Biomarker For Melanoma Research Articles

Identification and validation of matrix metalloproteinase hub genes as potential biomarkers for Skin Cutaneous Melanoma.

The role of matrix metalloproteinases (MMPs) in Skin Cutaneous Melanoma (SKCM) development and progression is unclear so far. This comprehensive study delved into the intricate role of MMPs in SKCM development and progression. RT-qPCR, bisulfite sequencing, and WES analyzed MMP gene expression, promoter methylation, and mutations in SKCM cell lines. TCGA datasets validated findings. DrugBank and molecular docking identified potential regulatory drugs, and cell line experiments confirmed the role of key MMP genes in tumorigenesis. Our findings unveiled significant up-regulation of MMP9, MMP12, MMP14, and MMP16, coupled with hypomethylation of their promoters in SKCM cell lines, implicating their involvement in disease progression. Mutational analysis highlighted a low frequency of mutations in these genes, indicating less involvement of mutations in the expression regulatory mechanisms. Prognostic assessments showcased a significant correlation between elevated expression of these genes and poor overall survival (OS) in SKCM patients. Additionally, functional experiments involving gene silencing revealed a potential impact on cellular proliferation, further emphasizing the significance of MMP9, MMP12, MMP14, and MMP16 in SKCM pathobiology. This study identifies Estradiol and Calcitriol as potential drugs for modulating MMP expression in SKCM, highlighting MMP9, MMP12, MMP14, and MMP16 as key diagnostic and prognostic biomarkers.

Recent advances in organelle-specific autophagy in melanoma

Abstract Organelle-specific autophagy, the selective degradation of distinct cellular organelles, plays a pivotal role in the pathogenesis and progression of various diseases, including melanoma. This review provides a comprehensive analysis of recent advances in organelle-specific autophagy in melanoma, focusing on key processes such as mitophagy, reticulophagy, lysophagy, nucleophagy, pexophagy, and ribophagy. Emerging evidence highlights the roles these autophagic pathways play in melanoma development, with each process contributing uniquely to tumor cell proliferation, migration, invasion, and resistance to therapy. Mitophagy, for example, can both support tumor growth by enhancing mitochondrial quality and suppress it by inducing cell death. Similarly, ER stress exhibits a dual regulatory role, promoting either drug resistance or apoptosis depending on the context, with reticulophagy playing a critical role in modulating these effects. These findings emphasize the importance of further exploring organelle-specific autophagy as both a potential therapeutic target and a prognostic biomarker in melanoma. This research holds significant promise for the development of novel clinical strategies aimed at improving patient outcomes.

Proteomic and metabolomic profiles of plasma-derived Extracellular Vesicles differentiate melanoma patients from healthy controls

BackgroundPlasma-derived Extracellular Vesicles (EVs) have been suggested as novel biomarkers in melanoma, due to their ability to reflect the cell of origin and ease of collection. This study aimed to identify novel EV biomarkers that can discriminate between disease stages. This was achieved by characterising the plasma-derived EVs of patients with melanoma, and comparing their proteomic and metabolomic profile to those from healthy controls. MethodsEVs were isolated from the plasma of 36 patients with melanoma and 13 healthy controls using Size Exclusion Chromatography. Proteomic and Metabolomic Analyses were performed, and machine learning algorithms were used to identify potential proteins and metabolites to differentiate the plasma-derived EVs from melanoma patients of different disease stages. ResultsThe concentration and size of the EV population isolated was similar between groups. Proteins (APOC4, PRG4, PLG, TNC, VWF and SERPIND1) and metabolites (lyso PC a C18:2, PC ae C44:3) previously associated with melanoma pathogenesis were identified as relevant in differentiating between disease stages. ConclusionThe results further support the continued investigation of circulating plasma-derived EVs as biomarkers in melanoma. Furthermore, the potential of combined proteo-metabolomic signatures for differentiation between disease stages may provide valuable insights into early detection, prognosis, and personalised treatment strategies.

