• bacteria
• drug delivery
• immunotherapy
• melanoma
• tumor microenvironment

• Melanoma/therapy
• Melanoma/pathology
• Melanoma/drug therapy
• Humans
• Animals
• Bacteria
• Drug Delivery Systems/methods
• Tumor Microenvironment/drug effects
• Skin Neoplasms/therapy
• Skin Neoplasms/drug therapy
• Skin Neoplasms/pathology
• Immunotherapy/methods

• 92059107 National Natural Science Foundation of China
• 32122048 National Natural Science Foundation of China
• 32471457 National Natural Science Foundation of China
• 82272755 National Natural Science Foundation of China
• 51825302 National Natural Science Foundation of China
• 11832008 National Natural Science Foundation of China
• 2023CDJXY-009 Fundamental Research Funds for the Central Universities
• 2024CDJYXTD-008 Fundamental Research Funds for the Central Universities
• 2022CDJYGRH-007 Fundamental Research Funds for the Central Universities
• 2023CDJYGRH-YB01 Fundamental Research Funds for the Central Universities
• 2024CDJXY016 Fundamental Research Funds for the Central Universities
• 2023CDJYGRH-ZD01 Fundamental Research Funds for the Central Universities
• 2023M740405 China Postdoc Science Foundation
• X20230241 Chongqing Municipal Science and Technology Bureau
• cstb2022nscq-msx0488 Chongqing Municipal Science and Technology Bureau
• cstc2021jcyj-jqX0022 Chongqing Municipal Science and Technology Bureau
• 2022TIAD-KPX0221 Chongqing Municipal Science and Technology Bureau
• CSTB2022TIAD-STX0015 Chongqing Municipal Science and Technology Bureau
• 2022NSCQ-MSX0706 Chongqing Municipal Science and Technology Bureau
• cstc2020jcyj-zdxmX0013 Chongqing Municipal Science and Technology Bureau

• FOXP3
• malignant melanoma
• metastasis
• prognosis
• tumor-infiltrating lymphocytes

• Humans
• Forkhead Transcription Factors/metabolism
• Melanoma/pathology
• Melanoma/metabolism
• Melanoma/immunology
• Melanoma/mortality
• Male
• T-Lymphocytes, Regulatory/immunology
• T-Lymphocytes, Regulatory/metabolism
• Female
• Middle Aged
• Prognosis
• Aged
• Adult
• Lymphatic Metastasis
• Biomarkers, Tumor/metabolism
• Retrospective Studies
• Skin Neoplasms/pathology
• Skin Neoplasms/immunology
• Skin Neoplasms/metabolism
• Skin Neoplasms/mortality
• Aged, 80 and over
• Neoplasm Recurrence, Local/pathology

• LAG-3
• PD-1
• TIM-3
• checkpoint receptors
• melanoma
• pulsed electric field

• Daina 2 - 2020/38/L/NZ7/00342 National Science Center
• Nr. S-LL-21-4 Lietuvos Mokslo Taryba
• GMIN.D260.22.005 WCA FAST II

• Diagnostic Techniques and Procedures
• Genes, Neoplasm
• MELANOMA
• Medical Oncology
• Pathology, Molecular

• Humans
• Proto-Oncogene Proteins B-raf/genetics
• Pathology, Molecular
• Workflow
• Prospective Studies
• Quality Improvement
• DNA Mutational Analysis/methods
• Melanoma/genetics
• Melanoma/therapy
• Melanoma/pathology
• Mutation
• High-Throughput Nucleotide Sequencing/methods
• Melanoma, Cutaneous Malignant

• Immunotherapy
• Melanoma
• Tumor Biomarkers

Objective: To reveal the potential mechanisms of curcumin for the treatment of skin cutaneous melanoma (SKCM) and its identify novel prognostic biomarkers.

Methods: We searched the Cancer Genome Atlas and Traditional Chinese Medicine Systems Pharmacology database for the data on SKCM and curcumin. We conducted data analysis using R and online tools. The propagation and migration of SKCM cells were assessed with CCK-8 and scratch wound assays, respectively. We assessed apoptosis by TUNEL assay and western blot.

