUMMARY A 45-year-old man presented with a rapidly enlarging tumour in an area of long-standing hypertrophic lichen planus of the lower leg. Histological examination of the resected specimen showed it to be a giant keratoacanthoma measuring 37 × 57 mm. Neoplastic change is a rarely reported complication of chronic variants of cutaneous lichen planus. To date there have been only two reports of keratoacanthoma development in association with lichen planus. [source]