Expression Profile of CD10, BCL-2, p63, and EMA in the Normal Skin and Basal Cell Carcinomas: An Immunohistochemical Reappraisal

BackgroundBasal cell carcinoma (BCC) is common cutaneous malignancy.AimsTo examine the expression patterns of CD10, p63, BCL-2, and epithelial membrane antigen (EMA) proteins in BCC.Materials and methodsWe used immunohistochemistry to evaluate the expression pattern of these proteins in 45 BCC specimens and their adjacent normal skin.ResultsWe found variations in the expression pattern of these proteins among normal skins and BCC. In normal skins, we found strong EMA cytoplasmic expression (adnexal structures). A strong nuclear p63 protein expression was found in basal and some suprabasal keratinocytes, external root sheath cells of the hair follicles, basal cells of the sebaceous glands, and in sweat glands.CD10 protein expression was seen in peri-adnexal mesenchymal spindle cells and myoepithelial cells of sweat glands.BCL-2 protein expression was confined to the basal cell keratinocytes, epidermal melanocytes, outer root sheath, and infundibulum of the hair follicle. In BCC, we found p63 (diffuse, strong nuclear staining), CD10 (focal, moderate cytoplasmic reactivity), and BCL-2 (focal, moderate cytoplasmic reactivity) protein expression in the neoplastic cells. BCC was consistently negative for EMA (except in areas of squamous differentiation).ConclusionsThere is an altered expression of these proteins in BCC. The underlying molecular mechanisms are open to further investigations.     

[Artículo traducido] Perfil de expresión de CD10, BCL-2, p63 y EMA en los carcinomas normales de piel y de células basales: Revaloración inmunohistoquímica

BackgroundBasal cell carcinoma (BCC) is common cutaneous malignancy.AimsTo examine the expression patterns of CD10, p63, BCL-2, and epithelial membrane antigen (EMA) proteins in BCC.Materials and methodsWe used immunohistochemistry to evaluate the expression pattern of these proteins in 45 BCC specimens and their adjacent normal skin.ResultsWe found variations in the expression pattern of these proteins among normal skins and BCC. In normal skins, we found strong EMA cytoplasmic expression (adnexal structures). A strong nuclear p63 protein expression was found in basal and some suprabasal keratinocytes, external root sheath cells of the hair follicles, basal cells of the sebaceous glands, and in sweat glands.CD10 protein expression was seen in peri-adnexal mesenchymal spindle cells and myoepithelial cells of sweat glands.BCL-2 protein expression was confined to the basal cell keratinocytes, epidermal melanocytes, outer root sheath, and infundibulum of the hair follicle. In BCC, we found p63 (diffuse, strong nuclear staining), CD10 (focal, moderate cytoplasmic reactivity), and BCL-2 (focal, moderate cytoplasmic reactivity) protein expression in the neoplastic cells. BCC was consistently negative for EMA (except in areas of squamous differentiation).ConclusionsThere is an altered expression of these proteins in BCC. The underlying molecular mechanisms are open to further investigations.     

皮肤鳞癌中p63表达和巨噬细胞反应的研究

采用免疫组化（Labelled streptravidin biotin,LSAB)方法研究60例皮肤鳞癌（SSCC）中p63的表达和CD68阳性的巨噬细胞反应，在原位观察其与SSCC增值、分化的关系。结果表明在正常表皮、毛囊中p63主要表达在具有增生潜能的基底层细胞，在终未分化的角质形成细胞中缺如。高分化癌中p63呈环状分布于癌巢周围，低分化癌中p63阳性细胞增多，分布紊乱。巨噬细胞规律性地分布于活路增殖的癌巢边缘区。本文结果提示SSCC分化程度越低p63表达强，而巨噬细胞浸润的量与SSCC分化呈反相关。癌中p63的表达越高癌周巨噬细胞反应减少。在SSCC中由p63过表达的癌细胞可能是更具增殖、侵袭和间变能力的细胞类型。     