Identification of SLC22A17 DNA methylation hotspot as a potential biomarker in cutaneous melanoma

BackgroundCancer onset and progression are driven by genetic and epigenetic alterations leading to oncogene activation and the silencing of tumor suppressor genes. Among epigenetic mechanisms, DNA methylation (methDNA) is gaining growing interest in cancer. Promoter hypomethylation is associated with oncogene activation while intragenic methDNA can be involved in transcriptional elongation, alternative spicing, and the activation of cryptic start sites. Several genes involved in the modulation of the tumor microenvironment are regulated by methDNA, including the Solute Carrier Family 22 Member 17 (SLC22A17), which is involved in iron trafficking and extracellular matrix remodeling cooperating with the Gelatinase-Associated Lipocalin (NGAL) ligand. However, the exact role of intragenic methDNA in cancer has not been fully investigated. Therefore, the aim of the present study is to explore the role of methDNA in the regulation of SLC22A17 in cutaneous melanoma (CM), used as a tumor model.MethodsCorrelation and differential analyses between SLC22A17 expression and methDNA were performed using the data contained in The Cancer Genome Atlas and Gene Expression Omnibus databases. Functional studies on melanoma cell lines treated with 5-Azacytidine (5-Aza) were conducted to assess the correlation between methDNA and SLC22A17 expression. A validation study on the diagnostic potential of the in silico-identified SLC22A17 methDNA hotspot was finally performed by analyzing tissue samples obtained from CM patients and healthy controls.ResultsThe computational analyses revealed that SLC22A17 was significantly downregulated in CM, and its expression was related to promoter hypomethylation and intragenic hypermethylation. Moreover, SLC22A17 overexpression and hypermethylation of two intragenic methDNA hotspots were associated with a better clinical outcome in CM patients. The correlation between SLC22A17 methDNA and expression was confirmed in 5-Aza-treated cells. In agreement with in silico analyses, the SLC22A17 promoter methylation hotspot showed higher methDNA levels in CM samples compared to nevi. In addition, the methDNA levels of this hotspot were positively correlated with advanced CM.ConclusionsThe SLC22A17 methDNA hotspot could represent a promising biomarker for CM, highlighting the regulatory role of methDNA on SLC22A17 expression. These results pave the way for the identification of novel epigenetic biomarkers and therapeutic targets for the management of CM patients.

Blood-based microRNAs as Potential Diagnostic Biomarkers for Melanoma: A Meta-Analysis.

Circulating microRNAs (miRNAs) serve as noninvasive diagnostic markers in many cancers. This meta-analysis aims to evaluate the diagnostic efficacy of circulating microRNAs for melanoma. The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and ROC curve were evaluated using the Meta-Disc V.1.4 and Comprehensive Meta-Analysis V.3.3 software packages. To investigate the heterogeneity, the I2 and Chi-square tests were used. The publishing bias was evaluated using Begg's rank correlation and Egger regression asymmetry tests. A total of 9 articles covering 13 studies (more than 50 miRs individually and in combination) were included, containing 1,355 participants (878 cases and 477 controls). The overall pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio (DOR), and AUC were 0.78 (95% CI: 0.76-0.81), 0.80 (95% CI: 0.77-0.83), 4.32 (95% CI: 3.21-5.82), 0.17 (95% CI: 0.09-0.32), 28.0 (95% CI: 15.34-51.09), and 0.91, respectively. According to Begg's and Egger's tests, there was no publication bias (Begg's p = 0.160 and Egger's p = 0.289). Circulating miRNAs can serve as fair and non-invasive diagnostic biomarkers for melanoma. Additionally, specific miRNAs still need to be discovered for diagnosing melanoma.

S100A9 and HMGB1 orchestrate MDSC-mediated immunosuppression in melanoma through TLR4 signaling

BackgroundImmunotherapies for malignant melanoma are challenged by the resistance developed in a significant proportion of patients. Myeloid-derived suppressor cells (MDSC), with their ability to inhibit antitumor T-cell responses, are a...