Results: The survival analysis revealed that the mRNA expressions of DPYD, DPYS, LYN, PRKCQ, and TLR1 were significantly related to a favorable overall survival in SKCM patients. Additionally, the mRNA expression level of DPYD was associated with GPI, LYN, PCSK9, PRKCQ, and TLR1 mRNAs. GSEA results showed that the prognostic hub genes were augmented with ultraviolet, apoptosis, and metastasis. Curcumin expressed proliferation and migration of SK-MEL-1 cells (p < 0.05), and induced apoptosis (p < 0.05) significantly.

Conclusion: Curcumin may have potential therapeutic effects in SKCM by inhibiting cell proliferation and migration and inducing apoptosis by regulating oxygen-related signaling pathways. The hub genes might be identified as novel biomarkers for SKCM.

Nowadays, many individuals, whether healthy or diagnosed with disease, tend to expose themselves to various easily accessible natural products in hopes of benefiting their health and well-being. Mediterranean populations have traditionally used olive oil not only in nutrition but also in cosmetics, including skincare. In this study, the phenolic profile—composed of twelve compounds altogether, including the secoiridoids oleocanthal (OCAL) and oleacein (OCEIN)—of extra virgin olive oil (EVOO) from autochthonous cultivars from Croatia was determined using ¹H qNMR spectroscopy and HPLC-DAD analysis, and its biological activity was investigated in melanoma cell lines. The EVOO with the highest OCEIN content had the strongest anti-cancer activity in A375 melanoma cells and the least toxic effect on the non-cancerous keratocyte cell line (HaCaT). On the other hand, pure OCAL was shown to be more effective and safer than pure OCEIN. Post-treatment with any of the EVOO phenolic extracts (EVOO-PEs) enhanced the anti-cancer effect of the anti-cancerous drug dacarbazine (DTIC) applied in pre-treatment, while they did not compromise the viability of non-cancerous cells. The metastatic melanoma A375M cell line was almost unresponsive to the EVOO-PEs themselves, as well as to pure OCEIN and OCAL. Our results demonstrate that olive oils and/or their compounds may have a potentially beneficial effect on melanoma treatment. However, their usage can be detrimental or futile, especially in healthy cells, due to inadequately applied concentrations/combinations or the presence of resistant cells.

High-dose ascorbate paradoxically acts as a pro-oxidant causing the formation of hydrogen peroxide in an oxygen dependent manner. Tumor cells (in particular melanoma cells) show an increased vulnerability to ascorbate induced reactive oxygen species (ROS). Therefore, high-dose ascorbate is a promising pharmacological approach to treating refractory melanomas, e.g., with secondary resistance to targeted BRAF inhibitor therapy. BRAF mutated melanoma cells were treated with ascorbate alone or in combination with the BRAF inhibitor vemurafenib. Viability, cell cycle, ROS production, and the protein levels of phospho-ERK1/2, GLUT-1 and HIF-1α were analyzed. To investigate the treatment in vivo, C57BL/6NCrl mice were subcutaneously injected with D4M.3A (Braf^V600E) melanoma cells and treated with intraperitoneal injections of ascorbate with or without vemurafenib. BRAF mutated melanoma cell lines either sensitive or resistant to vemurafenib were susceptible to the induction of cell death by pharmacological ascorbate. Treatment of Braf^V600E melanoma bearing mice with ascorbate resulted in plasma levels in the pharmacologically active range and significantly improved the therapeutic effect of vemurafenib. We conclude that intravenous high-dose ascorbate will be beneficial for melanoma patients by interfering with the tumor’s energy metabolism and can be safely combined with standard melanoma therapies such as BRAF inhibitors without pharmacological interference.

• BRAF inhibitor
• BRAFV600E
• D4M.3A melanoma cells
• ascorbate
• cancer
• malignant melanoma
• vemurafenib
• vitamin C

• 11β-hydroxysteroid dehydrogenase type 1-antisense RNA 1
• bioinformatics analysis
• cutaneous melanoma
• immune infiltration
• overexpression
• prognosis
• quantitative PCR

• ETS factors
• melanoma
• mouse models
• small molecule inhibitors
• therapeutics

• R01CA184001 NIH HHS
• R01AR062547 NIH HHS
• Stiefel Investigative Award American Skin Association
• Research grant Harry J. Lloyd Charitable Trust
• Dermatology Scholars Award Boston University

• BRAF
• acetylation stoichiometry
• driver mutations
• histopathology
• metastatic melanoma
• phosphorylation
• posttranslational-modification
• proteogenomics