中波紫外线对体外培养皮肤干细胞某些标记分子表达的影响

目的 探讨中波紫外线（UVB）对体外培养皮肤干细胞某些标记分子表达的影响。方法 利用快速贴壁法分离、培养皮肤干细胞,K15、β-连环素鉴定皮肤干细胞。利用峰值在305 nm的UVB照射皮肤干细胞,照射剂量为10 mJ/cm2。用免疫组化法分别检测经照射组与对照组皮肤干细胞CD34、β-连环素、p53的表达变化。结果 未经UVB照射的皮肤干细胞密度大,细胞呈圆形或多角形,细胞形态清晰,胞质均匀,可见有核分裂细胞,核质比例大。β-连环素主要在细胞膜和细胞质表达,其胞膜和胞核染色阳性率分别为64.74%和8.4%;p53主要在胞质表达,其胞核染色阳性率为6.9%。UVB照射后的细胞密度稀,细胞变形、不规则,胞质出现空泡,核质比例变小,部分细胞出现核固缩和凋亡。β-连环素主要在细胞质和细胞核表达,其胞膜和胞核染色阳性率分别为64.74%和0;p53主要在细胞核表达,其胞核染色阳性率为100%。CD34在两种情况下均不表达。结论 UVB能使CD34阴性皮肤干细胞β-连环素在细胞质聚集并移入细胞核,p53可定位于皮肤干细胞的细胞质,经UVB照射后可移入细胞核。     

Expression of sex-determining genes in the scalp of men with androgenetic alopecia

BACKGROUND: The regulation of the cutaneous steroidogenesis in patients with androgenetic alopecia remains largely unclear. OBJECTIVE: The purpose of this study was to quantify the expression of the sex-determining genes in different scalp areas. METHODS: Paired scalp specimens from frontal and occipital scalp areas of 10 patients were examined by real-time RT-PCR for mRNA expression and of 40 patients (mean age 34.9 years, range 22-58) by Western blotting for protein analysis. RESULTS: The SOX-9 mRNA was most abundant in the skin, while SF-1 mRNA was sparsely detected. The protein levels of DAX-1, SRY and WT-1 were significantly higher in the bald scalp (p=0.003, 0.004 and 0.03, respectively). Only the SRY expression showed a positive correlation with the baldness severity in Norwood-Hamilton classification (p=0.024). There was no association between patient's age and the protein levels. Immunostaining of SOX-9 was detected in the outer root sheath keratinocytes of hair follicles but not in the dermal papillae. CONCLUSION: Further study on a larger population, including normal subjects and female patients, is needed to confirm the pathogenic role of sex-determining genes in androgenetic alopecia.     

Centrifugal lipodystrophy of the scalp manifesting as centrifugal lipodystrophic alopecia

Centrifugal lipodystrophy (CLD), characterized by a depressed lesion in the abdominal skin, is a chronic disease occurring more often among younger patients of East Asian descent. We present an extremely unusual case of CLD of the scalp associated with reversible hair loss. The patient demonstrated alopecia in the frontal, temporal and occipital areas of the scalp, which connected to form a ring‐shaped area of hair loss. Curiously, the area of hair loss gradually expanded outwards while the central region showed normal hair regrowth. Immunohistochemical analysis demonstrated reduced expression of leptin, an adipokine capable of inducing the anagen phase of the hair cycle, in the adipose tissue, associated with active inflammation. By contrast, recovery of leptin expression was observed at sites of healed inflammatory lesions, suggesting that reversible hair loss might be caused by a change in leptin expression in adipose tissue.     

