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Journal of the European Academy of... Jul 2024
Topics: Humans; Skin Neoplasms
PubMed: 38932661
DOI: 10.1111/jdv.20067 -
Acta Dermato-venereologica Jun 2024
Topics: Humans; Female; Young Adult; Knee; Biopsy; Skin Neoplasms
PubMed: 38932593
DOI: 10.2340/actadv.v104.35391 -
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi =... Jun 2024Skin cancer is a significant public health issue, and computer-aided diagnosis technology can effectively alleviate this burden. Accurate identification of skin lesion...
Skin cancer is a significant public health issue, and computer-aided diagnosis technology can effectively alleviate this burden. Accurate identification of skin lesion types is crucial when employing computer-aided diagnosis. This study proposes a multi-level attention cascaded fusion model based on Swin-T and ConvNeXt. It employed hierarchical Swin-T and ConvNeXt to extract global and local features, respectively, and introduced residual channel attention and spatial attention modules for further feature extraction. Multi-level attention mechanisms were utilized to process multi-scale global and local features. To address the problem of shallow features being lost due to their distance from the classifier, a hierarchical inverted residual fusion module was proposed to dynamically adjust the extracted feature information. Balanced sampling strategies and focal loss were employed to tackle the issue of imbalanced categories of skin lesions. Experimental testing on the ISIC2018 and ISIC2019 datasets yielded accuracy, precision, recall, and F1-Score of 96.01%, 93.67%, 92.65%, and 93.11%, respectively, and 92.79%, 91.52%, 88.90%, and 90.15%, respectively. Compared to Swin-T, the proposed method achieved an accuracy improvement of 3.60% and 1.66%, and compared to ConvNeXt, it achieved an accuracy improvement of 2.87% and 3.45%. The experiments demonstrate that the proposed method accurately classifies skin lesion images, providing a new solution for skin cancer diagnosis.
Topics: Humans; Skin Neoplasms; Algorithms; Diagnosis, Computer-Assisted; Skin; Image Interpretation, Computer-Assisted
PubMed: 38932541
DOI: 10.7507/1001-5515.202305025 -
Skin Research and Technology : Official... Jul 2024Reports suggest that lipid profiles may be linked to the likelihood of developing skin cancer, yet the exact causal relationship is still unknown.
BACKGROUND
Reports suggest that lipid profiles may be linked to the likelihood of developing skin cancer, yet the exact causal relationship is still unknown.
OBJECTIVE
This study aimed to examine the connection between lipidome and skin cancers, as well as investigate any possible mediators.
METHODS
A two-sample Mendelian randomization (MR) analysis was conducted on 179 lipidomes and each skin cancer based on a genome-wide association study (GWAS), including melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). Then, Bayesian weighted MR was performed to verify the analysis results of two-sample MR. Moreover, a two-step MR was employed to investigate the impact of TNF-like weak inducer of apoptosis (TWEAK)-mediated lipidome on skin cancer rates.
RESULTS
MR analysis identified higher genetically predicted phosphatidylcholine (PC) (17:0_18:2) could reduce the risk of skin tumors, including BCC (OR = 0.9149, 95% CI: 0.8667-0.9658), SCC (OR = 0.9343, 95% CI: 0.9087-0.9606) and melanoma (OR = 0.9982, 95% CI: 0.9966-0.9997). The proportion of PC (17:0_18:2) predicted by TWEAK-mediated genetic prediction was 6.6 % in BCC and 7.6% in SCC. The causal relationship between PC (17:0_18:2) and melanoma was not mediated by TWEAK.
CONCLUSION
This study identified a negative causal relationship between PC (17:0_18:2) and keratinocyte carcinomas, a small part of which was mediated by TWEAK, and most of the remaining mediating factors are still unclear. Further research on other risk factors is needed in the future.
Topics: Humans; Skin Neoplasms; Cytokine TWEAK; Keratinocytes; Lipidomics; Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Mendelian Randomization Analysis; Genome-Wide Association Study; Melanoma; Polymorphism, Single Nucleotide; Genetic Predisposition to Disease; Bayes Theorem
PubMed: 38932454
DOI: 10.1111/srt.13781 -
Molecules (Basel, Switzerland) Jun 2024Halogenated boroxine K[BOFOH] (HB), an inorganic derivative of cyclic anhydride of boronic acid, is patented as a boron-containing compound with potential for the...
