The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Host immunity contributes to the anti-melanoma activity of BRAF inhibitors
Open accessAbstract
The BRAF mutant, BRAF(V600E), is expressed in nearly half of melanomas, and oral BRAF inhibitors induce substantial tumor regression in patients with BRAF(V600E) metastatic melanoma. The inhibitors are believed to work primarily by inhibiting BRAF(V600E)-induced oncogenic MAPK signaling; however, some patients treated with BRAF inhibitors exhibit increased tumor immune infiltration, suggesting that a combination of BRAF inhibitors and immunotherapy may be beneficial. We used two relatively resistant variants of Braf(V600E)-driven mouse melanoma (SM1 and SM1WT1) and melanoma-prone mice to determine the role of host immunity in type I BRAF inhibitor PLX4720 antitumor activity. We found that PLX4720 treatment downregulated tumor Ccl2 gene expression and decreased tumor CCL2 expression in both Braf(V600E) mouse melanoma transplants and in de novo melanomas in a manner that was coincident with reduced tumor growth. While PLX4720 did not directly increase tumor immunogenicity, analysis of SM1 tumor-infiltrating leukocytes in PLX4720-treated mice demonstrated a robust increase in CD8(+) T/FoxP3(+)CD4(+) T cell ratio and NK cells. Combination therapy with PLX4720 and anti-CCL2 or agonistic anti-CD137 antibodies demonstrated significant antitumor activity in mouse transplant and de novo tumorigenesis models. These data elucidate a role for host CCR2 in the mechanism of action of type I BRAF inhibitors and support the therapeutic potential of combining BRAF inhibitors with immunotherapy.
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Cites
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Self-citationCCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis
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Self-citationTumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion
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Self-citationCOT drives resistance to RAF inhibition through MAP kinase pathway reactivation
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The immune contexture in cancer prognosis and treatment
Fridman, W. H., Zitvogel, L., Sautès–Fridman, C., & Kroemer, G. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.101 · Cited by 2,263
T-cell invigoration to tumour burden ratio associated with anti-PD-1 response
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Immunological effects of conventional chemotherapy and targeted anticancer agents
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Loss of PTEN Promotes Resistance to T Cell–Mediated Immunotherapy
Peng, W., Chen, J. Q., Liu, C., Malu, S., Creasy, C., Tetzlaff, M. T., Xu, C., McKenzie, J. A., Zhang, C., Liang, X., et al. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0283 · Cited by 1,539
Loi, S., Michiels, S., Salgado, R., Sirtaine, N., Jose, V., Fumagalli, D., Kellokumpu-Lehtinen, P.-L., Bono, P., Kataja, V., Desmedt, C., et al. (2014) · Annals of Oncology · doi:10.1093/annonc/mdu112 · Cited by 1,256
Self-citation
Metadata
- Authors
- Knight, D. A., Ngiow, S. F., Li, M., Parmenter, T., Mok, S., Cass, A., Haynes, N. M., Kinross, K., Yagita, H., Koya, R. C., Graeber, T. G., Ribas, A., McArthur, G. A., & Smyth, M. J.
- Venue
- Journal of Clinical Investigation
- Published
- 2013-02-01
- Volume
- 123
- Issue
- 3
- Pages
- 1371-1381
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2102557111
- Cited by
- 269
- References
- 13
- FWCI
- 16.54
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- bronze
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- Knight, D. A., Ngiow, S. F., Li, M., Parmenter, T., Mok, S., Cass, A., Haynes, N. M., Kinross, K., Yagita, H., Koya, R. C., Graeber, T. G., Ribas, A., McArthur, G. A., & Smyth, M. J. (2013). Host immunity contributes to the anti-melanoma activity of BRAF inhibitors. Journal of Clinical Investigation. https://doi.org/10.1172/jci66236
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