Significant relationship between temporal hair loss and other scalp areas in female pattern hair loss

Female pattern hair loss affects the central scalp, sparing the frontal hairline. The temporal area can also be affected by hair loss. We investigated the degree of temporal hair loss and correlation of other sites of scalp hair loss in Korean female pattern hair loss patients. A total of 109 women with female pattern hair loss were enrolled in this retrospective analysis. We measured hair density and thickness in five scalp sites including the frontal, vertex, occipital and bilateral temporal areas by phototrichogram. Frontal and vertex area hair loss were classified according to the Basic and Specific (BASP) classification, and temporal scalp and occiput areas were also assessed. Eighty-nine patients showed temporal hair loss. The mean of the hair density was lowest in the temporal area among all scalp areas. Total and thick hair densities of the frontal scalp were correlated with those of the vertex, temporal scalp and occiput in descending order, and hair thickness of the frontal scalp was more related with that of the temporal scalp than the vertex. In this study, temporal involvement is evident in female pattern hair loss. We suggest that temporal involvement should be added to pattern hair loss classification, especially BASP classification.     

Acute telogen effluvium triad after resolution

Five cases of telogen effluvium undergoing resolution are shown, with the presence of frontal, bitemporal, and occipital hair regrowth. Diagnosing acute telogen effluvium after the end of the active phase can be challenging, especially when the pull test is negative. The differential diagnosis includes alopecia areata and traction alopecia. Clinical signs of hair regrowth after telogen effluvium can help in the diagnosis. The frontal and temporal areas have more telogen hairs and are more affected. On the occipital area, hairs seem to have the same behavior. The acute telogen effluvium triad during resolution is proposed: frontal fringe, temporal recess and occipital fringe.     

Changes in telogen rate, hair density, hair diameter and rate of growth in androgenetic alopecia of the male. Simultaneously a contribution to the significance of dysplastic hair

In a pilot study, comparative measurements of frontal and occipital trichograms, hair density, hair diameter and hair growth rate were performed on 26 male volunteers (ages 20-33 years) with androgenetic alopecia between stages II and V (Norwood scale). In the frontal region, the proportion of telogen hair was, in general, pathologically higher and increased according to stage. The density of the frontal hair was significantly lower (166 +/- 28/cm2) compared with that of the occipital region (193 +/- 24/cm2) and decreased according to stage. The average hair diameter in the higher Norwood stages decreased similarly in both the frontal and occipital regions, as shown by the correspondence between the two measurement points (frontal, 0.068 +/- 0.011 mm; occipital, 0.069 +/- 0.010 mm). Anagen and dysplastic hair from both the frontal and occipital regions was significantly thicker than telogen hair (0.07 mm vs 0.05 mm). The frontal growth rate (0.355 +/- 0.024 mm/day) was significantly lower than that of the occipital region (0.389 +/- 0.021 mm/day). In addition, the frontal growth rate decreased according to stage. Dysplastic hair exhibited high growth rates and diameters similar to those of typical anagen hair. In our opinion, dysplastic hair is growing hair, the roots of which have been artificially modified by plucking. - These intra-individual comparisons of frontal and occipital regions showed a reduction in the anagen phase, density, diameter and growth rate of the endangered frontal hair. A reduction in the size and dividing activity of the matrix is indicated by our data. It seems that these regressive changes occur primarily without a prior indication of accelerated hair growth.     

Expression of Ras homologous B protein in the human scalp skin and hair follicles: hair follicle cycle stages‐associated changes

