ReviewOncogene2017
Pathways from senescence to melanoma: focus on MITF sumoylation.
Review in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Loss of MITF activity leads to emergent cell states from the melanocyte stem cell lineage.bioRxiv : the preprint server for biology · 2026Article
- Cellular senescence: mechanisms and relevance to cancer and aging.Journal of biochemistry · 2025Review
- Unravelling tumour cell diversity and prognostic signatures in cutaneous melanoma through machine learning analysis.Journal of cellular and molecular medicine · 2024Article
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- Mapping cellular senescence networks in human diabetic foot ulcers.GeroScience · 2024Article
- Mechanisms of Melanoma Progression and Treatment Resistance: Role of Cancer Stem-like Cells.Cancers · 2024Review
- The journey from melanocytes to melanoma.Nature reviews. Cancer · 2023Review
- Cellular senescence in skin-related research: Targeted signaling pathways and naturally occurring therapeutic agents.Aging cell · 2023Review
- Disulfidptosis-related classification patterns and tumor microenvironment characterization in skin cutaneous melanoma.Melanoma management · 2023Article
- The Cross Talk between Cellular Senescence and Melanoma: From Molecular Pathogenesis to Target Therapies.Cancers · 2023Review
- Identification of anoikis-related subtypes and development of risk stratification system in skin cutaneous melanoma.Heliyon · 2023Article
- Leveraging a cuproptosis-based signature to predict the prognosis and drug sensitivity of cutaneous melanoma.Journal of translational medicine · 2023Article
- A unique hyperdynamic dimer interface permits small molecule perturbation of the melanoma oncoprotein MITF for melanoma therapy.Cell research · 2023Article
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice.Nature communications · 2022Article
- Clinical significance and immune landscape of KIR2DL4 and the senescence-based signature in cutaneous melanoma.Cancer science · 2022Article
- Detection of Cellular Senescence in Human Primary Melanocytes and Malignant Melanoma Cells In Vitro.Cells · 2022Article
- Targeted Therapy in Melanoma and Mechanisms of Resistance.International journal of molecular sciences · 2020Review
- WNT5A-Induced Activation of the Protein Kinase C Substrate MARCKS Is Required for Melanoma Cell Invasion.Cancers · 2020Article
- A conserved role for transcription factor sumoylation in binding-site selection.Current genetics · 2019Review
- Naturally-Occurring Canine Invasive Urothelial Carcinoma: A Model for Emerging Therapies.Bladder cancer (Amsterdam, Netherlands) · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous melanoma is a deadly skin cancer that originates from melanocytes. The development of cutaneous melanoma involves a complex interaction between environmental factors, mainly ultraviolet radiation from sunlight, and genetic alterations. Melanoma can also occur from a pre-existing nevus, a benign lesion formed from melanocytes harboring oncogenic mutations that trigger proliferative arrest and senescence entry. Senescence is a potent barrier against tumor progression. As such, the acquisition of mutations that suppress senescence and promote cell division is mandatory for cancer development. This topic appears central to melanoma development because, in humans, several somatic and germline mutations are related to the control of cellular senescence and proliferative activity. Consequently, primary melanoma can be viewed as a paradigm of senescence evasion. In support of this notion, a sumoylation-defective germline mutation in microphthalmia-associated transcription factor (MITF), a master regulator of melanocyte homeostasis, is associated with the development of melanoma. Interestingly, this MITF variant has also been recently reported to negatively impact the program of senescence. This article reviews the genetic alterations that have been shown to be involved in melanoma and that alter the process of senescence to favor melanoma development. Then, the transcription factor MITF and its sumoylation-defective mutant are described. How sumoylation misregulation can change MITF activity and impact the process of senescence is discussed. Finally, the contribution of such information to the development of anti-malignant melanoma strategies is evaluated.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.