Arch Dermatol Research Articles

The skin crease sign: A diagnostic sign of pilomatricoma

To the Editor: Pilomatricoma is a relatively common appendageal tumor that, despite well-described clinical features, is frequently misdiagnosed. 1 Julian C.G. Bowers P.W. A clinical review of 209 pilomatricomas. J Am Acad Dermatol. 1998; 39: 191-195 Abstract Full Text Full Text PDF PubMed Scopus (215) Google Scholar Most articles emphasize its histopathologic features. In most reported cases, the diagnosis was made retrospectively from the histopathologic findings and not from the clinical presentation. 2 Kleener J. Pilomatrixoma (epithelioma calcificans Malherbe). A clinical and histopathological survey of Danish material from 1954 to 1971. Acta Ophthalmol. 1973; 51: 692-699 Google Scholar , 3 Moehlenbeck F.W. Pilomatrixoma (calcifying epithelioma). A statistical study. Arch Dermatol. 1973; 108: 532-534 Crossref PubMed Scopus (220) Google Scholar

IgG Autoantibody Response against Keratinocyte Cadherins in Endemic Pemphigus Foliaceus (Fogo Selvagem)

It is well established that autoantibodies against desmoglein 3 and desmoglein 1 are relevant in the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including its endemic form, Fogo Selvagem (FS). Isolated reports have shown that in certain patients with these diseases, autoantibodies against other desmosomal cadherins and E-cadherin may also be present. The goal of this investigation was to determine if FS patients and normal individuals living in endemic areas possess autoantibodies against other desmosomal cadherins and E-cadherin. Testing a large number of FS and endemic control sera by ELISA we find a consistent and specific autoantibody response against desmoglein 1 and other keratinocyte cadherins in these individuals, which is quite different from US controls. Overall, the highest correlations among the autoantibody responses tested are in the endemic controls, followed by FS patients, and lowest in the US controls. These findings suggest that multiple, perhaps cross reactive, keratinocyte cadherins are recognized by FS patients and endemic controls.

Aggressive treatment of psoriasis associated with reduced MI risk

Nurse PrescribingVol. 10, No. 9 Research RoundupAggressive treatment of psoriasis associated with reduced MI riskMark GreenerMark GreenerSearch for more papers by this authorMark GreenerPublished Online:16 Aug 2013https://doi.org/10.12968/npre.2012.10.9.452AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Wu JJ, Poon KY, Channual JC et al. (2012) Association between tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. Arch Dermatol; advance online publication Crossref, Google Scholar FiguresReferencesRelatedDetails 1 September 2012Volume 10Issue 9ISSN (print): 1479-9189ISSN (online): 2052-2924 Metrics History Published online 16 August 2013 Published in print 1 September 2012 Information© MA Healthcare LimitedPDF download

Melanocortin 1 Receptor Function: Shifting Gears from Determining Skin and Nevus Phenotype to Fetal Growth

Variants in the MC1R gene influence skin pigmentation and thereby modulate risk of melanoma and basal and squamous cell carcinoma. In this issue, Kinsler et al. report an association between the MC1R genotype and the development of congenital melanocytic nevi. Further, higher birth weight was observed in carriers of MC1R variants, suggesting a role for the melanocortin network in fetal growth.

Amiodarone-induced facial pigmentation

British Journal of Hospital MedicineVol. 73, No. 8 Images in MedicineAmiodarone-induced facial pigmentationU Rao, A AgarwalU RaoSearch for more papers by this author, A AgarwalSearch for more papers by this authorU Rao; A AgarwalPublished Online:16 Aug 2013https://doi.org/10.12968/hmed.2012.73.8.473AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Karrer S, Hohenleutner U, Szeimies RM, Landthaler M (1999) Amiodarone-induced pigmentation resolves after treatment with the Q-switched ruby laser. Arch Dermatol 135: 251–3 Crossref, Medline, Google Scholar Kounis NG, Frangides C, Papadaki PJ, Zavras GM, Goudevenos J (1996) Dose-dependent appearance and disappearance of amiodarone-induced skin pigmentation. Clin Cardiol 19: 592–4 Crossref, Medline, Google Scholar FiguresReferencesRelatedDetailsCited byAmiodarone8 December 2012 | Reactions Weekly, Vol. 1431, No. 1 1 August 2012Volume 73Issue 8ISSN (print): 1750-8460ISSN (online): 1759-7390 Metrics History Published online 16 August 2013 Published in print 1 August 2012 Information© MA Healthcare LimitedPDF download

