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Cutaneous squamous cell carcinoma (cSCC) is the second most frequent form of skin cancer showing a rapidly increasing incidence worldwide. cSCC originates from alterations in keratinocyte stem cells which, in turn, disrupt epidermal homeostasis. In the skin, neurotrophins (NTs) and their receptors (CD271 and Trk receptors) form a complex network with regulatory functions. CD271 is implicated in the switch between stem and early progenitors, thus playing a key role in keratinocyte differentiation.
We assessed the role of macrophages in squamous cell carcinoma (SCC) behavior. We used mouse SCC cells derived from tumors harboring a Kras12D activation mutation and Smad4 deletion in keratin 15 (K15)-positive stem cells, and a human SCC cell line, FaDu. SCC cells were transplanted into immune-compromised or -competent (syngeneic) recipients. After tumors were established, we profiled tumor infiltrating leukocytes using CyTOF. CD45+ leukocytes comprised 10-25% of the total tumor cells, and tumor-associated macrophages (TAMs) were 5-10% of the CD45+ cells.
The aim of the study was to assess safety and efficacy of two formulations with SPF 50+ in patients with dermatoses such as acne vulgaris, rosacea and skin affected by aesthetic treatments. Both tested formulas provide wide spectrum protection from sun radiation in UV, HEV and IR as well as alleviate symptoms of the respective dermatoses. Product 14004 contained hesperidin, an ingredient used in care of rosacea and dilated capillaries or hypersensitivity caused by aesthetic treatments (chemical peels, laser therapy).
Given a known incidence of photosensitivity reactions with the predecessor drug, Flutamide, we explore another interesting case of photosensitivity following Bicalutamide therapy. Case: A 74-year-old man started on bicalutamide for prostate cancer. Approximately 4-6 weeks after starting bicalutamide the patient developed diffuse, tender erythema spreading caudally from facial sites. The distribution is symmetrical and follows a sun-exposed pattern with erythema seen across the face, shoulders, upper torso and upper limbs.
The effect of ultraviolet (UV) radiation is well studied by increasing inflammatory response and oxidative stress leading to degradation of extracellular matrix (ECM) proteins such as collagen. Additionally, increasing numbers of studies have indicated the atmospheric pollution induces intracellular reactive oxygen species. Among various substances with potentials to prevent deleterious effect of environmental ageing, antioxidants are most representative and well studied, Especially, the combination formulation of L-ascorbic acid, vitamin E and Ferulic acid have shown it’s in vitro and in vivo effect in the prevention of photoaging.
Poliosis, an absence of functional melanocytes of affected hair follicle, is considered a poor prognostic factor in treatment of vitiligo because the melanocytes of hair follicles are the major source of repigmentation. We sought to evaluate the clinical outcome of poliosis in treatment of vitiligo. An open-label pilot study was performed between January 2016 and March 2018. Patients with vitiligo who have poliosis in head and neck were treated with the combination therapy of 308-nm excimer laser, topical tacrolimus, and intralesional triamcinolone injection for more than 3 months.
Disruption of the dermal matrix secondary to photoaging is one of the proposed etiologies for rosacea. Matrix metalloproteinase-1-mediated collagen degeneration has been shown to impact endothelial cells, leading to the formation of vascular tubes resembling telangiectatic lumina. We performed a case-control study to examine the relationship between clinical presentation, collagen degeneration, and microvascular changes between 5 patients with erythematotelangiectatic rosacea ages 47-83 and 5 controls matched by age ±5 years and race.
The pigmentation of human skin (nevi, senile lentigines, melasma, etc) is regulated by a complex process involving the synthesis and distribution of melanin. Overexpression of melanin is induced by the off-balance between the signals which regulates melanin synthesis, this can be caused due to a response to external or internal stimulus that often affects the genes related to melanogenesis. To date, many studies have focused on developing direct enzymatic inhibitors of tyrosinase in order to achieve a skin-lightening effect.
Congenital melanocytic nevus (CMN) is a hamartoma derived from neural crest appearing at birth. CMN has a dynamic course and may show various changes even spontaneous regression. CMN may grow in size during childhood and show pigmentary regression with increasing age and develop a hypopigmentation halo and regress spontaneously after halo formation, or undergo malignant transformation resulting in melanoma. A 9-year-old boy presented with solitary brownish to blackish patch on the right forearm which had appeared since birth.
Silymarin is a phytophenol extracted from the seeds of milk thistle (Silibum marianum). Silymarin has been studied in skin UV-protection due to its antioxidant and anti-inflammatory effects. However, its possible phototoxic potential was also shown. Based on these findings the dermatological application of this polyphenol is questionable. Our aim was to study the effects of silymarin on cell viability, ROS production and mutagenesis in UVA-irradiated epithelial cells. HaCaT immortalized keratinocyte and CHO (Chinese hamster ovary) cell lines were treated with silymarin for 30 min, then exposed to 10 or 20 J/cm2 UVA.