Diagnostic Values of Ki67, Cox2, CD31, E-cadherin, VEGF, MMP2, and MMP9 Protein Expression in Human Melanoma

Background: Cutaneous melanoma, the most severe form of skin cancer, has an unpredictable behavior and a high mortality rate. Recent research has identified new biomarkers and their associations with certain histopathological features, offering essential insights into diagnosis, prognosis, and therapeutic strategies. Material and method: In this meticulously designed and executed study, we analyzed 85 formalin-fixed, paraffin-embedded (FFPE) tissue samples using the gold standard technique of immunohistochemistry (IHC) to characterize the protein expression profiles. We used a comprehensive panel of Ki67, Cox2, CD31, VEGF, MMP2, MMP9, and E-cadherin antibodies. Clinical stages were meticulously determined according to TNM classification, the thickness of the Breslow depth, and Clark levels. We employed robust statistical methods such as one-way ANOVA and curve estimation regression to analyze the data. The STRING database, a trusted resource, was used to identify protein-protein interactions and related pathways. Results: The results of our study unveiled novel pairwise positive correlations between CD31 and Ki67 (r = 0.72), and between VEGF and Ki67 protein expression (r = 0.63). We also found a significant inverse relationship between the expression of E-cadherin and some biomarkers, such as Ki67, CD31, and VEGF (p < 0.001 for all). Additionally, our findings revealed a strong positive association between the extent of tumor invasion and the expression levels of Ki67, CD31, and VEGF. The overexpression of these proteins was significantly correlated with advanced clinical stages (p < 0.001 for all). Conclusion: Our study suggests that the biomarkers we examined could be reliable potential diagnostic and prognostic biomarkers for cutaneous melanoma. These findings have the potential to significantly impact the diagnosis, prognosis, and treatment of this deadly disease, offering new avenues for improved patient care.

Circulating biomarkers literature in glioma patient populations.

Liquid biopsy, the process of identifying circulating biomarkers in patients with cancer, has emerged as clinically significant in population screening, tumor status & subclassification, and individualized patient treatment from tumor genotyping. While advances in genome sequencing and mass spectrometry have yielded large datasets available for mining and identified promising biomarkers in breast, melanoma, and lung cancers, among others, challenges persist in identifying biomarkers in neuro-oncology. Despite growing efforts in biomarker research and promise in their emergent clinical potential, there presently exists no validated circulating biomarker test for patients presenting with gliomas, the most common primary brain cancer.

Non-coding RNAs in BRAF-mutant melanoma: targets, indicators, and therapeutic potential.

Melanoma, a highly aggressive skin cancer, is often driven by BRAF mutations, such as the V600E mutation, which promotes cancer growth through the MAPK pathway and contributes to treatment resistance. Understanding the role of non-coding RNAs (ncRNAs) in these processes is crucial for developing new therapeutic strategies. This review aims to elucidate the relationship between ncRNAs and BRAF mutations in melanoma, focusing on their regulatory roles and impact on treatment resistance. We comprehensively reviewed current literature to synthesize evidence on ncRNA-mediated regulation of BRAF-mutant melanoma and their influence on therapeutic responses. Key ncRNAs, including microRNAs and long ncRNAs, were identified as significant regulators of melanoma development and therapy resistance. MicroRNAs such as miR-15/16 and miR-200 families modulate critical pathways like Wnt signaling and melanogenesis. Long ncRNAs like ANRIL and SAMMSON play roles in cell growth, invasion, and drug susceptibility. Specific ncRNAs, such as BANCR and RMEL3, intersect with the MAPK pathway, highlighting their potential as therapeutic targets or biomarkers in BRAF-mutant melanoma. Additionally, ncRNAs involved in drug resistance, such as miR-579-3p and miR-1246, target processes like autophagy and immune checkpoint regulation. This review highlights the pivotal roles of ncRNAs in regulating BRAF-mutant melanoma and their contribution to drug resistance. These findings underscore the potential of ncRNAs as biomarkers and therapeutic targets, paving the way for innovative treatments to improve outcomes for melanoma patients.

