Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LICHEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2001

Histology of lichen sclerosus varies according to site and proximity to carcinoma.

To investigate why vulvar but not extragenital lichen sclerosus is associated with squamous cell carcinoma, we performed a histologic study of extragenital lichen sclerosus, vulvar lichen sclerosus without carcinoma, and vulvar lichen sclerosus with carcinoma adjacent to and distant from the carcinoma. We compared epidermal thickness, rete ridge length, mitotic activity, atypia, dermal collagen change, dermal inflammation, and presence of other dermatoses in 30 women in each group. Extragenital lichen sclerosus showed thinner epidermis (mean thickness of 0.13 mm versus 0.41 mm; P < 0.0005), shorter rete ridges (P = 0.0001), more dermal edema (P = 0.16), and absence of associated dermatoses of spongiotic dermatitis and lichen planus (P < 0.005) compared with vulvar lichen sclerosus. The epidermal thickening seen in vulvar lichen sclerosus was indistinguishable from lichen simplex chronicus. Vulvar lichen sclerosus without carcinoma was generally similar to that distant from carcinoma. Vulvar lichen sclerosus adjacent to carcinoma showed increased epidermal thickness (0.61 mm versus 0.26 mm; P < 0.005), more dermal fibrosis (P < 0.0005), more inflammation (P < 0.0005), and more simplex (differentiated) vulvar intraepithelial neoplasia (18 cases versus 1 case; P < 0.0005) compared with that distant from carcinoma. We concluded that (1) the classic histologic features of lichen sclerosus are seen in both vulvar and extragenital sites; (2) vulvar lichen sclerosus without associated carcinoma has a mean epidermal thickness more than three times that of extragenital lichen sclerosus; (3) the epidermal thickening is histologically indistinguishable from lichen simplex chronicus; (4) there is a tendency for vulvar lichen sclerosus to have a more sclerotic and inflamed dermis; (5) lichen sclerosus 10 mm from cancer is more similar to vulvar lichen sclerosus without carcinoma than lichen sclerosus 1 mm from carcinoma; and (6) lichen sclerosus adjacent to carcinoma tends to show exaggerated epidermis thickness, basal atypia, and loss of the edematous-hyaline layer.

Adolescent↗
PubMed2000

Alterations in distribution of tenascin, fibronectin and fibrinogen in vulval lichen sclerosus.

BACKGROUND: The pathophysiology of lichen sclerosus remains uncertain. The clinical features, including increased fragility and scarring, and the histology suggest that significant reorganisation of the extracellular matrix is occurring. Tenascin, fibrinogen and fibronectin are extracellular matrix components that play a significant role in tissue remodelling, for example during wound repair. AIM: To examine the distribution of tenascin, fibrinogen and fibronectin in vulval lichen sclerosus. MATERIALS AND METHODS: Immunohistochemical staining was performed to study the distribution of tenascin, fibronectin and fibrinogen in 16 specimens of untreated vulval lichen sclerosus and 1 specimen of extragenital lichen sclerosus. Haematoxylin and eosin staining of the specimens was also performed to identify the position of the pale staining homogenous zone/zone of sclerosis and the inflammatory infiltrate below this. The control tissues studied included biopsies taken from the uninvolved thigh of 13 of the lichen sclerosus patients and 6 samples of normal vulva tissue obtained during gynaecological procedures from women of similar age to the lichen sclerosus women. RESULTS: All the lichen sclerosus specimens demonstrated increased immunostaining of tenascin in the upper dermis and comparing this with the haematoxylin and eosin staining this corresponded to the zone of sclerosis with relatively little tenascin staining associated with the inflammatory band. In 14 out of the 16 vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen fibrinogen immunostaining was increased in the upper dermis which corresponded--in haematoxylin and eosin staining --to the zone of sclerosis. There was also slightly increased fibrinogen staining in the mid dermis which corresponded to the inflammatory band. Fibronectin staining was reduced in the upper dermis of 12 of the vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen which corresponded to the zone of sclerosis. However, in 14 of the vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen, fibronectin was slightly increased in the mid and deeper dermis which corresponded to the zone of inflammatory cells and the area below this. There was also increased fibronectin staining around blood vessel walls both in the mid dermis and within the zone of sclerosis. CONCLUSION: The distribution of tenascin, fibrinogen and fibronectin is altered in lichen sclerosus and the alteration in these extracellular matrix components may be relevant to the initiation of scarring in lichen sclerosus and the associated increased skin fragility.

Extracellular Matrix Proteins↗
PubMed1998

Ki67 expression in lichen sclerosus of vulva in patients with and without associated squamous cell carcinoma.