Diffuse skin hyperpigmentation in CD30+ lymphoproliferation

CD30+ T-cell lymphoproliferative disorders (LD) comprise two main groups of diseases: CD30+ LD of the skin and systemic anaplastic large cell lymphoma (ALCL). The main feature of these disorders is the expression of CD30. We present a patient with an unusual clinical presentation of CD30+ lymphoproliferative disease in a 54-year old Caucasian male who presented with generalized lymphadenopathy and pronounced skin hyperpigmentation. In the lymph nodes and skin, CD30+ lymphoproliferation (ALCL) was diagnosed. The Prussian blue staining identified that the pigment responsible for the skin color was hemosiderin. Chemotherapy was started but the patient’s condition progressively worsened and he died a week after the first cycle. The complete color transformation of the entire skin due to hemosiderin accumulation is, to the best of our knowledge, the first reported observation in a CD30+ lymphoproliferation/ALCL patient. We speculate that hemosiderin-loaded macrophages resulted from the paraneoplastic process by some still unknown mechanism.

Prevalence survey of dermatological conditions in mountainous north India

Dermatological conditions account for a substantial proportion of the global burden of disease in low and middle income countries (Bickers D, Lim H, Margolis D, et al. The burden of skin diseases: 2004. A joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. J Am Acad Dermatol 2006; 55: 490-500) and place major pressures on primary healthcare centers (Satimia F, McBride S, Leppard B. Prevalence of skin disease in rural Tanzania and factors influencing the choice of health care, modern or traditional. Arch Dermatol 1998; 134: 1363-1366). In mountainous North India, where limited resources are available for skin care, no dermatological data exists on prevalence, treatment patterns, or associations. The study aimed to measure prevalence and treatment of dermatological conditions and associated factors in Uttarakhand so to inform delivery of dermatological care and prevention programs in India. Single stage cluster randomized sampling generated seven cluster units or villages. Household members (n = 1275) from each cluster were interviewed, and where possible, examined and offered treatment. Dermatological conditions were prevalent (45.3%), with 33% being of infectious etiology. Atopic dermatitis (9.2%), scabies (4.4%), tinea corporis (4.1%), and pityriasis alba (3.6%) were most prevalent. Multivariate analysis showed that cohabitation with animals (OR = 1.62, 95% CI-1.35, 1.95) was a predictor of any skin diseases. A health practitioner was not consulted in 64.7% of dermatological conditions, and where consulted, approximately 69% received inappropriate or ineffective treatments. Excessive spending on dermatological care was commonplace. Limitations associated with cross-sectional cluster methodology included the underrepresentation of seasonal conditions and conditions of short duration. Caste proved difficult to randomize across clusters given villages were often composed according to caste. These results demonstrate a high prevalence of dermatological conditions and a pattern of conditions somewhat distinctive to this mountainous area of North India. These findings will assist development of appropriate and cost-effective dermatological services in these mountainous regions.

TCF/Lef1-Mediated Control of Lipid Metabolism Regulates Skin Barrier Function

Defects in the function of the skin barrier are associated with a wide variety of skin diseases, many of which are not well characterized at the molecular level. Using Lef1 (lymphoid enhancer-binding factor 1) dominant-negative mutant mice, we demonstrate here that altered epidermal TCF (T cell factor)/Lef1 signaling results in severe impairment of the stratum corneum skin barrier and early postnatal death. Barrier defects were accompanied by major changes in lipid composition and ultrastructural abnormalities in assembly and extrusion of lipid lamellae of the interfollicular epidermis, as well as abnormal processing of profilaggrin. In contrast, tight-junction formation and stratified organization of the interfollicular epidermis was not obviously disturbed in Lef1 mutant mice. Molecular analysis revealed that TCF/Lef1 signaling regulates expression of lipid-modifying enzymes, such as Elovl3 and stearoyl coenzyme A desaturase 1 (SCD1), which are key regulators of barrier function. Promoter analysis and chromatin immunoprecipitation experiments indeed showed that SCD1 is a direct target of Lef1. Together, our data demonstrate that functional TCF/Lef1 signaling governs important aspects of epidermal differentiation and lipid metabolism, thereby regulating skin barrier function.

