Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain Article Swipe
Susanne Grünewald
,
Lillian R. Klug
,
Thomas Mühlenberg
,
Jonas Lategahn
,
Johanna Falkenhorst
,
Ajia Town
,
Christiane Ehrt
,
Eva Wardelmann
,
Wolfgang Hartmann
,
Hans‐Ulrich Schildhaus
,
Juergen Treckmann
,
Jonathan A. Fletcher
,
Sascha Jung
,
Paul Czodrowski
,
Stephen D. Miller
,
Oleg Schmidt-Kittler
,
Daniel Rauh
,
Michael C. Heinrich
,
Sebastian Bauer
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6548281.v1
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6548281.v1
Gastrointestinal stromal tumors (GIST) harboring activating mutations of PDGFRA respond to imatinib, with the notable exception of the most common mutation, D842V. Avapritinib is a novel, potent KIT/PDGFRA inhibitor with substantial clinical activity in patients with the D842V genotype. To date, only a minority of PDGFRA-mutant patients treated with avapritinib have developed secondary resistance. Tumor and plasma biopsies in 6 of 7 patients with PDGFRA primary mutations who progressed on avapritinib or imatinib had secondary resistance mutations within PDGFRA exons 13, 14, and 15 that interfere with avapritinib binding. Secondary PDGFRA mutations causing V658A, N659K, Y676C, and G680R substitutions were found in 2 or more patients each, representing recurrent mechanisms of PDGFRA GIST drug resistance. Notably, most PDGFRA-mutant GISTs refractory to avapritinib remain dependent on the PDGFRA oncogenic signal. Inhibitors that target PDGFRA protein stability or inhibition of PDGFRA-dependent signaling pathways may overcome avapritinib resistance.Significance:Here, we provide the first description of avapritinib resistance mechanisms in PDGFRA-mutant GIST.This article is highlighted in the In This Issue feature, p. 1
Related Topics
Concepts
PDGFRA
GiST
Cancer research
Mutation
Mutant
Imatinib mesylate
Imatinib
Biology
Stromal cell
Genetics
Gene
Myeloid leukemia
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/2159-8290.c.6548281.v1
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4362545773
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4362545773Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/2159-8290.c.6548281.v1Digital Object Identifier
- Title
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Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase DomainWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-04-03Full publication date if available
- Authors
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Susanne Grünewald, Lillian R. Klug, Thomas Mühlenberg, Jonas Lategahn, Johanna Falkenhorst, Ajia Town, Christiane Ehrt, Eva Wardelmann, Wolfgang Hartmann, Hans‐Ulrich Schildhaus, Juergen Treckmann, Jonathan A. Fletcher, Sascha Jung, Paul Czodrowski, Stephen D. Miller, Oleg Schmidt-Kittler, Daniel Rauh, Michael C. Heinrich, Sebastian BauerList of authors in order
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https://doi.org/10.1158/2159-8290.c.6548281.v1Publisher landing page
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YesWhether a free full text is available
- OA status
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goldOpen access status per OpenAlex
- OA URL
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https://doi.org/10.1158/2159-8290.c.6548281.v1Direct OA link when available
- Concepts
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PDGFRA, GiST, Cancer research, Mutation, Mutant, Imatinib mesylate, Imatinib, Biology, Stromal cell, Genetics, Gene, Myeloid leukemiaTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.target | 131 |
| abstract_inverted_index.tumors | 2 |
| abstract_inverted_index.within | 77 |
| abstract_inverted_index.article | 157 |
| abstract_inverted_index.causing | 92 |
| abstract_inverted_index.notable | 14 |
| abstract_inverted_index.primary | 65 |
| abstract_inverted_index.protein | 133 |
| abstract_inverted_index.provide | 146 |
| abstract_inverted_index.respond | 9 |
| abstract_inverted_index.signal. | 128 |
| abstract_inverted_index.stromal | 1 |
| abstract_inverted_index.treated | 47 |
| abstract_inverted_index.Notably, | 115 |
| abstract_inverted_index.activity | 32 |
| abstract_inverted_index.binding. | 88 |
| abstract_inverted_index.biopsies | 57 |
| abstract_inverted_index.clinical | 31 |
| abstract_inverted_index.feature, | 165 |
| abstract_inverted_index.imatinib | 72 |
| abstract_inverted_index.minority | 43 |
| abstract_inverted_index.overcome | 142 |
| abstract_inverted_index.pathways | 140 |
| abstract_inverted_index.patients | 34, 46, 62, 105 |
| abstract_inverted_index.Secondary | 89 |
| abstract_inverted_index.dependent | 123 |
| abstract_inverted_index.developed | 51 |
| abstract_inverted_index.exception | 15 |
| abstract_inverted_index.genotype. | 38 |
| abstract_inverted_index.harboring | 4 |
| abstract_inverted_index.imatinib, | 11 |
| abstract_inverted_index.inhibitor | 28 |
| abstract_inverted_index.interfere | 85 |
| abstract_inverted_index.mutation, | 20 |
| abstract_inverted_index.mutations | 6, 66, 76, 91 |
| abstract_inverted_index.oncogenic | 127 |
| abstract_inverted_index.recurrent | 108 |
| abstract_inverted_index.secondary | 52, 74 |
| abstract_inverted_index.signaling | 139 |
| abstract_inverted_index.stability | 134 |
| abstract_inverted_index.Inhibitors | 129 |
| abstract_inverted_index.KIT/PDGFRA | 27 |
| abstract_inverted_index.activating | 5 |
| abstract_inverted_index.inhibition | 136 |
| abstract_inverted_index.mechanisms | 109, 153 |
| abstract_inverted_index.progressed | 68 |
| abstract_inverted_index.refractory | 119 |
| abstract_inverted_index.resistance | 75, 152 |
| abstract_inverted_index.Avapritinib | 22 |
| abstract_inverted_index.avapritinib | 49, 70, 87, 121, 143, 151 |
| abstract_inverted_index.description | 149 |
| abstract_inverted_index.highlighted | 159 |
| abstract_inverted_index.resistance. | 53, 114 |
| abstract_inverted_index.substantial | 30 |
| abstract_inverted_index.representing | 107 |
| abstract_inverted_index.PDGFRA-mutant | 117, 155 |
| abstract_inverted_index.substitutions | 98 |
| abstract_inverted_index.PDGFRA-dependent | 138 |
| abstract_inverted_index.<i>PDGFRA</i> | 8, 64, 78, 90 |
| abstract_inverted_index.<i>PDGFRA</i>-mutant | 45 |
| abstract_inverted_index.1</i></p></div> | 167 |
| abstract_inverted_index.GIST.</p><p><i>This | 156 |
| abstract_inverted_index.<div>Abstract<p>Gastrointestinal | 0 |
| abstract_inverted_index.resistance.</p>Significance:<p>Here, | 144 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 19 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.6800000071525574 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.12341804 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |