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Open research questions in Melanoma and MAPK Pathways

96 gap statements mined from Melanoma and MAPK Pathways papers in our 4.5M-paper local library, which holds 535 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • Due to these diverse effects, it remains unclear whether NGFR agonists or antagonists would be more beneficial for melanoma treatment. In our previous work, we used the small molecule NGFR inhibitor THX-B and found that it reduced melanoma lymph node metastasis; however, its impact on distant metastasis has not been tested (Garcia-Silva et al, 2021).

    NGFR induces melanoma invasion and immunotherapy resistance through myosin light chain 2 modulation · 2026 · DOI

  • A 2025 systematic review and meta-analysis of clinical studies suggested a potential association between β-blocker use and improved disease-free survival, although evidence remains insufficient to support clinical recommendation for cancer treatment, including melanoma [75].

    Antihypertensive Drugs as Potential Repositioning Options for Melanoma: A Map of Pre-Clinical Evidence · 2026 · DOI

  • To our knowledge, electronegative ERG has not been established as a characteristic electrophysiologic feature of MEK inhibitor-associated retinopathy.

    Electronegative ERG revealing melanoma-associated retinopathy in a patient with trametinib-associated retinopathy · 2026 · DOI

  • These insights position the SCAMP3-ERK1/2 axis as a relevant modulator of TNBC behavior and support further investigation of SCAMP3 in strategies to improve ERK1/2-targeted therapy, particularly in tumors where receptor-proximal signaling remains a dominant driver of ERK activity.

    Secretory carrier membrane protein 3 modulates nuclear ERK1/2 signaling and drug response in triple-negative breast cancer · 2026 · DOI

  • However, the molecular mechanisms underlying the dysregulation of apoptosis in pathological conditions associated with oxidative stress, including tumor growth, are still not fully understood.

    Regulation and Implementation of Apoptosis in Melanoma Tumor Cells with BRAF, NRAS, and NF1 Gene Mutations · 2026 · DOI

  • However, the specific contribution of HCQ to thera- peutic efficacy in the clinic remains incompletely characterized.

    Mutant and Wild-type RAS Crosstalk and Stoichiometric Deficiencies are Determinants of Sensitivity to Targeted Therapies in KRASG12R Pancreatic Ductal Adenocarcinoma. · 2026 · DOI

  • The signaling basis for differential RAF activity across mutant KRAS-expressing lines remains unclear.

    MEK interactions tune RAF kinase sensitivity to conformation-selective inhibition · 2026 · DOI

  • Whether these organoid systems can stably maintain long- term melanocyte-lineage populations, particularly cells with MeSC-like properties, remains unclear.

    Recent Advances in Genetically Engineered Mouse Models of Melanoma: Insights into Tumor Initiation and Oncogenic Signaling Pathways · 2026 · DOI

  • Confidence in these findings is further limited by the frequent high or unclear risk of bias among animal studies, incomplete methodological reporting, and the absence of a formal quality assessment for the in vitro evidence.

    Antihypertensive Drugs as Potential Repositioning Options for Melanoma: A Map of Pre-Clinical Evidence · 2026 · DOI

  • ABSTRACT While adjuvant immunotherapy and BRAF/MEK inhibitors improve the outcomes for BRAF V600‐mutant stage III melanoma, comparisons of long‐term survival and safety of these therapeutic modalities are currently lacking in Chinese patients.

    Optimal Adjuvant Therapy Selection for Chinese BRAF V600‐Mutant Stage III Melanoma: A Multicenter Efficacy Comparison of Targeted Agents, Immunotherapy, and Combinatorial Strategies · 2026 · DOI

  • However, therapeutic success is often limited by the emergence of drug-resistant cancer cell populations within a few months.

    BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer · 2026 · DOI

  • In contrast to many other cancer types, with the exception of poly (ADP-ribose) polymerase inhibition in DNA repair defective cancers, clinically actionable molecular subtypes are lacking.

    Decoding the Raf-Mek-Erk-Rsk pathway in prostate cancer: from molecular mechanisms to clinical opportunities · 2026 · DOI

  • Herein, we describe the structure-guided development of IACS-56676, a selective and potent NRAS G12D inhibitor useful as a tool compound for further studies of NRAS biology.