AIMS: To investigate the malignant potential of lichen sclerosus, a study using the cell proliferation marker Ki67 comparing lichen sclerosus with and without associated squamous cell carcinoma was performed. METHODS AND RESULTS: Formalin-fixed, paraffin-embedded slides of 13 cases of lichen sclerosus with associated carcinoma, and 31 cases without associated carcinoma, including 16 random cases, seven with epidermal thickening and eight with epidermal thinning, were examined by the immunoperoxidase technique for Ki67, a cell proliferation marker. Ki67 reactivity was mostly seen in the basal and parabasal cells in both groups of lichen sclerosus and this pattern was similar to normal skin, squamous cell hyperplasia and analogous to that of one form of squamous cell carcinoma. There was a mean of 50 Ki67 positive cells per 100 basal cells in lichen sclerosus with associated squamous cell carcinoma; however, in squamous cell hyperplasia adjacent to carcinoma this rose to 90 Ki67 positive cells per 100 basal cells. In lichen sclerosus without associated carcinoma, the random cases had a count of 53 per 100 basal cells, those with epidermal thickening 53 and those with thinning 42. Non-genital normal skin had a count of 71 per 100 basal cells. CONCLUSION: The lack of qualitative differences of Ki67 expression in normal skin, in lichen sclerosus with and without carcinoma, in squamous cell hyperplasia and in one form of squamous cell carcinoma indicates that these conditions share a common localized pattern of cell proliferation and does not support or deny the malignant potential of lichen sclerosus. The higher Ki67 count in squamous cell hyperplasia adjacent to carcinoma could indicate premalignancy or a reaction to the carcinoma. In patients without carcinoma, the higher Ki67 count in thickened lichen sclerosus compared to thinned suggests that some or all of the cases of thickened lichen sclerosus were lichen sclerosus with squamous cell hyperplasia or that lichen simplex chronicus superimposed on lichen sclerosus has a higher Ki67 expression or that the distinction between squamous cell hyperplasia and lichen simplex chronicus is only one of terminology.

Basal Cell Carcinoma↗
PubMed2001

Major fungal lineages are derived from lichen symbiotic ancestors.

About one-fifth of all known extant fungal species form obligate symbiotic associations with green algae, cyanobacteria or with both photobionts. These symbioses, known as lichens, are one way for fungi to meet their requirement for carbohydrates. Lichens are widely believed to have arisen independently on several occasions, accounting for the high diversity and mixed occurrence of lichenized and non-lichenized (42 and 58%, respectively) fungal species within the Ascomycota. Depending on the taxonomic classification chosen, 15-18 orders of the Ascomycota include lichen-forming taxa, and 8-11 of these orders (representing about 60% of the Ascomycota species) contain both lichenized and non-lichenized species. Here we report a phylogenetic comparative analysis of the Ascomycota, a phylum that includes greater than 98% of known lichenized fungal species. Using a Bayesian phylogenetic tree sampling methodology combined with a statistical model of trait evolution, we take into account uncertainty about the phylogenetic tree and ancestral state reconstructions. Our results show that lichens evolved earlier than believed, and that gains of lichenization have been infrequent during Ascomycota evolution, but have been followed by multiple independent losses of the lichen symbiosis. As a consequence, major Ascomycota lineages of exclusively non-lichen-forming species are derived from lichen-forming ancestors. These species include taxa with important benefits and detriments to humans, such as Penicillium and Aspergillus.

Ascomycota↗
PubMed2006

[Lichen sclerosus in urological practice].

UNLABELLED: Lichen sclerosus in urological practice. INTRODUCTION: Lichen sclerosus is a sclerosing, inflammatory skin disease with unknown origin which causes secondary phimosis of the foreskin and stricture of the urethra. In the case of long term existence of it the prevalence of intraepithelial squamous cell neoplasia is increased. AIM: To identify the role of lichen sclerosus in adulthood phimosis and to categorize urological treatment. To define the proper therapy of lichen sclerosus, causing meatal and urethral stricture. To measure the incidence of lichen sclerosus in patients with squamous cell neoplasia. METHOD: There was looked the incidence of lichen sclerosus in patient suffering with phimosis, recurrent urethral stricture, therapeutical options and presence of lichen sclerosus in patient with penile squamous cell neoplasia. RESULTS: There were 123 foreskins sent for histological examination from 624 patients operated with circumcision in the last 5 years in the clinic. There were 76 (62%) times lichen sclerosus justified in 123 foreskins. There were lichen sclerosus found in 90% (9/10) of excised tissues of recurrent urethral strictures. There were lichen sclerosus noticed in 3 of 10 (33%) penile squamous cell carcinoma slides. CONCLUSIONS: Lichen sclerosus can be detected in significant proportion of phimosis in adulthood. Lichen sclerosus can be found very often as the cause of recurrent urethral strictures, which takes necessary to perform 2 steps reconstructive operation with complete excision of the urethra and buccal graft emplacement. In the third of our all squamous cell carcinoma cases lichen sclerosus could be histologically shown, which give good reason for the opportunity of malignant disease development of this dermatological illness.