The prognostic implications of cuproptosis-related gene signature and the potential of PPIC as a promising biomarker in cutaneous melanoma.

Cutaneous melanoma is the most lethal of all skin tumors. Recently, cuproptosis, a novel form of cell death linked to oxidative phosphorylation, has emerged as an important factor. However, the precise role of cuproptosis in melanoma remains unclear. Our research explored the potential links between cuproptosis-related genes, prognosis, immune microenvironments, and melanoma treatments. Significantly, cuproptosis regulators showed remarkable differences between melanoma and normal tissues, establishing their relevance to melanoma. The newly developed cuproptosis-related gene signature (CGS) demonstrated a robust ability to predict overall survival (OS) in melanoma. We constructed a novel nomogram that combined clinical features with CGS to improve predictive accuracy. In addition, the study revealed correlations between CGS and immune cell populations, including CD8+T cells, Tfh cells, B cells, and myeloid-derived suppressor cells. Within the CGS, Peptidylprolyl isomerase C (PPIC) emerged as the most strongly associated with poor prognosis and drug resistance in melanoma. PPIC was identified as a promoter of melanoma progression, enhancing cell invasiveness while concurrently suppressing CD8+T cell activation. This comprehensive study not only elucidated the intricate connections between CGS, melanoma prognosis, immune microenvironment, and drug resistance but also provided compelling evidence supporting PPIC as a promising biomarker for predicting OS in melanoma treatment.

PRAME expression in melanoma is negatively regulated by TET2-mediated DNA hydroxymethylation.

Melanoma biomarker PRAME expression is negatively regulated epigenetically by TET2-mediated DNA hydroxymethylation.

TRP channel-related LncRNAs, AC092535.4 and LINC01637, as novel prognostic biomarkers for uveal melanoma.

Transient receptor potential (TRP) channels function as cellular sensors with a broad impact, and their dysregulation is linked to numerous cancers. The influence of TRP channel-related long noncoding RNAs (TCRLs) on uveal melanoma (UM) remains poorly understood. We employed bioinformatics to examine the RNA-seq data and relevant clinical information of UM in the TCGA databases. By implementing coexpression analysis, we identified differentially expressed TCRLs. Using univariate Cox regression analysis, selection operator (LASSO) algorithm and stepwise regression, five key prognostic biomarkers were chosen. The high- and low-risk groups were divided based on the risk scores. Afterwards, the prediction performance of the signature was evaluated by receiver operating characteristic (ROC) curve and Kaplan-Meier (K-M) survival analysis. The functional enrichment analysis of TCRLs was also investigated. Following that, we examined immune cell infiltration, immune checkpoint expression, and tumor immune microenvironment between patients in high and low risk groups. TCRLs were validated using Random forests and multifactor Cox analysis. Candidate biomarkers were identified and screened. Finally, the effects of the candidate biomarkers on the proliferation, migration and invasion of UM cells were detected by CCK-8 assay, migration assay and perforation invasion assay. The risk score generated by five TCRLs demonstrated robust predictive power. The high-risk group exhibited a poorer prognosis, increased immune cell infiltration, and an active tumor immune microenvironment compared to the low-risk group. Furthermore, two TCRLs of risk score, AC092535.4 and LINC01637, were screened to multiplex modelling. The in vitro experiments demonstrated that UM cells were suppressed following AC092535.4 or LINC01637 knockdown. Two TCRLs, AC092535.4 and LINC01637, serve as novel prognostic biomarkers for uveal melanoma and may present potential therapeutic targets.

CTHRC1 is associated with BRAF(V600E) mutation and correlates with prognosis, immune cell infiltration, and drug resistance in colon cancer, thyroid cancer, and melanoma.