    Structure-Guided Development of NRAS G12D Inhibitors Based on a 5-Azaindole Core · 2026 · DOI

  • Despite this, crucial questions about its activation have not been fully explored on the foundational, conformational level.

    ERK Allosteric Activation: The Importance of Two Ordered Phosphorylation Events · 2025 · DOI

  • Abstract Anti‐PD‐1 immunotherapy and targeted therapy (TT) represent two major therapeutic modalities for BRAFV600‐mutant advanced melanoma, but the efficacy of combination therapy in Asian populations remains unknown.

    Addition of anti‐PD‐1 immunotherapy to BRAF inhibitor‐based targeted therapy improves real‐world survival and delays brain metastases in patients with BRAFV600‐mutant advanced melanoma: a multicenter cohort study · 2025 · DOI

  • Transcriptional dysregulation has emerged as a critical driver of melanoma progression, yet the molecular mechanisms governing this process and their potential as therapeutic targets remain inadequately characterized.

    FRA1 drives melanoma metastasis through an actionable transcriptional network · 2025 · DOI

  • However, the mechanisms underlying cell death in this context and how damaged tissue contributes to tumor progression remain unclear.

    Involvement of p38 MAPK and MAPKAPK2 in promoting cell death and the inflammatory response to ischemic stress associated with necrotic glioblastoma · 2025 · DOI

  • Accordingly, MAPKi/ERK5i co-inhibition was capable of triggering a sustained cell cycle arrest in NRAS-mutant melanoma cells, but the key mediator(s) of its vigorous anti-proliferative effect remain elusive.

    MEK5/ERK5 inhibition sensitizes NRAS-mutant melanoma to MAPK-targeted therapy by preventing Cyclin D/CDK4-mediated G1/S progression · 2025 · DOI

  • Although transcriptional and epigenetic mechanisms driving these transitions have been extensively studied, the role of post-translational regulation, particularly the ubiquitin-proteasome system, remains poorly understood.

    Ubiquitin E3 ligase KPC1 governs mesenchymal metastatic melanoma reprogramming via proteasomal degradation of ZEB1 · 2025 · DOI

  • Necroptosis is an inflammatory form of regulated cell death implicated in a range of human pathologies, whose execution depends on the poorly understood pseudokinase mixed lineage kinase domain-like (MLKL).

    MLKL activity requires a splicing-regulated, druggable intramolecular interaction · 2025 · DOI

  • Despite remarkable advancements in therapies targeted against mutant KRAS, NRAS-specific pharmacologics are lacking.

    Inhibition and degradation of NRAS with a pan-NRAS monobody · 2024 · DOI

  • Abstract Background Resistance mechanisms to combination therapy with dabrafenib plus trametinib remain poorly understood in patients with BRAF V600E -mutant advanced non-small-cell lung cancer (NSCLC).

    Resistance to BRAF inhibition explored through single circulating tumour cell molecular profiling in BRAF-mutant non-small-cell lung cancer · 2024 · DOI

  • Our hypothesis posits that Bim is a direct target of miR-92b-3p, an understudied microRNA, prompting an investigation into its role in regulating apoptosis in SMCs.

    MiR-92b-3p modulates apoptosis in smooth muscle cells through BCL2L11 regulation, unravelling novel therapeutic strategies for unstable plaques · 2024 · DOI

  • RAF kinases interpret signals from the three major RAS isoforms to initiate MAPK pathway activation, yet the molecular logic that governs isoform-specific RAS recruitment and the early events that relieve RAF autoinhibition are not yet fully understood.

    Divergent CRD-Dependent Mechanisms Govern RAS Isoform-Selective Recruitment of CRAF and ARAF · 2026 · DOI

  • Further study of FGFR1 as a therapeutic target for intrinsic BRAFi resistance. Investigation of the mechanisms by which FGFR1 drives intrinsic BRAFi resistance.

    FGFR1 but not S6K1/2 drives intrinsic BRAF inhibitor resistance in melanoma · 2026 · DOI

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96 gap statements have been mined from Melanoma and MAPK Pathways papers in our 4.5M-paper local library, which holds 535 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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