Final Results of Phase II Trial of Pegylated Liposomal Doxorubicin (PLD) Followed by Bexarotene (Bex) in Advanced Cutaneous T-Cell Lymphoma (CTCL)

Abstract 882 Background:PLD is approved for treatment of Kaposi’s sarcoma and concentrates highly in the skin. Overall response (ORR: complete response [CR] + partial response [PR] rates) ranging from 56% to 88%, and CRs from 20% to 44% have been reported with PLD in CTCL patients (pts) without strictly defined response criteria (Cancer 2003; 98: 993–1001; Arch Dermatol 2008; 144: 727–33) Bex is a synthetic retinoid with an ORR of approximately 50% in relapsed/refractory CTCL (J Clin Oncol 2001; 19: 2456–71; Arch Dermatol 2001; 137: 581–93). To clarify the true ORR for PLD and to assess whether the ORR and remission durations can be improved by sequential Bex following PLD, a multi-institutional phase II trial was undertaken for pts with advanced stage/refractory CTCL. Methods:Pts were treated with PLD 20mg/m2 IV every 2 weeks for 8 doses (16 weeks) followed by 16 weeks with Bex 300mg/m2 orally. Response assessments were performed after 8 (PLD) and 16 weeks (Bex). The Severity-Weighted Assessment Tool (SWAT) (Arch Dermatol 2002; 138: 42–8) was the primary measure of skin response with the Composite Assessment of Index Lesion Severity (J Clin Oncol 2001; 19: 2456–71) and a self-reported pruritus scale as secondary measures. For stage IV pts with baseline lymphadenopathy, CT of chest, abdomen and pelvis was repeated. Sézary cell count and/or flow cytometry were repeated for patients with Sézary syndrome. Pts with complete disappearance of skin lesions on examination were deemed to have a clinical CR (CCR) in skin. A repeat skin biopsy without evidence of disease changed CCR to full CR. Results:All of the planned 37 pts with stages IV (21 including 7 Sézary syndrome), IIB (10) or refractory earlier stage (6) CTCL have been enrolled and have completed 32 weeks of treatment. Median age was 56 years (27–81). There were 20 males and 17 females. All pts had prior topical treatment with or without irradiation. Fourteen pts had no prior systemic therapy; while23 pts had prior systemic therapies (median 2, range 1–11). Median follow-up for surviving pts is 7.54 months (0.7–41.9). Thirty-four pts were assessable for response (2 withdrew consent, 1 died of disease progression 5 days after initiation of 1st cycle). For 34 assessable pts: ORR 14/34 (41%: PR 12, CCR 2). Maximum responses were all seen after 16 weeks PLD. Median progression free survival (PFS) is 4.82 months. To date, 18 pts have died of disease progression and 1 patient died of CHF which occurred 3 months after last study intervention. That patient had a pretreatment left ventricular ejection fraction of 60%. Treatment-related grade 3/4 serious adverse events occurred in 9 pts: 4 tumor pain, 2 (grade 3) hand-foot syndrome, 1 infection- unknown ANC- skin (cellulitis), 1 infection- normal ANC- skin (cellulitis), 1 neutropenia. Conclusions:With strict criteria, PLD ORR is among the highest reported for single agents in CTCL but lower than previously reported. The population contained a high proportion of patients with advanced disease as reflected in the initial stage and the poor survival. Sequential bexarotene did not increase the response rate or duration. Disclosures:Horwitz:Celgene: Consultancy, Research Funding; Allos: Consultancy, Research Funding; Seattle Genetics: Consultancy; Novartis: Consultancy; Merck: Honoraria; Millennium: Consultancy; Genzyme: Research Funding.

Tongue Hyperpigmentation Resulting from Peginterferon Alfa-2b and Ribavirin Treatment in a Patient with Chronic Hepatitis C

Hepatitis C virus (HCV) infection has been associated with several cutaneous diseases such as lichen planus, porphyria cutanea tarda, chronic pruritus, and cutaneous necrotizing vasculitis (Doutre, Arch Dermatol 135:1401-1403, 1999). The antiviral treatment for chronic HCV with interferon alfa (INF) or peginterferon alfa (PEG-INF) combined with rivabirin also leads to many skin side effects including injection site reaction, generalized skin rashes, pruritus, dry skin, alopecia, and exacerbation of autoimmune processes, particularly psoriasis, lichen planus or vitiligo (Dalekos et al., Eur J Gastroenterol Hepatol 10:933-939, 1998; Sookoian et al., Arch Dermatol 135:1000-1000, 1999). There are case reports of tongue hyperpigmentation during combination therapy of PEG IFN and RBV in chronic hepatitis C both in dark-skined as well as Caucasian. We report the first case of tongue hyperpigmentation associated with PEG-INF-2b plus ribavirin administration in a non-Caucasian patient with genotype 4.