UVB-induced cyclobutane pyrimidine dimers (CPDs) are considered to be the main cause of acute sunburn and epidermal carcinogenesis. In humans, these lesions are repaired by nucleotide excision repair, but marsupials and lower organisms present photolyase enzyme which rapidly removes CPDs in a visible light-dependent process (photoreactivation). Previously we established an in vitro pseudouridin-modified mRNA encoding CPD-specific photolyase transfection on human keratinocyte cell lines, which was proved to be a proper method to avoid UVB-induced apoptosis.
PCE-DP (D-pantothenyl alcohol) is an active ingredient in pharmaceuticals and cosmetics that prevents inflammation and promotes hair growth. In our previous randomized double-blind placebo-controlled UVB irradiation-induced pigmentation study using healthy Japanese men and women, we found that topical PCE-DP has brightening effects when used for 4 weeks. In this study, we examined four studies to clarify the molecular mechanism of PCE-DP activity: (i) epidermal turnover, (ii) melanosomal uptake of keratinocytes, (iii) melanocyte activation by keratinocytes, or (iv) melanin production in melanocytes.
UVA1 phototherapy selectively uses the longer UVA1 wavelengths (340-400 nm), and does not include the shorter UVA2 wavelengths (320-340 nm) or UVB wavelengths (290-320 nm) that cause an erythema reaction. Several studies report the effectiveness of UVA1 phototherapy for various diseases such as atopic dermatitis, T-cell lymphoma, and systemic sclerosis. While UVA1 phototherapy has a high therapeutic effect, it also causes immediate pigment darkening (IPD) as a deleterious effect. IPD is a dull grayish-brown pigment enhancement observed during or immediately after UVA irradiation.
Premature skin aging evidenced by a rough skin texture and wrinkles is known to be driven by external factors, mainly by sunlight and in particular UV radiation including UVB (280-320 nm) and UVA (320-400 nm). However, recent advance highlighted the role of visible light and especially the blue light part (400-500nm) in skin aging. As the blue light is the highest energetic wavelength of the visible light, it penetrates deeper into the skin and damages the skin by inducing oxidative stress and production of proteases which degrade the extracellular matrix of the dermis.
Imatinib mesylate is a tyrosine kinase inhibitor (TKI) that regulates cell growth, thereby inhibiting cancer cell proliferation. It has been used to treat various neoplasms such as chronic myeloid leukemia (CML). The most common side effect in skin is hypopigmentation. However, hyperpigmentation has also been rarely reported. A 48-year-old woman diagnosed as chronic myeloid leukemia presented with bluish to grayish macules and patches on face, shoulder, and buttock. She had got a treatment of CML with imatinib mesylate for 9 years.
Skin is the largest organ of the human body and possesses a unique microbiome which is known to play a significant role in skin barrier function. Throughout life, both cutaneous cells and skin microorganisms are exposed to solar ultraviolet radiation (UVR). Although the effects of UVR on keratinocytes have been investigated in many studies, little is known about the effects of UVR on the skin microbiome, and the potential effect of the altered skin microbiome on skin cells. The aims of this study were to test the hypothesis that irradiation of fourspecific skin commensal bacteria (Staphylococcus epidermidis, Staphylococcus hominis,Staphylococcus capitis and Cutibacterium acnes) change their interactions with normal human epidermal keratinocytes (NHEKs).
Visible light between 400 to 500nm was identified as an additional contributor to cutaneous photo-aging. Clinical studies showing clear effects of blue light on photo-aging are, however, still scarce. While there is evidence for increased skin pigmentation, the underlying mechanisms of photo-aging in vivo are still not clear. Furthermore, there is still a lack of means to significantly protect from blue light induced signs of photo-aging in vivo. We conducted a randomized, double-blind and placebo controlled clinical study on 33 female Caucasian and Asian volunteers with skin phototype III and IV.
Wrinkling has been attributed to the cumulative effects of acute Ultraviolet Radiation (UVR) exposure on the dermis. Previous studies have shown that the collagenase MMP-1 is secreted by dermal fibroblasts and degrades collagen immediately after UV exposure. However, skin ages gradually, and not intermittently after sun exposure. In this study we sought to examine the mechanism underpinning the gradual appearance of wrinkles, and to determine whether this is a result of intrinsic changes in the biology of the dermis.
It is well known that solar radiation accelerates photoaging. To protect the skin especially from the early phase of ultraviolet (UV)-induced damage, we have focused on ultraweak photon emission (UPE), which is also called biophoton, to evaluate the photodamage in a quick and simple manner. Our previous research revealed that the amount of UV-induced long-lasting UPE predominantly from lipid peroxidation would be a valuable indicator to assess cutaneous photodamage even at a suberythemal dose, though it was only applied to acute UV damage.
To protect the human body against environmental stress, such as UVB, a multifunctional enzymatic and antioxidant defense system is expressed in the skin. A key regulator of this pathway is the transcription factor Nrf2. Thus, we have speculated that target activation of this pathway may provide therapeutic options against oxidative stress-related disorders. A novel pharmacological Nrf2 activator (E)-5-oxo-1-(4-((2,4,6-trihydroxybenzylidene)amino)phenyl)pyrrolidine-3-carboxylic acid (SK-119) was synthesis and evaluated on several in vitro skin models.