Cited by 183Melanoma and MAPK PathwaysNeurofibromatosis and Schwannoma CasesProtein Kinase Regulation and GTPase Signaling

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Mutually exclusive NRASQ61R and BRAFV600E mutations at the single-cell level in the same human melanoma

Sensi, M, Nicolini, G, Petti, C, Bersani, I, Lozupone, F, Molla, A, Vegetti, C, Nonaka, D, Mortarini, R, Parmiani, G, Fais, S, Anichini, A·2006·Oncogene

DOI 10.1038/sj.onc.1209379

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Abstract

Activating BRAF or NRAS mutations have been found in 80% of human sporadic melanomas, but only one of these genetic alterations could be detected in each tumour. This suggests that BRAF and NRAS 'double mutants' may not provide advantage for tumour growth, or may even be selected against during tumorigenesis. However, by applying mutant-allele-specific-amplification-PCR method to short-term melanoma lines, one out of 14 tumours was found to harbour both BRAFV600E and the activating NRASQ61R mutations. On the other hand, analysis of 21 melanoma clones isolated by growth in soft agar from this tumour indicated that 16/21 clones harboured a BRAFV600E, but were wild-type for NRAS, whereas the remaining had the opposite genotype (NRASQ61R/wild-type BRAF). When compared to BRAFV600E clones, NRASQ61R clones displayed reduced growth in soft agar, but higher proliferative ability in vitro in liquid medium and even in vivo after grafting into SCID/SCID mice. These data suggest that NRAS and BRAF activating mutations can coexist in the same melanoma, but are mutually exclusive at the single-cell level. Moreover, the presence of NRASQ61R or BRAFV600E is associated with distinct in vitro and in vivo growth properties of neoplastic cells.

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1 retracted

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Retracted
Mutations of the BRAF gene in human cancer
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BRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
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“The most common point mutations affect codon 61 (Q61R and Q61K) and result in the expression of p21RAS oncoproteins with a single substituted amino acid that remain constitutively GTP bound and active (Malumbres and Barbacid, 2003).”
Background
High frequency of BRAF mutations in nevi
Pollock, P. M., Harper, U. L., Hansen, K. S., Yudt, L. M., Stark, M., Robbins, C. M., Moses, T. Y., Hostetter, G., Wagner, U., Kakareka, J., et al. (2003) · Nature Genetics · doi:10.1038/ng1054 · Cited by 1,730
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Authors: Sensi, M., Nicolini, G., Petti, C., Bersani, I., Lozupone, F., Molla, A., Vegetti, C., Nonaka, D., Mortarini, R., Parmiani, G., Fais, S., & Anichini, A.
Affiliations: Fondazione IRCCS Istituto Nazionale dei Tumori (IT)
Istituto Superiore di Sanità (IT)
Corresponding author: Sensi, M
ORCID: Sensi, M
Lozupone, F
Nonaka, D
Mortarini, R
Parmiani, G
Fais, S
Anichini, A
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2006-02-06
Volume: 25
Issue: 24
Pages: 3357-3364
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1209379
OpenAlex: W2057818550
Cited by: 183
References: 33
Citations by year: 2026: 2 · 2024: 8 · 2023: 4 · 2022: 14 · 2021: 13 · 2020: 9 · 2019: 12 · 2018: 11 · 2017: 6 · 2016: 11 · 2015: 17 · 2014: 14 · 2013: 8 · 2012: 13
FWCI: 3.67
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: Associazione Italiana per la Ricerca sul Cancro
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
Health Sciences › Medicine › Clinical Neurology › Neurofibromatosis and Schwannoma Cases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords: melanoma, NRAS Q61R mutation, BRAF V600E mutation, co-occurring mutations, mutually exclusive mutations, single-cell analysis, soft agar growth, tumorigenicity, SCID mouse xenograft
MeSH terms: Animals, Base Sequence, Female, Genotype, Humans, Melanoma, Molecular Sequence Data, Mutation, Neoplasm Transplantation, Genes, ras, Mice, SCID, Cell Line, Tumor, Proto-Oncogene Proteins B-raf, Mice

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Mutually exclusive NRASQ61R and BRAFV600E mutations at the single-cell level in the same human melanoma

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