Latitude and psoriasis prevalence

Latitude and psoriasis prevalence

Smoking and psoriasis: A meta-analysis of case–control studies

Psoriasis is one of the most common dermatological disorders with a genetic predisposition and potentially being caused or triggered by environmental factors [ [1] Lowes M.A. Bowcock A.M. Krueger J.G. Pathogenesis and therapy of psoriasis. Nature. 2007; 445: 866-873 Crossref PubMed Scopus (1377) Google Scholar ]. Many epidemiologic studies have pointed to a significant association between smoking and psoriasis [ 2 Gerdes S. Zahl V.A. Weichenthal M. Mrowietz U. Smoking and alcohol intake in severely affected patients with psoriasis in Germany. Dermatology. 2010; 220: 38-43 Crossref PubMed Scopus (77) Google Scholar , 3 Kramer U. Esser C. Cigarette smoking, metabolic gene polymorphism, and psoriasis. J Invest Dermatol. 2006; 126 (author reply 5): 693-694 Crossref PubMed Scopus (23) Google Scholar , 4 Naldi L. Chatenoud L. Linder D. Belloni Fortina A. Peserico A. Virgili A.R. et al. Cigarette smoking, body mass index, and stressful life events as risk factors for psoriasis: results from an Italian case-control study. J Invest Dermatol. 2005; 125: 61-67 Crossref PubMed Scopus (528) Google Scholar , 5 Herron M.D. Hinckley M. Hoffman M.S. Papenfuss J. Hansen C.B. Callis K.P. et al. Impact of obesity and smoking on psoriasis presentation and management. Arch Dermatol. 2005; 141: 1527-1534 Crossref PubMed Scopus (398) Google Scholar , 6 Mills C.M. Srivastava E.D. Harvey I.M. Swift G.L. Newcombe R.G. Holt P.J. et al. Smoking habits in psoriasis: a case control study. Br J Dermatol. 1992; 127: 18-21 Crossref PubMed Scopus (105) Google Scholar , 7 Zhang X. Wang H. Te-Shao H. Yang S. Wang F. Frequent use of tobacco and alcohol in Chinese psoriasis patients. Int J Dermatol. 2002; 41: 659-662 Crossref PubMed Scopus (49) Google Scholar ]. However, to our knowledge, the meta-analysis of smoking and psoriasis has not been assessed systematically and the gender and ethnicity features of these studies have not been assessed fully to further characterize this potential association and its determinants.

A Large Mutational Study in Pachyonychia Congenita

Pachyonychia congenita (PC) is a rare autosomal dominant skin disorder characterized predominantly by nail dystrophy and painful palmoplantar keratoderma. Additional clinical features include oral leukokeratosis, follicular keratosis, and cysts (steatocysts and pilosebaceous cysts). PC is due to heterozygous mutations in one of four keratin genes, namely, KRT6A, KRT6B, KRT16, or KRT17. Here, we report genetic analysis of 90 new families with PC in which we identified mutations in KRT6A, KRT6B, KRT16, or KRT17, thereby confirming their clinical diagnosis. A total of 21 previously unreported and 22 known mutations were found. Approximately half of the kindreds had mutations in KRT6A (52%), 28% had mutations in KRT16, 17% in KRT17, and 3% of families had mutations in KRT6B. Most of the mutations were heterozygous missense or small in-frame insertion/deletion mutations occurring within one of the helix boundary motif regions of the keratin polypeptide. More unusual mutations included heterozygous splice site mutations, nonsense mutations, and a 1-bp insertion mutation, leading to a frameshift and premature termination codon. This study, together with previously reported mutations, identifies mutation hotspot codons that may be useful in the development of personalized medicine for PC.

Merkel cell polyomavirus in naevoid basal cell carcinoma syndrome-associated basal cell carcinomas and sporadic trichoblastomas