• Antineoplastic Agents/therapeutic use
• Blood Proteins/metabolism
• Cell Line
• Chromatography, High Pressure Liquid
• Databases, Factual
• Humans
• Melanoma/drug therapy
• Melanoma/metabolism
• Melanoma/pathology
• Mutation
• Protein Processing, Post-Translational/genetics
• Proteome/metabolism
• Proteomics/methods
• Proto-Oncogene Proteins B-raf/genetics
• Proto-Oncogene Proteins B-raf/metabolism
• Tandem Mass Spectrometry
• Transcriptome

• Conselho Nacional de Desenvolvimento Científico e Tecnológico
• Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
• Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
• Országos Tudományos Kutatási Alapprogramok
• Fru Berta Kamprads Stiftelse
• National Research Foundation of Korea

Prognosis of metastatic melanoma has undergone substantial improvement with the discovery of checkpoint inhibitors. Immunotherapies and targeted therapies have improved the median overall survival (OS) of metastatic melanoma from 6 months to more than 3 years. However, still about half of the patients die due to uncontrolled disease. Therefore, multiple strategies are currently being investigated to improve outcomes. One such strategy is intralesional/intratumoral (IT) therapies which can either directly kill the tumor cells or make the tumor more immunogenic to be recognized by the immune system. Talimogene laherparepvec (T-VEC), an oncolytic virus, is the first FDA approved IT therapy. This review focuses on the current status of IT agents currently under clinical trials in melanoma. Reviewed therapies include T-VEC, T-VEC with immune checkpoint inhibitors including ipilimumab and pembrolizumab or other agents, RP1, OrienX010, Canerpaturev (C-REV, HF10), CAVATAK (coxsackievirus A21, CVA21) alone or in combination with checkpoint inhibitors, oncolytic polio/rhinovirus recombinant (PVSRIPO), MAGE-A3-expressing MG1 Maraba virus, VSV-IFNbetaTYRP1, suicide gene therapy, ONCOS-102, OBP-301 (Telomelysin), Stimulation of Interferon Genes Pathway (STING agonists) including DMXAA, MIW815 (ADU-S100) and MK-1454, PV-10, toll-like receptors (TLRs) agonists including TLR-9 agonists (SD-101, CMP-001, IMO-2125 or tilsotolimod, AST-008 or cavrotolimod, MGN1703 or lefitolimod), CV8102, NKTR-262 plus NKTR-214, LHC165, G100, intralesional interleukin-2, Daromun (L19IL2 plus L19TNF), Hiltonol (poly-ICLC), electroporation including calcium electroporation and plasmid interleukin-12 electroporation (pIL-12 EP), IT ipilimumab, INT230-6 (cisplatin and vinblastine with an amphiphilic penetration enhancer), TTI-621 (SIRPαFc), CD-40 agonistic antibodies (ABBV-927 and APX005M), antimicrobial peptide LL37 and other miscellaneous agents.

• Melanoma
• intralesional
• intratumoral
• talimogene laherparepvec (T-VEC)

• Ca2+ overload
• Melanoma
• Mitochondrial impairment
• Paraptosis
• ROS production
• Tocotrienols

• Antineoplastic Agents/pharmacology
• Calcium/metabolism
• Cell Line, Tumor
• Endoplasmic Reticulum/drug effects
• Endoplasmic Reticulum/metabolism
• Endoplasmic Reticulum/pathology
• Humans
• Melanoma/metabolism
• Melanoma/pathology
• Membrane Potential, Mitochondrial/drug effects
• Mitochondria/drug effects
• Mitochondria/metabolism
• Mitochondria/pathology
• Mitochondrial Swelling/drug effects
• Mitogen-Activated Protein Kinases/metabolism
• Reactive Oxygen Species/metabolism
• Regulated Cell Death/drug effects
• Signal Transduction/drug effects
• Vitamin E/analogs & derivatives
• Vitamin E/pharmacology

• MIUR Progetto di Eccellenza
• AIRC Fellowship
• Università degli Studi di Milano