Colon cancer, thyroid cancer, and melanoma are common malignant tumors that seriously threaten human health globally. The B-Raf proto-oncogene, serine/threonine kinase (BRAF)(V600E) mutation is an important driver gene mutation in these cancer types. In this study, we identified that collagen triple helix repeat containing 1 (CTHRC1) expression was associated with the BRAF(V600E) mutation in colon cancer, thyroid cancer, and melanoma. Based on database analysis and clinical tissue studies, CTHRC1 was verified to correlate with poor prognosis and worse clinicopathological features in colon cancer and thyroid cancer patients, but not in patients with melanoma. Several signaling pathways, immune cell infiltration, and immunotherapy markers were associated with CTHRC1 expression. Additionally, a high level of CTHRC1 was correlated with decreased sensitivity to antitumor drugs (vemurafenib, PLX-4720, dabrafenib, and SB-590885) targeting the BRAF(V600E) mutation. This study provides evidence of a significant correlation between CTHRC1 and the BRAF(V600E) mutation, suggesting its potential utility as a diagnostic and prognostic biomarker in human colon cancer, thyroid cancer, and melanoma.

Silencing Exosomal circ102927 Inhibits Foot Melanoma Metastasis via Regulating Invasiveness, Epithelial-Mesenchymal Transition and Apoptosis.

Exosomes contain abundant circular RNAs (circRNAs), playing an important role in intercellular communication. However, the function and underlying molecular mechanism of exosomal circRNAs in foot metastatic melanoma remain unclear. Twelve differentially expressed exosomal circRNAs between patients with metastatic and primary foot melanoma were screened through high-throughput sequencing, and their expression levels were detected by the real-time reverse transcriptase-polymerase chain reaction (RT-qPCR). CircRNA102927 silencing and overexpression A2058 cell line was constructed, and the effects of circRNA102927 on cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) were assessed using cell counting kit-8 (CCK-8), flow cytometry, wound healing, Transwell, and Western blot assays, respectively. Twelve differentially expressed exosomal circRNAs were screened and ROC curve showed that six circRNAs could be used as the diagnostic biomarkers for metastatic melanoma. Melanoma-secreted exosomes induced the differentiation of CD4+ T cells into Treg cells. CircRNA102927 was highly expressed in metastatic melanomas. Functionally, circRNA102927 silencing inhibited proliferation, EMT, migration, and invasion in metastatic melanoma cells, while promoting apoptosis. Meanwhile, overexpression of circRNA102927 had the opposite effects. Our investigation suggests that silencing exosomal circRNA102927 may suppress foot melanoma metastasis by inhibiting invasiveness, EMT and promoting apoptosis.

RARRES1 identified by comprehensive bioinformatic analysis and experimental validation as a promising biomarker in Skin Cutaneous Melanoma

Skin cutaneous melanoma (SKCM) is a highly malignant form of skin cancer, known for its unfavorable prognosis and elevated mortality rate. RARRES1, a gene responsive to retinoic acid receptors, displays varied functions in various cancer types. However, the specific role and underlying mechanisms of RARRES1 in SKCM are still unclear. GSE15605 was utilized to analyze the expression of RARRES1 in SKCM. Subsequently, the TCGA and GEO databases were employed to investigate the relationships between RARRES1 and clinicopathological parameters, as well as the prognostic implications and diagnostic efficacy of RARRES1 in SKCM. GO, KEGG, and GSEA analyses were conducted to explore the potential functions of RARRES1. Furthermore, the associations between RARRES1 and immune infiltration were examined. Genomic alterations and promoter methylation levels of RARRES1 in SKCM were assessed using cBioPortal, UALCAN, and the GEO database. Finally, RARRES1 expression in SKCM was validated through immunohistochemistry, and its functional role in SKCM progression was elucidated via in vivo and in vitro experiments. We found that RARRES1 was downregulated in SKCM compared with normal tissues, and this low expression was associated with worse clinicopathological features and poor prognosis of SKCM. The diagnostic efficacy of RARRES1, as determined by ROC analysis, was 0.732. Through GO, KEGG, and GSEA enrichment analysis, we identified 30 correlated genes and pathways that were mainly enriched in the tumor immune microenvironment, proliferation, apoptosis, and autophagy. Additionally, RARRES1 expression was found to be positively related to the infiltration of various immune cells in SKCM, particularly macrophages and T helper cells, among others. Analysis of genomic alterations and promoter methylation revealed that shallow deletion and hypermethylation of the RARRES1 promoter could lead to reduced RARRES1 expression. IHC validation confirmed the downregulation of RARRES1 in SKCM. Moreover, overexpression of RARRES1 inhibited the proliferation and migration of A375 cells, promoted apoptosis, and inhibited autophagic flux. In the mouse xenograft model, RARRES1 overexpression also suppressed SKCM tumor growth. Collectively, these findings suggest that RARRES1 may function as a suppressor and could potentially serve as a prognostic biomarker and therapeutic target for SKCM.