Merkel cell carcinoma (MCC) is a very aggressive neuroendocrine non-melanoma skin cancer (NMSC) of elderly or immunosuppressed individuals [ [1] Swann M.H. Yoon J. Merkel cell carcinoma. Semin Oncol. 2007; 34: 51-567 Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar ]. Approximately 80% of MCC harbor the recently detected Merkel cell polyomavirus (MCPyV) within the tumor DNA [ [2] Feng H. Shuda M. Chang Y. Moore P.S. Clonal integration of a polyomavirus in human Merkel cell carcinoma. Science. 2008; 319: 1096-1100 Crossref PubMed Scopus (2328) Google Scholar ]. MCPyV-positive MCC reveal tumor specific truncating mutations within the large T antigen (LTAg) of MCPyV which are not found in the MCPyV wildtype [ [3] Shuda M. Feng H. Kwun H.J. et al. T antigen mutations are a human tumor-specific signature for Merkel cell polyomavirus. Proc Natl Acad Sci USA. 2008; 105: 16272-16277 Crossref PubMed Scopus (553) Google Scholar ]. Thus epidemiology, clonal integration and tumor specific mutations within the LTAg of MCPyV are strongly supporting an important role of MCPyV in the etiopathogenesis of human MCC. However, the presence of MCPyV has been reported in NMSC of immunosuppressed and immunocompetent patients, including squamous cell carcinomas (SCC), Bowen's disease (BD) and basal cell carcinoma (BCC) [ 4 Kassem A. Technau K. Kurz A.K. et al. Merkel cell polyomavirus sequences are frequently detected in nonmelanoma skin cancer of immunosuppressed patients. Int J Cancer. 2009; 125: 356-361 Crossref PubMed Scopus (122) Google Scholar , 5 Becker J.C. Houben R. Ugurel S. Trefzer U. Pföhler C. et al. MC Polyomavirus is frequently present in Merkel cell carcinoma of European patients. J Invest Dermatol. 2009; 129: 248-250 Crossref PubMed Scopus (282) Google Scholar , 6 Wieland U. Mauch C. Kreuter A. Krieg T. Pfister H. Merkel cell polyomavirus DNA in persons without Merkel cell carcinoma. Emerg Infect Dis. 2009; 15: 1496-1498 Crossref PubMed Scopus (115) Google Scholar , 7 Andres C, Belloni B, Puchta U, Sander CA, Flaig MJ. Prevalence of MCPyV in Merkel cell carcinoma and non-MCC tumors. J Cutan Pathol 2009; July 14 PMID: 19615033. Google Scholar ]. BCCs are among the most common malignant skin tumors and show differentiation towards germinative cells of the hair follicle. In addition to sporadic forms, BCCs may occur in the context of the naevoid basal cell carcinoma syndrome (NBCCS) which is a rare disease with an autosomal dominant trait with high penetrance and variable phenotype. The underlying molecular causes of NBCCS are germline mutations of the tumor suppressor gene PTCH1 located on the long arm of chromosome 9q22.3 [ [8] Johnson R.L. Rothman A.L. Xie J. Goodrich L.V. Bare J.W. Bonifas J.M. et al. Human homolog of patched, a candidate gene for the basal cell nevus syndrome. Science. 1996; 272: 1668-1671 Crossref PubMed Scopus (1624) Google Scholar ]. It is of interest that sporadic trichoblastoma which is a relatively rare benign counterpart of BCC, also showing differentiation toward germinative cells of the hair follicle, has been linked to chromosome 9p22.3 [ [9] Matt D. Xin H. Vortmeyer A.O. Zhuang Z. Burg G. Boni R. Sporadic trichoepithelioma demonstrates deletions at 9q22.3. Arch Dermatol. 2000; 136: 657-660 Crossref PubMed Scopus (55) Google Scholar ].

A protocol for enrichment of CD34+ stromal cell fraction through human skin disaggregation and magnetic separation

A protocol for enrichment of CD34+ stromal cell fraction through human skin disaggregation and magnetic separation

Long‐term management of vulval lichen sclerosus in adult women

Adult vulval lichen sclerosus (VLS) is usually a lifelong disease with an estimated remission rate after treatment of only 16% [Arch Dermatol 2004; 140 (6): 709]. Although superpotent topical corticosteroid (TCS) is the validated gold standard treatment to induce remission, little data are available on how remission should be maintained. We present a retrospective chart review of 129 adult patients with VLS who have been under surveillance by the authors for a minimum duration of three years. Remission was maintained in most patients with low-to-moderate potency TCS. All subjects' symptoms, signs, treatment regimes and response to treatment including compliance, symptom remission, disease progression with scarring, squamous cell carcinoma and side effects were recorded. Data were compared for the compliant and non-compliant groups. Fischer's exact test was used to identify significant differences. The mean age at presentation was 53.6 years and mean duration of follow-up was 6.2 years. Compliance was excellent: 84 (65%) of patients' self-reporting as being fully compliant. Symptom remission was achieved in 98% of compliant and 75% of non-compliant patients (P = 0.001) Progression of disease with scarring was not encountered in any of the compliant patients, but was seen in 35% of non-compliant patients (P = 0.0001). One patient had squamous cell carcinoma on first presentation. Carcinoma subsequently occurred in none of the compliant patients, and in five partly compliant patients (P = 0.004). Mild, reversible corticosteroid side effects were encountered in 7% of patients. Long-term treatment of adult VLS with individualised regimes using moderate potency TCS is safe and effective. Patients require long-term follow-up.