Bacillus Calmette–Guérin (BCG), an attenuated vaccine from Mycobacterium bovis, was initially developed as an agent for vaccination against tuberculosis. BCG proved to be the first successful immunotherapy against established human bladder cancer and other neoplasms. The use of BCG has been shown to induce a long-lasting antitumor response over all other forms of treatment against intermediate, non-invasive muscle bladder cancer Several types of tumors may now be treated by releasing the immune response through the blockade of checkpoint inhibitory molecules, such as CTLA-4 and PD-1. In addition, Toll-Like Receptor (TLR) agonists and BCG are used to potentiate the immune response against tumors. Studies concerning TLR-ligands combined with BCG to treat melanoma have demonstrated efficacy in treating mice and patients This review addresses several interventions using BCG on neoplasms, such as Leukemia, Bladder Cancer, Lung Cancer, and Melanoma, describing treatments and antitumor responses promoted by this attenuated bacillus. Of essential importance, BCG is described recently to participate in an adequate microbiome, establishing an effective response during cell-target therapy when combined with anti-PD-1 antibody, which stimulates T cell responses against the melanoma. Finally, trained immunity is discussed, and reprogramming events to shape innate immune responses are addressed.

• BCG
• cancer
• trained immunity

Even though melanoma represents a small percentage of all cutaneous cancers, it is responsible for most deaths from skin neoplasms. In early stages it can be successfully treated with surgery, but as the disease expands the survival rate drops significantly. For many years the mainstay of treatment for metastatic melanoma was chemotherapeutic agents, even though they failed to prove survival prolongation. After the advent of ipilimumab, a survival benefit and better overall response rate could be offered to the patients. Other new therapies, such as immunotherapies, targeted therapies, vaccines, and small molecules, are currently being studied. Also, combination regimens have demonstrated superiority to some monotherapies. Nowadays, ipilimumab should no longer be considered the first-line therapy given its severe toxicity and lower efficacy, while nivolumab remains efficacious and has a good safety profile. T-VEC as monotherapy has been shown to be an elegant alternative even for the elderly or cases of head and neck melanomas. If the BRAF mutation status is positive, the combination of dabrafenib and trametinib could be an option to consider. Despite the success of the novel treatments, their effectiveness is still limited. New studies have opened up new avenues for future research in melanoma treatment, which is expected to lead to better therapeutic outcomes for our patients. The objective of this review is to discuss the novel therapies for metastatic melanoma that have been tested in humans during the last 3 years to obtain a sharper perspective of the available treatment options for specific patient characteristics.

• Immune checkpoint inhibitors
• Melanoma
• Metastatic melanoma
• Small molecules
• Targeted therapy
• Vaccines

• cell proliferation
• dihydrocapsaicin
• melanoma
• metastasis
• ubiquitination
• β-catenin

• National Natural Science Foundation of China
• Natural Science Foundation of Chongqing
• Fundamental Research Funds for the Central Universities

Background: Total saponins from Rubus parvifolius L. (TSRP) are the main bioactive fractions responsible for the anti-tumor activities. The work was aimed to evaluate the anti-tumor effect of TSRP in malignant melanoma (MM) in vitro and in vivo.

Methods and results: Anti-melanoma cell proliferation, invasion and migration effect of TSRP were detected in human MM A375 cells under the indicated time and dosages. In vivo anti-tumor effect of TSRP was measured in A375 xenograft immunodeficient nude mice. Sixty A375 xenografts were randomly divided into five groups: Vehicle, cyclophosphamide (CTX, 20 mg/kg), TSRP (25 mg/kg), TSRP (50 mg/kg) and TSRP (100 mg/kg) groups for 14 days’ treatment. In addition, the melanoma metastasis in lung in vivo of TSRP was detected in A375 tail vein injection mice, and the histopathalogical analysis of the lung metastasis was detected by Hematoxylin–Eosin (H&E) staining. TSRP significantly inhibited the cell proliferation, invasion and migration of A375 in vitro at the indicated time and dosages. TSRP treatment effectively blocked the tumor growth in immunodeficient nude mice. In addition, TSRP also significantly inhibited the lung metastasis of melanoma.

Conclusion: The present study indicated that the TSRP has a remarkable anti-MM effect, which mainly through the inhibition of the cell invasion, migration and tumor metastasis.