Halogenated boroxine K[BOFOH] (HB), an inorganic derivative of cyclic anhydride of boronic acid, is patented as a boron-containing compound with potential for the treatment of both benign and malignant skin changes. HB has effectively inhibited the growth of several carcinoma cell lines. Because of the growing interest in autophagy induction as a therapeutic approach in bladder carcinoma (BC), we aimed to assess the effects of HB on metabolic phenotype and autophagy levels in 5637 human bladder carcinoma cells (BC). Cytotoxicity was evaluated using the alamar blue assay, and the degree of autophagy was determined microscopically. Mitochondrial respiration and glycolysis were measured simultaneously. The relative expression of autophagy-related genes BECN1, P62, BCL-2, and DRAM1 was determined by real-time PCR. HB affected cell growth, while starvation significantly increased the level of autophagy in the positive control compared to the basal level of autophagy in the untreated negative control. In HB-treated cultures, the degree of autophagy was higher compared to the basal level, and metabolic phenotypes were altered; both glycolysis and oxidative phosphorylation (OXPHOS) were decreased by HB at 0.2 and 0.4 mg/mL. Gene expression was deregulated towards autophagy induction and expansion. In conclusion, HB disrupted the bioenergetic metabolism and reduced the intracellular survival potential of BC cells. Further molecular studies are needed to confirm these findings and investigate their applicative potential.
Topics: Humans; Autophagy; Cell Line, Tumor; Urinary Bladder Neoplasms; Cell Proliferation; Glycolysis; Phenotype; Oxidative Phosphorylation; Cell Survival; Mitochondria; Antineoplastic Agents; Gene Expression Regulation, Neoplastic; Halogenation
PubMed: 38930984
DOI: 10.3390/molecules29122919 -
Medicina (Kaunas, Lithuania) May 2024: While the management of noninvasive cutaneous melanoma (CM) is typically limited to a secondary excision to reduce recurrence risk and periodic follow-up, treating... (Review)
Review
: While the management of noninvasive cutaneous melanoma (CM) is typically limited to a secondary excision to reduce recurrence risk and periodic follow-up, treating patients with advanced melanoma presents ongoing challenges. : This review provides a comprehensive examination of both established and emerging pharmacologic strategies for advanced CM management, offering an up-to-date insight into the current therapeutic milieu. The dynamic landscape of advanced CM treatment is explored, highlighting the efficacy of immune checkpoint inhibitors and targeted therapies, either in monotherapy or combination regimens. Additionally, ongoing investigations into novel treatment modalities are thoroughly discussed, reflecting the evolving nature of melanoma management. : The therapeutic landscape for melanoma management is undergoing significant transformation. Although various treatment modalities exist, there remains a critical need for novel therapies, particularly for certain stages of melanoma or cases resistant to current options. : Consequently, further studies are warranted to identify new treatment avenues and optimize the utilization of existing drugs.
Topics: Humans; Melanoma; Skin Neoplasms; Immune Checkpoint Inhibitors; Melanoma, Cutaneous Malignant; Molecular Targeted Therapy
PubMed: 38929501
DOI: 10.3390/medicina60060884 -
International Journal of Molecular... Jun 2024Chitosan is a natural polymer with numerous biomedical applications. The cellular activity of chitosan has been studied in various types of cancer, including melanoma,...
Chitosan is a natural polymer with numerous biomedical applications. The cellular activity of chitosan has been studied in various types of cancer, including melanoma, and indicates that these molecules can open new perspectives on antiproliferative action and anticancer therapy. This study analyzes how different chitosan conformations, such as α-chitosan (CH) or β-oligochitosan (CO), with various degrees of deacetylation (DDA) and molar mass (MM), both in different concentrations and in CH-CO mixtures, influence the cellular processes of SK-MEL-28 melanocytes, to estimate the reactivity of these cells to the applied treatments. The in vitro evaluation was carried out, aiming at the cellular metabolism (MTT assay), cellular morphology, and chitinase-like glycoprotein YKL-40 expression. The in vitro effect of the CH-CO mixture application on melanocytes is obvious at low concentrations of α-chitosan/β-oligochitosan (1:2 ratio), with the cell's response supporting the hypothesis that β-oligo-chitosan amplifies the effect. This oligochitosan mixture, favored by the β conformation and its small size, penetrates faster into the cells, being more reactive when interacting with some cellular components. Morphological effects expressed by the loss of cell adhesion and the depletion of YKL-40 synthesis are significant responses of melanocytes. β-oligochitosan (1.5 kDa) induces an extension of cytophysiological effects and limits the cell viability compared to α-chitosan (400-900 kDa). Statistical analysis using multivariate techniques showed differences between the CH samples and CH-CO mixtures.
Topics: Chitosan; Melanocytes; Humans; Chitin; Oligosaccharides; Chitinase-3-Like Protein 1; Cell Survival; Cell Proliferation; Cell Line, Tumor; Melanoma
PubMed: 38928474
DOI: 10.3390/ijms25126768 -
International Journal of Molecular... Jun 2024Cutaneous melanoma is the most dangerous and deadly form of human skin malignancy. Despite its rarity, it accounts for a staggering 80% of deaths attributed to cutaneous...