Background: RhoB belongs to the Ras homologous (Rho) subfamily which consists of low molecular weight mass GTP‐binding proteins. Rho proteins are regulatory molecules that mediate changes in cell shape, contractility, motility and gene expression. Aim: To test the hypothesis that ‘RhoB protein is expressed in the human skin and its expression undergoes hair follicle cycle dependent changes'. To test this hypothesis, we examined the expression of RhoB in the normal human skin and hair follicles (HFs) using immunohistochemical methods. Methods: A total of 50 normal human scalp skin specimens were obtained from 50 females (age: 53–57 years) undergoing elective cosmetic plastic surgery. The specimens were obtained from both frontal and temporal regions of the scalp. A total of 50 HF, (35 anagen, 10 catagen and 5 telogen) were examined in each case using immunohistologic staining methods. Semiquantitative analysis was done. Results: RhoB protein was strongly expressed in the various elements of the human scalp skin and hair follicles. In the epidermis, a moderate RhoB immunoreactivity was found in all layers except stratum corneum where RhoB protein was completely absent. In sebaceous glands, a strong RhoB immunoreactivity was detected in all sebaceocytes. In the hair follicles, the expression of RhoB protein showed hair follicle cycle stages‐associated changes, i.e. strong expression during anagen, but weak and completely absent expressions during catagen and telogen phases, respectively. Semiquantitative analysis revealed statistically significant high expression values (staining intensity, percentage of positive cells and immunoreactivity scores) in the anagen VI hair follicles compared to either cantagen or telogen ones (p < 0.05). Similarly, RhoB protein expression was significantly high in the stratum basale, stratum spinosum and sebaceous glands compared to stratum granulosum (p < 0.05). Conclusions: Here we report, for the first time, the distribution of RhoB protein in the human scalp skin and hair follicles. We also provide the first indication that there are variations in the expression of this protein in the different stages of the hair cycle. Adly M.A, Assaf H.A, Hussein M.R.A. Expression of Ras homologous B protein in the human scalp skin and hair follicles: hair follicle cycle stages‐associated changes     

Proliferation, DNA repair and apoptosis in androgenetic alopecia

Background   Androgenetic alopecia is a common hair disorder, resulting from interplay of genetic, endocrine and ageing factors. Meanwhile, it is unclear if an altered degree of proliferation or increased apoptosis could contribute to its pathogenesis.
Objective   To evaluate the role of proliferation, DNA damage and apoptosis in the pathogenesis of androgenetic alopecia.
Methods   Thirty biopsies were taken from the frontal (bald) area and occipital (hairy) area of 15 male patients with androgenetic alopecia, as well as five specimens from frontal area of five age-matched controls. These specimens were used for immunohistochemical staining of cell proliferation [proliferating cell nuclear antigen (PCNA)] and DNA repair markers (XRCC1, APE1, PARP-1) as well as apoptosis regulatory protein p53.
Results   The frontal bald area of patients showed significantly higher levels of X-ray Cross Complementing-1 (XRCC1; P  < 0.001) and p53 ( P  < 0.001) expression when compared with occipital hairy area of patients and frontal area of controls ( P  = 0.003 and 0.04, respectively). On the other hand, there were significantly lower expression of PCNA ( P  < 0.001) and apurinic/apyridinic endonuclease 1 (APE1; P  = 0.001 and 0.02) when compared with the frontal area of controls and occipital area of patients, respectively. Meanwhile, APE1 showed significant inverse correlation with p53 overexpression ( P  = 0.03).
Conclusion   The frontal bald area of patients with androgenetic alopecia has lower proliferation rate that result in follicular miniaturization. There is increased DNA damage that would be beyond the capacity of cells to repair in advanced cases. An alternative pathway would take place in order to eliminate the damaged cells through apoptosis.     

Phototrichogram findings in women with androgenetic alopecia

BACKGROUND/PURPOSE: Androgenetic alopecia (AGA) in women is characterized by diffuse thinning in the frontal and parietal areas of the scalp; preservation of the frontal hairline is norm. Hair over the occipital scalp is preserved. The purpose of this work was to investigate the findings of phototrichogram (PTG) of the affected and the spared areas in women with AGA and to compare them with those of healthy subjects. METHODS: Twenty-two controls and 60 untreated women with AGA (32 with Ludwig I, 28 with Ludwig II) were included in this study. Hair density, percentages of thin hair, and non-growing hair were estimated both on the midscalp and on the occiput by using PTG with digital camera attached to a dermoscope. RESULTS: In the control group, hair density was higher on the midscalp than the occiput. In AGA groups, hair density was lower on the midscalp than the occiput and percentages of thin hair and non-growing hair were higher on the midscalp than the occiput. These findings were more prominent in Ludwig II group. In the occiput there were findings mimicking the changes seen on the midscalp. These were less striking than those seen on the midscalp yet the difference between the control and Ludwig II group was statistically significant. CONCLUSION: We concluded that the hair is not equally distributed on the scalp, the occiput may be affected in females with AGA and further studies are necessary to support these findings.     