Correlation of eTILs with recurrence free survival (RFS) in stage IIB-IIIA melanoma and use as biomarker for stratification for clinical trials.

9567 Background: Immunotherapy is approved for resected stage IIB-IIIC, but treatment of all patients, particularly those with IIB-IIIA disease, incurs unneeded expense and toxicity. Biomarkers are urgently needed for patient stratification. Time constraints in clinical trial design have led to the adoption of recurrence free survival (RFS) as a primary endpoint in adjuvant melanoma trials. Tumor infiltrating lymphocytes (TILs) are a well-established biomarker in primary melanoma, but quantification is subjective. Electronic TILs (eTILs) are a previously published automated digital pathology tool to quantify TILs. Methods: A retrospective cohort of 194 patients with Stage II-III melanoma from Roswell Park Comprehensive Cancer Center (RPCCC, n=133) and Geisinger Medical Center (GMC, n=61) were evaluated for eTILS by blinded investigators. Patients were included based on a search of dermatopathology databases and tissue availability. Digital images of diagnostic slides were analyzed using quPath, a publicly available software. Briefly, tumor areas were selected to include infiltrating lymphocytes with minimal adjacent stroma. Color variations in H&E images were standardized, and cell types quantified utilizing a machine learning algorithm. A previously published threshold of 16.6% eTILs, calculated as lymphocytes/tumor cells x 100, was used. Patients were staged using American Joint Committee on Cancer (AJCC) guidelines, version 8. Survival was assessed using Kaplan-Meier Curves and correlation of clinic-pathologic features with survival was tested using Cox Proportional Hazards Models. Results: Of 194 patients, 56 were stage IIA, 85 were IIB-IIIA, and 53 were IIIB-D. Median follow up was 47.5 months. 103 patients had eTILs >16.6% of whom 13 (12.6%) died and 84 had eTILS <16.6% of whom 23 (27.4%) died during follow-up. HR for death from melanoma within 5 years for the high eTIL group was 0.53 (CI 0.21-0.90, p=0.024). DSS was significantly longer in the high eTIL group than the low eTIL group (p=0.0095). Among 85 stage IIB-IIIA patients, local and distant recurrence data was available for the RPCCC cohort of 68 patients. 46 of these patients had high eTILs of whom 9(19.6%) recurred and 22 had low eTILS of whom 10 (45.95%) recurred. HR for recurrence within 5 years for the high eTIL group was 0.44 (CI0.23-0.83, p=0.012). RFS was significantly longer in the high TIL group (p=0.016) as was distant metastatic recurrent survival (p= 0.0063). eTIL score correlated with RFS in a univariable Cox model (p=0.033) and added to stage and depth in a multivariable Cox model (p=0.018). Conclusions: eTILs, readily evaluable at low cost using diagnostic slides, correlate with clinical outcome in a retrospective cohort of 194 patients. eTILS should be prospectively evaluated as a biomarker to stratify early-stage melanoma patients for adjuvant clinical trials.

