Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.

By N. Wagle, Caroline M. Emery, M. Berger, Matthew J. Davis, Allison M. Sawyer, Panisa Pochanard, Sarah M. Kehoe, Cory M. Johannessen, L. Macconaill, William C. Hahn and 2 more. Journal of Clinical Oncology, 2011

983 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/17eae740073eba93b151fcdadb38dbf61157bae3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. N. Ferrara
2. A. Adamis
3. R. Apte
4. Daniel Chen
5. D. Hicklin
6. D. Gilliland
7. Meenhard Herlyn
8. S. Roychowdhury

In Oncology

1. Daniel Chen
2. R. Apte
3. N. Ferrara
4. A. Adamis
5. K. Flaherty
6. Meenhard Herlyn
7. D. Hicklin
8. S. Roychowdhury

Citations in the corpus

• VEGF in Signaling and Disease: Beyond Discovery and Development (2019, background): “Interestingly, the mechanisms of reduced response/resistance to anti-VEGF in cancer are likely different from those in response to treatment with inhibitors of well-defined oncogenic pathways, as there is no evidence of selection of preexisting or acquiredmutations in VEGF itself or in its signaling”
• Lessons from the cancer genome. (2013, neutral): “Multiple genetic mechanisms of resistance have been described (oncogenicNRASmutations, COT/MAP3K8 gains,BRAF amplification, activatingMEK1mutations, and NF1 loss), each of which produces sustained MAP kinase (ERK) activity in the presence of drug (Emery et al., 2009; Johannessen et al., 2010; Nazari”
• BRAF inhibition is associated with enhanced melanoma antigen expression and a more favorable tumor microenvironment in patients with metastatic melanoma (2013, background): “It is unclear whether the use of a different BRAF inhibitor (dabrafenib) or the addition of the MEK inhibitor contributed to this phenomenon, although recent literature would suggest that it is more likely to be the latter (21).”
• Ten years of anti-vascular endothelial growth factor therapy (2016, background): “…the key TIE2 ligands, ANG2, in cancer as well as in ophthalmology are ongoing 154 . typically occurring during treatment with inhibitors of well-defined oncogenic pathways that render a drug ineffective (that is, selection of pre-existing or acquired mutations in the target or in the pathway) 170 .”
• Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors. (2013, background): “Importantly, BRAF amplification has been demonstrated to mediate cross-resistance to MEK inhibitors (10) while MEK mutations mediate cross-resistance to BRAF inhibitors (17, 20).”
• Overcoming intrinsic multi-drug resistance in melanoma by blocking the mitochondrial respiratory chain of slow-cycling JARID1Bhigh cells (2013, background): “…receptor 1 [Nazarian et al., 2010; Villanueva et al., 2010], dimerization of aberrantly spliced BRAF isoforms [Poulikakos et al., 2011], or by secondary genetic events, such as genomic amplification of COT, NRAS mutations, or the MEK1C121S mutation [Johannessen et al., 2010; Wagle et al., 2011]).”
• Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq (2016, neutral): “Although this regimen improves survival, virtually all tumors eventually develop resistance to these drugs (12, 13).”
• Precision Cancer Medicine: Challenges and Opportunities (2019, methodology): “One of the largest basket trial endeavors launched to date is the NCI-MATCH (National Cancer Institute-Molecular Analysis for Therapy Choice) [26].”