Association of p53 Arg72Pro polymorphism and beta-catenin accumulation in mycosis fungoides

BACKGROUND: Aberrant activation of beta-catenin contributes to the onset of a variety of tumours. There are many tumours that display beta-catenin accumulation in the absence of mutations in its gene. Recently, abnormal accumulation of wild-type beta-catenin has been associated with mutational inactivation of the p53 tumour suppressor. OBJECTIVES: To investigate the potential role of p53 and its homologue p63 in beta-catenin deregulation and to correlate this with disease outcome. METHODS: We analysed a panel of 24 samples of mycosis fungoides (MF), the most frequent manifestation of cutaneous T-cell lymphoma (CTCL), for beta-catenin, p53 and p63 protein expression by immunohistochemistry. Based on the immunostaining results for beta-catenin protein, 11 positive cases were selected for laser microdissection, genomic DNA isolation and subsequent mutation analysis of beta-catenin exon 3 and p53 exons 4-8. RESULTS: Our findings revealed overexpression of beta-catenin, p53 and p63 in 46%, 38% and 17% of cases, respectively. The number of p53-positive cases of MF was significantly higher (P < 0.05) in the beta-catenin-positive group (73%). Sequence analysis demonstrated that wild-type beta-catenin accumulation in MF is not associated with mutational inactivation of the p53 gene and, more importantly, our data provide evidence that a common polymorphic form of p53 (Arg72Pro) is significantly associated with beta-catenin overexpression (P < 0.05). No significant differences in the three genotypes were observed between the CTCL cases and the control group, demonstrating that Arg72Pro polymorphism of the p53 gene is not associated with the risk of developing cutaneous lymphomas (P > 0.05). CONCLUSIONS: We found an association of beta-catenin and p53 overexpression without detection of structural alteration in the genes, suggesting that p53 mutation is not an important mechanism for beta-catenin activation in primary CTCL. Additionally, we speculate that the p53 codon 72 polymorphism may influence negative feedback control involving beta-catenin and p53.     

p63 expression in normal human epidermis and epidermal appendages and their tumors

BACKGROUND: p63, a member of the p53 gene family, is expressed in basal cells of several different organs. METHODS: The immunoreactivity of p63 was examined in normal human epidermis and epidermal appendages and their tumors, and compared with proliferative activity as evaluated by Ki-67. RESULTS: In normal skin, p63 expression was seen in basal/suprabasal cells of the epidermis, outer root sheath and hair matrix cells of the hair follicle, seboblast situated in the outermost layer of sebaceous glands, and outer layer cells of the ductal portion and myoepithelial cells of the secretory portion of the sweat glands. p63 expression was confined to the cells forming a continuous basal rim along the normal epithelial structure. In tumors, p63 expression resembled that in normal tissue in that tumor components originating from p63-positive cells were constantly positive for p63. In normal and tumor tissues, not all p63-positive cells were positive for Ki-67. CONCLUSIONS: p63 expression may be a marker of basal/progenitor cells in tumors of epidermis and epidermal appendages, and may be a diagnostic marker of these tumors.     

Expression of vascular endothelial growth factor, apoptosis inhibitors (survivin and p16) and CCL27 in alopecia areata before and after diphencyprone treatment: an immunohistochemical study

