The BRAF inhibitors vemurafenib, dabrafenib and encorafenib are used in the treatment of patients with BRAF-mutant melanoma. They selectively target BRAF kinase and thus interfere with the mitogen-activated protein kinase (MAPK) signalling pathway that regulates the proliferation and survival of melanoma cells. In addition to their molecularly targeted activity, BRAF inhibitors have immunomodulatory effects. The MAPK pathway is involved in T-cell receptor signalling, and interference in the pathway by BRAF inhibitors has beneficial effects on the tumour microenvironment and anti-tumour immune response in BRAF-mutant melanoma, including increased immune-stimulatory cytokine levels, decreased immunosuppressive cytokine levels, enhanced melanoma differentiation antigen expression and presentation of tumour antigens by HLA 1, and increased intra-tumoral T-cell infiltration and activity. These effects promote recognition of the tumour by the immune system and enhance anti-tumour T-cell responses. Combining BRAF inhibitors with MEK inhibitors provides more complete blockade of the MAPK pathway. The immunomodulatory effects of BRAF inhibition alone or in combination with MEK inhibition provide a rationale for combining these targeted therapies with immune checkpoint inhibitors. Available data support the synergy between these treatment approaches, indicating such combinations provide an additional beneficial effect on the tumour microenvironment and immune response in BRAF-mutant melanoma.

This systematic review investigated the literature on acquired v-raf murine sarcoma viral oncogene homolog B1 (BRAF) inhibitor resistance in patients with melanoma. We searched MEDLINE for articles on BRAF inhibitor resistance in patients with melanoma published since January 2010 in the following areas: (1) genetic basis of resistance; (2) epigenetic and transcriptomic mechanisms; (3) influence of the immune system on resistance development; and (4) combination therapy to overcome resistance. Common resistance mutations in melanoma are BRAF splice variants, BRAF amplification, neuroblastoma RAS viral oncogene homolog (NRAS) mutations and mitogen-activated protein kinase kinase 1/2 (MEK1/2) mutations. Genetic and epigenetic changes reactivate previously blocked mitogen-activated protein kinase (MAPK) pathways, activate alternative signaling pathways, and cause epithelial-to-mesenchymal transition. Once BRAF inhibitor resistance develops, the tumor microenvironment reverts to a low immunogenic state secondary to the induction of programmed cell death ligand-1. Combining a BRAF inhibitor with a MEK inhibitor delays resistance development and increases duration of response. Multiple other combinations based on known mechanisms of resistance are being investigated. BRAF inhibitor-resistant cells develop a range of ‘escape routes’, so multiple different treatment targets will probably be required to overcome resistance. In the future, it may be possible to personalize combination therapy towards the specific resistance pathway in individual patients.

Recent data support the theory of the involvement of IL‐17 in the pathogenesis of several chronic inflammatory skin diseases (psoriasis, atopic dermatitis, acne, hidradenitis suppurativa) and autoimmune skin diseases (alopecia areata, vitiligo, bullous diseases). Even if the role of IL‐17 in inflammatory and autoimmune diseases has been reported extensively, its role in tumor is still controversial. Some reports show that Th17 cells eradicate tumors, while others reveal that they promote the initiation and early growth of tumors. Herein, we review the role of IL‐17 in the involvement of some common dermatologic diseases: psoriasis, atopic dermatitis, hidradenitis suppurativa, acne, vitiligo, melanoma, and nonmelanoma skin cancers.

The growing interest in maintaining a youthful appearance has encouraged an accelerated development of innovative, minimally invasive aesthetic treatments for facial rejuvenation and regeneration. The close correlation between tissue repair, regeneration, and aging has paved the way for the application of regenerative medicine principles in cosmetic dermatology. The theoretical substrates of regenerative medicine applications in dermo-aesthetics are plentiful. However, regenerative dermatology is an emerging field and needs more data and in vivo trials to reach a consensus on the standardization of methods. In this review, we summarize the principles of regenerative medicine and techniques as they apply to cosmetic dermatology, suggesting unexplored fields and future directions.

Cosmetic dermatology increasingly utilizes laser technologies to address various aesthetic concerns. This study evaluates the efficacy of the flash-lamp pulsed-dye laser (FPDL) in treating vascular and scar-related conditions. A cohort of 71 patients with diverse vascular lesions, including facial telangiectasia, port-wine stains (PWSs), striae rubrae, erythematous acne scars, facial traumatic scars, and keloids, was treated using the FPDL (Synchro Vas-Q, Deka MELA). Treatment protocols varied based on lesion type, with sessions ranging from one to eight at intervals of four to eight weeks. Clinical outcomes were assessed using a four-point grading scale and patient satisfaction surveys. Results indicated that 70.4% of patients achieved excellent clearance of lesions, while 16.9% and 9.9% showed moderate-good and slight clearance, respectively. Minimal or no improvement was observed in 2.8% of cases. High patient satisfaction was reported, correlating with effective lesion reduction and manageable side effects, primarily post-operative purpura. The study underscores FPDL’s selective efficacy for hemoglobin-rich lesions and its safety profile, advocating for its continued use in cosmetic dermatological practices. These findings contribute to the growing evidence supporting laser therapy as a pivotal tool in aesthetic medicine, emphasizing the importance of tailored treatment protocols and patient education for optimal outcomes.