ArticleThe American journal of pathology2009
The role of BRAF mutation and p53 inactivation during transformation of a subpopulation of primary human melanocytes.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- Review
- Comparing P53 expression and genome-wide transcriptome profiling to Comet assay in lymphocytes from melanoma patients and healthy controls.Scientific reports · 2023Article
- NAD+ depletion enhances reovirus-induced oncolysis in multiple myeloma.Molecular therapy oncolytics · 2022Article
- miR-138-5p induces aggressive traits by targeting Trp53 expression in murine melanoma cells, and correlates with poor prognosis of melanoma patients.Neoplasia (New York, N.Y.) · 2021Article
- Article
- Article
- Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAFeLife · 2019Article
- Molecular background of skin melanoma development and progression: therapeutic implications.Postepy dermatologii i alergologii · 2019Review
- Cancer modeling by Transgene Electroporation in Adult Zebrafish (TEAZ).Disease models & mechanisms · 2018Article
- Targeting the hedgehog transcription factors GLI1 and GLI2 restores sensitivity to vemurafenib-resistant human melanoma cells.Oncogene · 2017Article
- Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines.Pigment cell & melanoma research · 2016Article
- Phytochemicals for the Management of Melanoma.Mini reviews in medicinal chemistry · 2016Review
- MicroRNA-3151 inactivates TP53 in BRAF-mutated human malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The dynamic control of signal transduction networks in cancer cells.Nature reviews. Cancer · 2015Review
- The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics.Cancer discovery · 2015Review
- Three-dimensional modeling of ovarian cancer.Advanced drug delivery reviews · 2014Review
- Mechanisms of chromosomal instability in melanoma.Environmental and molecular mutagenesis · 2014Article
- Human skin neural crest progenitor cells are susceptible to BRAF(V600E)-induced transformation.Oncogene · 2014Article
- Establishment and characterization of a primary and a metastatic melanoma cell line from Grey horses.In vitro cellular & developmental biology. Animal · 2014Article
- The role of AKT/mTOR pathway in stress response to UV-irradiation: implication in skin carcinogenesis by regulation of apoptosis, autophagy and senescence.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Melanocytic nevi frequently harbor oncogenic BRAF mutations, but only a minority progress to melanoma. In human melanocytes, persistent BRAF(V600E) expression triggers oncogene-induced senescence, which implies that bypass of oncogene-induced senescence is necessary for malignant transformation of melanocytes. We show that a subpopulation of primary human melanocytes with persistent expression of BRAF(V600E) do not enter oncogene-induced senescence, but instead survive despite heightened MAPK activity. Disruption of the p53 pathway using short-hairpin RNA initiated rapid growth of these V600E(+) melanocytes in vitro. The resultant V600E(+)/p53(sh) melanocytes grew anchorage-independently in soft agar, formed pigmented lesions reminiscent of in situ melanoma in artificial skin reconstructs, and were weakly tumorigenic in vivo. Array comparative genomic hybridization analysis demonstrated that the transformed melanocytes acquired a substantial deletion in chromosome 13, which encodes the Rb1 tumor suppressor gene. Gene expression profiling study of nevi and melanomas showed that p53 target genes were differentially expressed in melanomas compared with nevi, suggesting a dysfunctional p53 pathway in melanoma in vivo. In summary, these data demonstrate that a subpopulation of melanocytes possesses the ability to survive BRAF(V600E)-induced senescence, and suggest that p53 inactivation may promote malignant transformation of these cells.
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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.