GLI Transcriptional Targets S100A7 and KRT16 Show Upregulated Expression Patterns in Epidermis Overlying the Tumor Mass in Melanoma Samples.

Although not completely understood, the role of the Hedgehog-GLI (HH-GLI) signaling pathway in melanoma and epithelial skin tumors has been reported before. In this study, we confirmed in various melanoma cell line models that keratin 16 (KRT16) and S100 Calcium-Binding Protein A7 (S100A7) are transcriptional targets of GLI Family Zinc Finger (GLI) proteins. Besides their important role in protecting and maintaining the epidermal barrier, keratins are somehow tightly connected with the S100 family of proteins. We found that stronger expression of KRT16 indeed corresponds to stronger expression of S100A7 in our clinical melanoma samples. We also report a trend regarding staining of GLI1, which corresponds to stronger staining of GLI3, KRT16, and S100A7 proteins. The most interesting of our findings is that all the proteins are detected specifically in the epidermis overlying the tumor, but rarely in the tumor itself. The examined proteins were also not detected in the healthy epidermis at the edges of the sample, suggesting that the staining is specific to the epidermis overlaying the tumor mass. Of all proteins, only S100A7 demonstrated a statistically significant trend regarding tumor staging and staining intensity. Results from our clinical samples prove that immune infiltration is an important feature of melanoma. Pigmentophages and tumor-infiltrating lymphocytes (TIL) demonstrate a significant association with tumor stage, while mononuclear cells are equally present in all stages. For S100A7, we found an association between the number of TILs and staining intensity. Considering these new findings presented in our study, we suggest a more detailed examination of the possible role of the S100A7 protein as a biomarker in melanoma.

Transdermal Sensing of Enzyme Biomarker Enabled by Chemo-Responsive Probe-Modified Epidermal Microneedle Patch in Human Skin Tissue.

Wearable bioelectronics represents a significant breakthrough in healthcare settings, particularly in (bio)sensing which offers an alternative way to track individual health for diagnostics and therapy. However, there has been no notable improvement in the field of cancer, particularly for skin cancer. Here, a wearable bioelectronic patch is established for transdermal sensing of the melanoma biomarker, tyrosinase (Tyr), using a microneedle array integrated with a surface-bound chemo-responsive smart probe to enable target-specific electrochemical detection of Tyr directly from human skin tissue. The results presented herein demonstrate the feasibility of a transdermal microneedle sensor for direct quantification of enzyme biomarkers in an ex vivo skin model. Initial performance analysis of the transdermal microneedle sensor proves that the designed methodology can be an alternative for fast and reliable diagnosis of melanoma and the evaluation of skin moles. The innovative approach presented here may revolutionize the landscape of skin monitoring by offering a nondisruptive means for continuous surveillance and timely intervention of skin anomalies, such as inflammatory skin diseases or allergies and can be extended to the screening of multiple responses of complementary biomarkers with simple modification in device design.

Melanin-Targeting Radiotracers and Their Preclinical, Translational, and Clinical Status: From Past to Future.

Melanin is one of the representative biomarkers of malignant melanoma and a potential target for diagnosis and therapy. With advancements in chemistry and radiolabeling technologies, promising strides have been made to synthesize radiolabeled melanin-binding molecules for various applications. We present an overview of melanin-targeted radiolabeled molecules and compare their features reported in preclinical studies. Clinical practice and trials are also discussed to elaborate on the safety and validity of the probes, and expanded applications beyond melanoma are reviewed. Melanin-targeted imaging holds potential value in the diagnosis, staging, and prognostic assessment of melanoma and other applications. Melanin-targeted radionuclide therapy possesses immense potential but requires more clinical validation. Furthermore, an intriguing avenue for future research involves expanding the application scope of melanin-targeted probes and exploring their value.

3150: Biological correlates of radiomic biomarkers in malignant melanoma treated with immunotherapy

3150: Biological correlates of radiomic biomarkers in malignant melanoma treated with immunotherapy