BACKGROUND: Alopecia areata (AA) is a relatively common inflammatory form of nonscarring hair loss of unknown pathogenesis, but possibly of autoimmune origin. Topical immunotherapy, using a potent contact allergen such as diphencyprone (DPC), is currently considered the most effective mode of treatment. However, the way in which DPC operates on hair follicles in AA still remains to be elucidated. Vascular endothelial growth factor (VEGF), essential for angiogenesis and vascular permeability, may be responsible for maintaining proper vasculature around hair follicles, and several studies provide evidence that apoptosis is a central element in the regulation of hair follicle and vascular regression. The cutaneous lymphocyte-associated antigen (CLA) and the skin-associated chemokine CCL27 highlight an important role for epithelial cells in controlling homeostatic lymphocyte trafficking. OBJECTIVES: To determine the expression pattern of VEGF, factor (F)VIII, survivin, p16, CD4, CD8, CLA and CCL27 in alopecic skin before and after treatment with DPC. Methods Immunohistochemical staining methods were applied to skin biopsy specimens obtained from alopecic areas of 14 patients before and after DPC treatment and from five healthy subjects. Sections were incubated with monoclonal antibodies against VEGF, FVIII, survivin, p16, CCL27, CLA, CD4 and CD8, and their immunohistochemical expression was evaluated by light microscopy. RESULTS: The intensity of VEGF staining in alopecic human hair follicles was significantly lower than in healthy scalp tissue. FVIII immunostaining showed a significantly reduced development of the microvasculature in AA in comparison with healthy scalp tissue. After DPC therapy, cells of alopecic hair follicles showed a significant increase of VEGF immunopositivity, and the number of capillary vessels expressing FVIII was markedly increased in comparison with untreated scalp tissue. The increase in microvessels was associated with strong survivin expression in endothelial cells after treatment. All alopecic specimens showed expression of p16 in the hair follicle outer root sheath (ORS), with a significant increase after therapy. After treatment we observed a significantly decreased number of CD4+ cells and an increase of CD8+ cells (CD4/CD8 ratio 0.85) in alopecic skin compared with untreated scalp tissue (CD4/CD8 ratio 3.45). Most of the T lymphocytes found in inflammatory skin lesions expressed CLA antigen and after therapy we observed a significantly higher CLA positivity in hair follicles (50% or more) in comparison with untreated alopecic scalp tissue. Alopecic patients showed a CCL27 immunopositivity significantly lower than in normal scalp tissue. After DPC therapy the labelling intensity for CCL27 showed a significant increase both in the ORS and in the inner root sheath; similarly, in the basal interfollicular keratinocytes we observed a moderate increase in CCL27 expression. CONCLUSIONS: Topical immunotherapy exerts an important role in angiogenesis, upregulating VEGF in human hair follicle keratinocytes and upregulating survivin to preserve endothelial cell viability. Moreover, it considerably alters the peribulbar CD4/CD8 ratio, restoring a condition close to normal scalp skin. Our study could contribute to explaining some aspects of AA pathogenesis that are still unknown and aid understanding of how DPC could act in this complex disease.     

表皮p63和CD44与年龄及曝光部位的相关性

目的 探讨p63与CD44在皮肤衰老过程中与年龄、紫外线的关系。方法 采用免疫组化方法检测121例正常全厚皮肤标本中p63与CD44的表达,光镜下观察并计算表皮基底层p63阳性细胞百分比,用图像分析软件image proplus 6.0测量表皮层p63与CD44表达的吸光度值。结果 ①表皮基底层p63阳性细胞百分比与年龄呈负相关（r = -0.218,P < 0.05）,51 ~ 79岁组最低;但在曝光部位、半曝光部位与非曝光部位间的差异无统计学意义。②表皮p63的表达强度与年龄在曝光部位呈负相关（r = -0.389,P = 0.010）,在半曝光部位无相关性,在非曝光部位呈正相关（r = 0.341,P < 0.05）;三个部位表达强度的差异在10 ~ 30岁组无统计学意义,在31 ~ 50岁组与51 ~ 79岁组由强至弱依次为非曝光部位、半曝光部位、曝光部位。③表皮CD44的表达强度与年龄之间呈微弱负相关（r = -0.083,P < 0.05）,10 ~ 30岁组最高;但在曝光部位、半曝光部位与非曝光部位间的差异无统计学意义。结论 表皮基底层p63阳性细胞百分比、表皮CD44的表达强度和年龄呈负相关,和紫外线照射量无关。表皮p63表达强度在31 ~ 50岁组与51 ~ 79岁组的表达强度依曝光多少而递减。     