Review of the Literature: Dermatology

1. Marc R. Avram, MD 1. New York, New York 2. Nicole E. Rogers, MD 1. Metairie, Louisiana Citation: Tilstra, J.S., et al. Scalp dermatomyositis revisited. Arch Dermatol. 2009; 145:1062-1063. Dermatologists in Pittsburgh recently investigated the incidence of hair loss in the setting

Malignancy Is (Still) Associated with Dermatomyositis

In the late 1970s, during my residency, I collaborated with rheumatologists on a study (Arch Dermatol 1980; 116:295) showing that malignancy was

Follow up study of dermal hyaluronic acid injection by high frequency ultrasound and magnetic resonance imaging

In the last few years, increasing use of injectable resorbable fillings has been reported for facial wrinkle treatment and for soft tissue augmentation of HIV-associated facial lipodystrophy [ 1 Buck D.W. Alam M. Kim J.Y.S. Injectable fillers for facial rejuvenation: a review. J Plast Reconstr Aesthet Surg. 2009 Jan; 62: 11-18 Abstract Full Text Full Text PDF PubMed Scopus (112) Google Scholar , 2 Gooderham M. Solish N. Use of hyaluronic acid for soft tissue augmentation of HIV-associated facial lipodystrophy. Dermatol Surg. 2005 Jan; 31: 104-108 Crossref PubMed Scopus (31) Google Scholar ]. However, important practical information concerning the localization and subsequent diffusion of the injected product in skin tissues are poorly documented. Histological analysis has been previously used to compare different kinds of fillers [ [3] Lemperle G. Morhenn V. Charrier U. Human histology and persistence of various injectable filler substances for soft tissue augmentation. Aesthetic Plast Surg. 2003; 27: 354-366 Crossref PubMed Scopus (399) Google Scholar ], to evaluate remanescence of the injected material [ [4] Duranti F. Salti G. Bovani B. Calandra M. Rosati M.L. Injectable hyaluronic acid gel for soft tissue augmentation. A clinical and histological study. Dermatol Surg. 1998; 24: 1317-1325 Crossref PubMed Scopus (413) Google Scholar ], or to observe the product placement at the injection site [ [5] Arlette J.P. Trotter M.J. Anatomic location of hyaluronic acid filler material injected into nasolabial fold: a histologic study. Dermatol Surg. 2008; 34 (discussion S62-3: S56–S62): S56-S62 Crossref PubMed Scopus (49) Google Scholar ]. Wang et al. have recently proposed a mechanism in which the filler-induced mechanical tension solicits local fibroblasts and activates collagen synthesis [ [6] Wang F. Garza L.A. Kang S. Varani J. Orringer J.S. Fisher G.J. et al. In vivo stimulation of de novo collagen production caused by cross-linked hyaluronic acid dermal filler injections in photodamaged human skin. Arch Dermatol. 2007; 143: 155-163 Crossref PubMed Scopus (356) Google Scholar ].

Significance of cyclin D1-, product of retinoblastoma (pRb), p53, p63 and p73 expression in eccrine poroma and eccrine porocarcinoma

Eccrine porocarcinoma (EPC) is a rare malignant tumor arising from the intraepidermal portion of the eccrine sweat gland duct epithelium or from pre-existing eccrine poroma (EP) [ [1] Mehregan A.H. Hasimoto K. Rahbari H. Eccrine adenocarcinoma—a clinicopathologic study of 35 cases. Arch Dermatol. 1983; 119: 104-114 Crossref PubMed Scopus (320) Google Scholar ], and the precise pathogenesis remains unclear. We have previously reported that activating transcription factor-2- and signal transducer and activator of transcription-3 signaling pathways might contribute to the formation of both EP and EPC [ [2] Chen S.Y. Takeuchi S. Urabe K. Kido M. Hayashida S. Tomoeda H. et al. Overexpression of phosphorylated ATF2 and STAT3 in eccrine porocarcinoma and eccrine poroma. J Dermatol Sci. 2008; 49: 170-173 Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar ], but neither factor was able to dissect EPC from EP.