Carcinoma, Squamous Cell↗
PubMed2002

Vertical evolution and intragenic spread of lichen-fungal group I introns.

One family within the Euascomycetes (Ascomycota), the lichen-forming Physciaceae, is particularly rich in nuclear ribosomal [r]DNA group I introns. We used phylogenetic analyses of group I introns and lichen-fungal host cells to address four questions about group I intron evolution in lichens, and generally in all eukaryotes: 1) Is intron spread in the lichens associated with the intimate association of the fungal and photosynthetic cells that make up the lichen thallus? 2) Are the multiple group I introns in the lichen-fungi of independent origins, or have existing introns spread into novel sites in the rDNA? 3) If introns have moved to novel sites, then does the exon context of these sites provide insights into the mechanism of intron spread? and 4) What is the pattern of intron loss in the small subunit rDNA gene of lichen-fungi? Our analyses show that group I introns in the lichen-fungi and in the lichen-algae (and lichenized cyanobacteria) do not share a close evolutionary relationship, suggesting that these introns do not move between the symbionts. Many group I introns appear to have originated in the common ancestor of the Lecanorales, whereas others have spread within this lineage (particularly in the Physciaceae) putatively through reverse-splicing into novel rRNA sites. We suggest that the evolutionary history of most lichen-fungal group I introns is characterized by rare gains followed by extensive losses in descendants, resulting in a sporadic intron distribution. Detailed phylogenetic analyses of the introns and host cells are required, therefore, to distinguish this scenario from the alternative hypothesis of widespread and independent intron gains in the different lichen-fungal lineages.

Ascomycota↗
PubMed2003

Are lichens active under snow in continental Antarctica?

Photosynthetic activity, detected as chlorophyll a fluorescence, was measured for lichens under undisturbed snow in continental Antarctica using fibre optics. The fibre optics had been buried by winter snowfall after being put in place the previous year under snow-free conditions. The fibre optics were fixed in place using specially designed holding devices so that the fibre ends were in close proximity to selected lichens. Several temperature and PPFD (photosynthetic photon flux density) sensors were also installed in or close to the lichens. By attaching a chlorophyll a fluorometer to the previously placed fibre optics it proved possible to measure in vivo potential photosynthetic activity of continental Antarctic lichens under undisturbed snow. The snow cover proved to be a very good insulator for the mosses and lichens but, in contrast to the situation reported for the maritime Antarctic, it retained the severe cold of the winter and prevented early warming. Therefore, the lichens and mosses under snow were kept inactive at subzero temperatures for a prolonged time, even though the external ambient air temperatures would have allowed metabolic activity. The results suggest that the major activity period of the lichens was at the time of final disappearance of the snow and lasted about 10-14 days. The activation of lichens under snow by high air humidity appeared to be very variable and species specific. Xanthoria mawsonii was activated at temperatures below -10 degrees C through absorption of water from high air humidity. Physcia dubia showed some activation at temperatures around -5 degrees C but only became fully activated at thallus temperatures of 0 degrees C through liquid water. Candelariella flava stayed inactive until thallus temperatures close to zero indicated that liquid water had become available. Although the snow cover represented the major water supply for the lichens, lichens only became active for a brief time at or close to the time the snow disappeared. The snow did not provide a protected environment, as reported for alpine habitats, but appeared to limit lichen activity. This provides at least one explanation for the observed negative effect of extended snow cover on lichen growth.

Adaptation, Physiological↗
PubMed2004

Lichen palatability depends on investments in herbivore defence.