Caveolin-1 is expressed on multipotent cells of hair follicles and might be involved in their resistance to chemotherapy

BACKGROUND: Caveolin-1 is the principal protein that composes caveolae, which are vesicular invaginations present on the plasma membrane of different cell types. Caveolae are involved in a variety of cellular functions including regulation of proliferation rate and resistance to chemotherapeutic drugs. Chemotherapy frequently induces alopecia which is reversible most probably due to the low proliferative rate of hair follicle stem cells and due to the expression of proteins which confer resistance. OBJECTIVES: Using a specific animal model and immunohistochemistry, we analysed the expression of both caveolin-1 and the cell proliferation marker beta-catenin, at different stages of the hair follicle cycle, both before and after doxorubicin (DXR) -induced alopecia. METHODS: Seven-week-old C57BL/6 mice were depilated in order to synchronize hair follicle cycle in the anagen phase. Chemotherapy with DXR 15 mg kg(-1) was used to induce alopecia. Control and treated mice were then sacrificed at precise time points and caveolin-1 expression in hairs at different stages of the cycle were analysed by immunohistochemistry. By double immunofluorescence, colocalization of caveolin-1 and cytokeratin-15 was confirmed in the bulge region. The state of proliferation of cells composing hair follicle was assessed by beta-catenin immunohistochemistry. RESULTS: Caveolin-1 was expressed by the cells of the bulge area, the multipotent compartment of the hair follicle, during all phases of growth (anagen), regression (catagen) and resting (telogen). During the anagen phases, nuclear beta-catenin labelling was not observed in bulge cells, but rather in the deeper portion of the follicle. Damaged hair follicles from DXR-treated mice presented bulge cells which still expressed caveolin-1, suggesting that this protein might play a role in their drug resistance. As expected, no beta-catenin nuclear staining was detectable in DXR-treated hair follicles, indicating the complete lack of proliferative processes. The differential localization of caveolin-1 and beta-catenin suggests that the mutually exclusive expression of these proteins is useful for correct hair regrowth, whether during the physiological cycle or after chemotherapy-induced alopecia. CONCLUSIONS: Expression of caveolin-1 within the multipotent cell compartment of the hair follicle can explain the resistance of bulge cells to many chemotherapeutics, suggested by the reversibility of chemotherapy-induced alopecia.     

The expression of p63 in basal cell carcinomas and association with histological differentiation

BACKGROUND: We aim to examine p63 expression in basal cell carcinomas (BCCs) and to investigate association with their histopathological differentiation subtypes. METHODS: Eighty-four BCCs were classified according to the histopathologic differentiation subtypes. Immunohistochemistry using monoclonal antibody against p63 was performed. RESULTS: In nontumoral skin, p63 expression was consistently seen in basal/suprabasal cells of epidermis, hair matrix cells, and outer root sheath of the hair follicle. In BCCs, the cases were distributed as 47 undifferentiated, 28 differentiated (16 adenoid and 12 keratotic), and nine superficial. The nuclear p63 expression was negative in two cases, whereas 64 BCCs (76.2%) showed homogeneous p63 immunostaining. There was no statistically significant difference between p63 expression and histological differentiation subtypes (p > 0.05). The expression of p63 was found strongly and diffuse in 72.3% of solid undifferentiated and 82.1% differentiated and in 77.8% of superficial type BCCs. CONCLUSIONS: p63 is consistently expressed in epidermal basal/suprabasal and adnexal basal cells. Most BCCs have higher homogeneous p63 expression than nontumoral epidermis, which is not changed according to histological differentiation subtypes. Thus, overexpression of p63 in all histological subtypes may confirm that basaloid progenitor cells are linked tumor-cell lineage and have a role in the tumorigenesis of BCC.