• Malignant melanoma
• Metastasis
• Rubus parvifolius
• Total saponins

• Hippo pathway
• Melanoma
• Metastasia
• Triptonide

Tumor vasculature constitutes a formidable hurdle for the efficient delivery of cancer nanomedicine into tumors. The leverage of passive pathway through inter-endothelial gaps in tumor blood vessels might account for limited extravasation of nanomedicine into tumor microenvironment (TME). Herein, Annexin A1 antibody-installed mesoporous organosilica nanoplatforms carrying immunotherapeutics of anti-PD-L1 antibody (aPD-L1) and Indoximod are developed to target at caveolar Annexin-A1 protein of luminal endothelial cells and to trigger the active trans-endothelial transcytosis of nanomedicine mediated by caveolae. Such strategy enables rapid nanomedicine extravasation across tumor endothelium and relatively extensive accumulation in tumor interstitium. aPD-L1 and Indoximod release from aPD/IND@MON-aANN in a reduction-responsive manner and synergistically facilitate the intratumoral infiltration of cytotoxic T lymphocytes and reverse the immunosuppressive TME, thus demonstrating substantial anti-tumor efficacy in subcutaneous 4T1 breast tumors and remarkable anti-metastatic capacity to extend the survival of 4T1 tumor metastasis model. Moreover, aPD/IND@MON-aANN nanomedicine also exhibits distinct superiority over the combination therapy of free drugs to potently attenuate the progression of urethane-induced orthotopic lung cancers. Collectively, aPD/IND@MON-aANN nanoplatforms with boosted delivery efficiency via antibody-activated trans-endothelial pathway and enhanced immunotherapeutic efficacy provides perspectives for the development of cancer nanomedicines.

•

The nanomedicine overcomes tumor vascular barrier by active transcytosis via caveolae initiated by the conjugated aANXA1.

• Active transcytosis
• Cancer immunotherapy
• Drug delivery
• Extravasation
• Stimulus-responsive nanomedicine

• BRAF
• molecular oncology
• predictive molecular pathology
• prognostic biomarker

• Biomarkers, Tumor/genetics
• Humans
• Mutation/genetics
• Neoplasms/genetics
• Proto-Oncogene Proteins B-raf/genetics
• Signal Transduction/genetics

• PD-1
• antibiotics
• melanoma
• microbiome
• microbiota

• Diazepine
• Hybrid particles
• Lipid-based drug delivery system
• Melanoma
• Vegetable oil

• BRAF
• Lung cancer
• Melanoma
• Precision medicine
• Predictive molecular pathology

• Advanced melanoma
• Expert views
• Health technology assessment
• Implementation
• Tumor-infiltrating lymphocytes

• Alkaloid
• Apoptosis
• Cyclodextrin
• Harman
• Skin cancer

Indoleamine 2,3-dioxygenase 1 (IDO1) catalyzes the first, rate-limiting step of the so-called “kynurenine pathway”, which converts the essential amino acid L-tryptophan (Trp) into the immunosuppressive metabolite L-kynurenine (Kyn). While expressed constitutively by some tissues, IDO1 can also be induced in specific subsets of antigen-presenting cells that ultimately favor the establishment of immune tolerance to tumor antigens. At least in part, the immunomodulatory functions of IDO1 can be explained by depletion of Trp and accumulation of Kyn and its derivatives. In animal tumor models, genetic or pharmacological IDO1 inhibition can cause the (re)activation of anticancer immune responses. Similarly, neoplasms expressing high levels of IDO1 may elude anticancer immunosurveillance. Therefore, IDO1 inhibitors represent promising therapeutic candidates for cancer therapy, and some of them have already entered clinical evaluation. Here, we summarize preclinical and clinical studies testing IDO1-targeting interventions for oncologic indications.

• Dendritic cells
• epacadostat
• immune checkpoint blockers
• indoximod
• navoximod

• Anti-sMIC antibody
• Melanoma
• NKG2D ligands
• PD1/PDL1 blockade
• Soluble MHC I chain-related molecule (sMIC)

• Melanoma
• Metabolic adaptation
• Mitochondria
• OXPHOS
• Phenotype shifting
• Resistance
• Slow-cycling

• Cancer unit
• Colorectal cancer
• KRAS
• Metastasis
• outcome

Melanoma is the less common but the most malignant skin cancer. Since the survival rate of melanoma metastasis is about 10–15%, many different studies have been carried out in order to find a more effective treatment. Although the development of target-based therapies and immunotherapeutic strategies has improved chances for patient survival, melanoma treatment still remains a big challenge for oncologists. Here, we collect recent data about the emerging role of melanoma-associated microRNAs (miRNAs) currently available treatments, and their involvement in drug resistance. We also reviewed miRNAs as prognostic factors, because of their chemical stability and resistance to RNase activity, in melanoma progression. Moreover, despite miRNAs being considered small conserved regulators with the limitation of target specificity, we outline the dual role of melanoma-associated miRNAs, as oncogenic and/or tumor suppressive factors, compared to other tumors.

