C-Kit non-mutated metastatic melanoma showing positive response to Nilotinib

Melanoma is an aggressive tumor with advanced disease characterized by widespread metastatic lesions and the tumor hastraditionally been resistant to most forms of treatment. Indeed, metastatic melanoma has a very poor prognosis with a median survival time of 8–9 months and an estimated 3-year survival rate of less than 15 % [1].Recent advances in our understanding of the genetic profile of melanoma cells and the molecular factors that drive malignant transformation have resulted in the identification of numerous new therapeutic targets.KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate [2].Nilotinib is an inhibitor of ligand-induced PDGFRα and PDFGRβ kinase activity and autophosphorylation of constitutively activated KIT harboring exon 13 or exon 11 mutations (IC50 values of 0.2 and 0.027 μmol/L, respectively), with efficacy comparable to that of imatinib [2].We report a case of non-kit mutated metastatic vaginal melanoma showing impressive response to nilotinib

C-Kit non-mutated metastatic melanoma showing positive response to Nilotinib

Melanoma is an aggressive tumor with advanced disease characterized by widespread metastatic lesions and the tumor hastraditionally been resistant to most forms of treatment. Indeed, metastatic melanoma has a very poor prognosis with a median survival time of 8–9 months and an estimated 3-year survival rate of less than 15 % [1].Recent advances in our understanding of the genetic profile of melanoma cells and the molecular factors that drive malignant transformation have resulted in the identification of numerous new therapeutic targets.KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate [2].Nilotinib is an inhibitor of ligand-induced PDGFRα and PDFGRβ kinase activity and autophosphorylation of constitutively activated KIT harboring exon 13 or exon 11 mutations (IC50 values of 0.2 and 0.027 μmol/L, respectively), with efficacy comparable to that of imatinib [2].We report a case of non-kit mutated metastatic vaginal melanoma showing impressive response to nilotinib

Occasional acne; an acne variant

Yaser Taha Melibary,1 Salim Alkeraye,2 Kholood Abdulaziz Alnutaifi,3 Nouran Taha Melibary,4 Mariam Khalfan Alsuwaidi,5 Haitham Ibrheem Algzlan61Private Cinic for Dermatology, Allergy and Aesthetic Medicine, Coesfeld, Muensterland, Germany; 2Department of Dermatology, College of Medicine, King Saud University, Riyadh, Saudi Arabia; 3Department of Dermatology, National Guard Hospital, Dammam, Eastern Province, Saudi Arabia; 4Department of Family Medicine, Prince Sultan Military Hospital, Riyadh, Saudi Arabia; 5Department of Dermatology, Sheikh Khalifa Medical City, Abu Dhabi, UAE; 6Department of Dermatology, Ichan School of Medicine at Mount Sinai, New York, NY, USAAbstract: This article is about a common skin eruption that dermatologists face regularly in their clinics. It is a form of acne that patients frequently refer to as nightshifts acne, stress acne or airplane acne (after experiencing a prior occasion that might aggravate it). Physical or psychological stress is not the only causative factor, therefore we took into consideration of naming it based on its presentation irrespectively of the skin proneness to acne and self-limiting tendency, we name the entity as “occasional acne”. This article will discuss the similarities and differences between this entity and other forms of acne, as well as different causative factors that are involved in the eruption. These factors vary individually whether single or multiple factors might provoke it; maladaptation driven by mental and/or physical stress, temporary imbalance of sebum lipids and nicotine effect, etc.Keywords: temporary acne, night shifts acne, airplane acne, acne &nbsp

Alopecia Areata: Clinical Treatment

Alopecia areata is a complex immune-mediated disease that targets anagen hair follicles. Therapeutic strategies must be directed as either immunosuppressive or immunomodulating and may consist of monotherapy or combination therapy and should be different depending on patient’s age, extent, and chronicity of the disease. The physician must discuss mild and aggressive options, as well as the possibility of no treatment, camouflage options, and social/psychological support. Topical, intralesional, and systemic steroids, as well as corticosteroid-sparing agents and disease-modifying antirheumatic drugs are useful as local or systemic immunosuppressors. Topical immunotherapy, anthralin, and phototherapy have proved useful as immunomodulators. Target therapy with JAK inhibitors is useful in alopecia areata totalis or universalis. Treatment in special areas such as eyelashes, eyebrows, or beard benefit from treatment with steroids, minoxidil, prostaglandin F2a analogs, and topical tofacitinib. Vitamin D3, ezetimibe/simvastatin, platelet-rich plasma, antihistamines, and aromatherapy may be used as adjuvant therapies. We discuss a practical but evidence-based approach for treatment in different cases of alopecia areata with detailed information about doses, administration, and possible side effects