Cutaneous melanoma is the most dangerous and deadly form of human skin malignancy. Despite its rarity, it accounts for a staggering 80% of deaths attributed to cutaneous cancers overall. Moreover, its final stages often exhibit resistance to drug treatments, resulting in unfavorable outcomes. Hence, ensuring access to novel and improved chemotherapeutic agents is imperative for patients grappling with this severe ailment. Pyrazole and its fused systems derived thereof are heteroaromatic moieties widely employed in medicinal chemistry to develop effective drugs for various therapeutic areas, including inflammation, pain, oxidation, pathogens, depression, and fever. In a previous study, we described the biochemical properties of a newly synthesized group of imidazo-pyrazole compounds. In this paper, to improve our knowledge of the pharmacological properties of these molecules, we conduct a differential proteomic analysis on a human melanoma cell line treated with one of these imidazo-pyrazole derivatives. Our results detail the changes to the SKMEL-28 cell line proteome induced by 24, 48, and 72 h of imidazo-pyrazole treatment. Notably, we highlight the down-regulation of the Ras-responsive element binding protein 1 (RREB1), a member of the zinc finger transcription factors family involved in the tumorigenesis of melanoma. RREB1 is a downstream element of the MAPK pathway, and its activation is mediated by ERK1/2 through phosphorylation.
Topics: Humans; Melanoma; Pyrazoles; Proteomics; Cell Line, Tumor; Transcription Factors; Antineoplastic Agents; Skin Neoplasms; DNA-Binding Proteins; Imidazoles; Gene Expression Regulation, Neoplastic; Proteome
PubMed: 38928466
DOI: 10.3390/ijms25126760 -
International Journal of Molecular... Jun 2024The ability of tumor-derived extracellular vesicles (EVs) to modulate the function of myeloid cells is widely recognized. Hence, a comprehensive understanding of the...
The ability of tumor-derived extracellular vesicles (EVs) to modulate the function of myeloid cells is widely recognized. Hence, a comprehensive understanding of the distinct components associated with EVs and the signals that they deliver to myeloid cells could provide potential approaches to impede the immunosuppression by myeloid-derived suppressor cells (MDSCs). We investigated melanoma EV-associated microRNAs (miRs) using the RET transgenic melanoma mouse model and simulated their transfer to normal myeloid cells by transfecting immature mouse myeloid cells and human monocytes. We observed elevated levels of miR-125a-5p, -125b-5p, and let-7e-5p in mouse melanoma-infiltrating MDSCs. In addition, miR-125a-5p levels in the tumor microenvironment correlated with mouse melanoma progression. The delivery of miR-125a-5p, alone or in combination with let-7e-5p and miR-99b-5p from the same genomic cluster, to normal myeloid cells resulted in their conversion to MDSC-like cells. Our findings indicate that miR-125a-5p could modulate myeloid cell activation in the melanoma microenvironment via a NF-κB-dependent mechanism.
Topics: MicroRNAs; Myeloid-Derived Suppressor Cells; Animals; Humans; Mice; Tumor Microenvironment; Melanoma; Mice, Transgenic; NF-kappa B; Extracellular Vesicles; Cell Line, Tumor; Gene Expression Regulation, Neoplastic; Mice, Inbred C57BL; Monocytes
PubMed: 38928399
DOI: 10.3390/ijms25126693 -
International Journal of Molecular... Jun 2024NF2-related schwannomatosis (NF2) is a genetic syndrome characterized by the growth of benign tumors in the nervous system, particularly bilateral vestibular... (Review)
Review
NF2-related schwannomatosis (NF2) is a genetic syndrome characterized by the growth of benign tumors in the nervous system, particularly bilateral vestibular schwannomas, meningiomas, and ependymomas. This review consolidates the current knowledge on NF2 syndrome, emphasizing the molecular pathology associated with the mutations in the gene of the same name, the gene, and the subsequent dysfunction of its product, the Merlin protein. Merlin, a tumor suppressor, integrates multiple signaling pathways that regulate cell contact, proliferation, and motility, thereby influencing tumor growth. The loss of Merlin disrupts these pathways, leading to tumorigenesis. We discuss the roles of another two proteins potentially associated with deficiency as well as Merlin: Yes-associated protein 1 (YAP), which may promote tumor growth, and Raf kinase inhibitory protein (RKIP), which appears to suppress tumor development. Additionally, this review discusses the efficacy of various treatments, such as molecular therapies that target specific pathways or inhibit neomorphic protein-protein interaction caused by deficiency. This overview not only expands on the fundamental understanding of NF2 pathophysiology but also explores the potential of novel therapeutic targets that affect the clinical approach to NF2 syndrome.
Topics: Humans; Neurofibromatoses; Neurofibromin 2; Neurilemmoma; Skin Neoplasms; Animals; Neurofibromatosis 2; Mutation; Signal Transduction; Molecular Targeted Therapy
PubMed: 38928264
DOI: 10.3390/ijms25126558