Lichens are well-suited organisms for experimental herbivory studies because their secondary compounds, assumed to deter grazing, can be non-destructively extracted. Thalli of 17 lichen species from various habitats were cut in two equal parts; compounds were extracted from one part by acetone, the other served as a control. These two pieces were offered as a paired choice to the generalist herbivore snail Cepaea hortensis. Control thalli of all lichens were consumed at a low rate regardless of their investments in acetone-extractable lichen compounds; naturally compound-deficient lichen species were not preferred compared to those with high contents. However, for extracted thalli, there was a highly significant positive correlation between rate of consumption and the extracted compound contents. These data imply that herbivore defence has evolved in different directions in different lichens. Studied members of Parmeliaceae, common in oligotrophic habitats, have high contents of carbon-rich acetone-soluble compounds; these lichens became highly palatable to snails subsequent to acetone rinsing. Extracted lichen compounds were applied to pieces of filter paper and fed to snails. Extracts from members of the Parmeliaceae significantly deterred feeding on paper. Such data suggest that generalist herbivores may have shaped evolution in the widespread and highly diverse Parmeliaceae towards high investments in lichen compounds. On the other hand, lichens belonging to the Physciaceae and Teloschistales, common in nutrient-enriched habitats, are deficient in, or have low concentrations of, lichen compounds. Such lichens did not become more palatable after acetone rinsing. The orange anthraquinone compound parietin, restricted to the Teloschistales, and which has previously been found to protect against excess light, did not deter grazing.

Acetone↗
PubMed2005

On monitoring anthropogenic airborne uranium concentrations and (235)U/(238)U isotopic ratio by Lichen - bio-indicator technique.

Lichens are widely used to assess the atmospheric pollution by heavy metals and radionuclides. However, few studies are available in publications on using lichens to qualitatively assess the atmospheric pollution levels. The paper presents research results applying epiphytic lichens as bio-monitors of quantitative atmospheric contamination with uranium. The observations were conducted during 2.5 years in the natural environment. Two experimental sites were used: one in the vicinity of a uranium contamination source, the other one - at a sufficient distance away to represent the background conditions. Air and lichens were sampled at both sites monthly. Epiphytic lichens Hypogimnia physodes were used as bio-indicators. Lichen samples were taken from various trees at about 1.5m from the ground. Air was sampled with filters at sampling stations. The uranium content in lichen and air samples as well as isotopic mass ratios (235)U/(238)U were measured by mass-spectrometer technique after uranium pre-extraction. Measured content of uranium were 1.45 mgkg(-1) in lichen at 2.09 E-04 microgm(-3) in air and 0.106 mgkg(-1) in lichen at 1.13 E-05 microgm(-3) in air. The relationship of the uranium content in atmosphere and that in lichens was determined, C(AIR)=exp(1.1 x C(LICHEN)-12). The possibility of separate identification of natural and man-made uranium in lichens was demonstrated in principle.

Air Pollutants, Radioactive↗
PubMed2002

Overexpression of wild-type p53 in lichen sclerosus adjacent to human papillomavirus-negative vulvar cancer.

Human papillomavirus is a risk factor for vulvar cancer, whereas human papillomavirus-negative late onset vulvar carcinoma is associated with the dermatologic condition, lichen sclerosus. Human papillomavirus E6 protein targets TP53 for degradation and by inference it has been assumed that human papillomavirus-negative vulvar cancer is dependent upon the acquisition of p53 somatic mutations and subsequent allelic loss. To investigate this, TP53 expression, loss of heterozygosity, and p53 genomic sequence were examined in 29 cases of human papillomavirus-negative vulvar carcinoma with adjacent lichen sclerosus. We examined 37 cases of lichen sclerosus without vulvar carcinoma, 10 cases of nongenital lichen sclerosus, and 12 cases of normal vulvar epithelium served as controls. TP53 was evident in 72% of vulvar carcinoma, 48% in epithelium adjacent to vulvar carcinoma, but was minimal in normal samples. When lichen sclerosus cases were selected to exclude samples with absolutely no TP53 expression through probable failed antigen retrieval or homozygous p53 loss the number of epithelial cells expressing TP53 increased progressively from nongenital lichen sclerosus to lichen sclerosus without vulvar carcinoma, then to lichen sclerosus with vulvar carcinoma (p<0.0001). These data suggest elevated TP53 is a feature of vulvar lichen sclerosus. Seventy-four percent of vulvar carcinoma had chromosome 17p-linked loss of heterozygosity, whereas 47% of adjacent lichen sclerosus featured loss of heterozygosity, but only 31% of vulvar carcinoma had p53 mutations, a frequency less than reported previously. Seven percent of adjacent lichen sclerosus had mutations, showing for the first time the presence of an identical mutation to the matched vulvar carcinoma. These data, however, implicate p53 mutations as a later event in vulvar carcinoma and in marked contrast to the original expectation, our loss of heterozygosity data are consistent with loss of another locus (not p53) on 17p operating as a tumor suppressor in lichen sclerosus destined to develop vulvar carcinoma.

Carcinoma, Squamous Cell↗