• drug resistance
• melanoma
• metastasis
• miRNAs

• 2-deoxy-D-glucose
• T-regulatory cells
• cyclophosphamide
• dendritic cells
• immune enhancement
• metabolic inhibitor
• targeted cancer therapy

• CTLA-4
• IFNα-2b
• IL-2
• Immune checkpoint inhibitors
• Immunotherapy
• Malignant melanoma
• PD-1

Primary malignant melanoma of the esophagus accounts for 0.1%-0.2% of all esophageal malignancies, including melanotic and amelanotic melanomas. Primary amelanotic malignant melanoma of the esophagus is extremely rare, and only about 20 cases have been published in the literature to date. Most primary malignant melanomas of the esophagus are diagnosed following development of metastatic lesions and thus have a very poor prognosis. The median survival duration of patients with metastatic melanoma has been reported to be 6.2 mo.

A 49-year-old woman was referred to our hospital with a diagnosis of esophageal cancer. Endoscopy, biopsy, imaging evaluation, and physical examination at our hospital indicated a diagnosis of advanced primary amelanotic malignant melanoma of the esophagus. Immunohistochemical staining confirmed melanoma. Nuclear medicine examination revealed a left iliac bone metastatic lesion. After discharge, the patient self-administered apatinib for 3 mo, followed by oral treatment with Chinese medicines (also self-administered) for 2 mo. No treatments had been taken since then. The patient has survived with no growth out to the most recent follow-up (24 mo post diagnosis), and she always presented with a positive attitude about her condition during this period.

Survival following metastatic melanoma might be related to the pharmaceutical and Chinese medicine treatment and the patient's positive attitude.

• Esophagus
• Amelanotic malignant melanoma
• Immune
• Emotion
• Psychological intervention
• Case report

• Hypophysitis
• Immune related adverse side effects
• Immunotherapy
• Ipilimumab
• Malignant melanoma

• Aged
• Aged, 80 and over
• Antineoplastic Agents, Immunological/adverse effects
• Antineoplastic Agents, Immunological/therapeutic use
• Female
• Humans
• Hypophysitis/chemically induced
• Hypophysitis/diagnosis
• Ipilimumab/adverse effects
• Ipilimumab/therapeutic use
• Male
• Melanoma/drug therapy
• Middle Aged
• Progression-Free Survival
• Retrospective Studies
• Risk Factors

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that responds to a wide range of chemicals, including chemical carcinogens such as dioxins and carcinogenic polyaromatic hydrocarbons, and induces a battery of genes associated with detoxification, proliferation, and immune regulation. Recent reports suggest that AHR plays an important role in carcinogenesis and maintenance of various types of skin cancers. Indeed, AHR is a susceptibility gene for squamous cell carcinoma and a prognostic factor for melanoma and Merkel cell carcinoma. In addition, the carcinogenic effects of ultraviolet (UV) and chemical carcinogens, both of which are major environmental carcinogenetic factors of skin, are at least partly mediated by AHR, which regulates UV-induced inflammation and apoptosis, the DNA repair system, and metabolic activation of chemical carcinogens. Furthermore, AHR modulates the efficacy of key therapeutic agents in melanoma. AHR activation induces the expression of resistance genes against the inhibitors of V600E mutated B-Raf proto-oncogene, serine/threonine kinase (BRAF) in melanoma and upregulation of programmed cell death protein 1 (PD-1) in tumor-infiltrating T cells surrounding melanoma. Taken together, these findings underscore the importance of AHR in the biology of skin cancers. Development of therapeutic agents that modulate AHR activity is a promising strategy to advance chemoprevention and chemotherapy for skin cancers.

• BRAF inhibitor
• PD-1
• air pollutant
• aryl hydrocarbon (Ah) receptor
• melanoma
• squamous cell carcinoma
• ultraviolet

• Antitumor activity
• Bacillus Calmette–Guérin
• Immunotherapy
• Recombinant BCG
• Skin cancer