Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer

Abstract Understanding mechanisms of resistance to active therapies is crucial for developing more effective treatments. Here, we investigate resistance to anti-EGFR and anti-VEGF plus chemotherapy treatment in colorectal cancer (CRC) patients from the IMblaze370 trial (NCT02788279). While anti-VEGF...

Full description

Saved in:
Bibliographic Details
Main Authors: Xueping Qu, Habib Hamidi, Radia M. Johnson, Ethan S. Sokol, Eva Lin, Cathy Eng, Tae Won Kim, Johanna Bendell, Smruthy Sivakumar, Benjamin Kaplan, Felipe de Sousa e Melo, Andrew Mancini, Matthew Wongchenko, Yi Shi, David Shames, Yibing Yan, Fortunato Ciardiello, Carlos Bais
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59588-3
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849729063732641792
author Xueping Qu
Habib Hamidi
Radia M. Johnson
Ethan S. Sokol
Eva Lin
Cathy Eng
Tae Won Kim
Johanna Bendell
Smruthy Sivakumar
Benjamin Kaplan
Felipe de Sousa e Melo
Andrew Mancini
Matthew Wongchenko
Yi Shi
David Shames
Yibing Yan
Fortunato Ciardiello
Carlos Bais
author_facet Xueping Qu
Habib Hamidi
Radia M. Johnson
Ethan S. Sokol
Eva Lin
Cathy Eng
Tae Won Kim
Johanna Bendell
Smruthy Sivakumar
Benjamin Kaplan
Felipe de Sousa e Melo
Andrew Mancini
Matthew Wongchenko
Yi Shi
David Shames
Yibing Yan
Fortunato Ciardiello
Carlos Bais
author_sort Xueping Qu
collection DOAJ
description Abstract Understanding mechanisms of resistance to active therapies is crucial for developing more effective treatments. Here, we investigate resistance to anti-EGFR and anti-VEGF plus chemotherapy treatment in colorectal cancer (CRC) patients from the IMblaze370 trial (NCT02788279). While anti-VEGF does not select for secondary mutations, anti-EGFR leads to simultaneous mutations in EGFR and MAPK, but not PI3K pathway genes. Notably, we observe frequent acquired mutations in the EGFR extracellular but not intracellular domain and that patients with higher baseline expression of EGFR-ligands are prone to acquire resistant mutations. This data reveals a ligand-activated EGFR/MAPK-signaling dependency in CRC. We also observe enrichment for 8q gains in anti-EGFR treated patients, potentially linked to MYC amplification, a finding further supported by baseline expression analysis. This work adds to the evidence supporting broader evaluation of EGFR and pan-KRAS inhibitor combinations in CRC patients. It also underscores the utility of EGFR ligands as anti-EGFR efficacy biomarkers and provides a rationale for developing ligand blockers to complement and/or improve conventional anti-EGFR therapies in CRC.
format Article
id doaj-art-99c3444279284575bbfdef9db628dc0e
institution DOAJ
issn 2041-1723
language English
publishDate 2025-05-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-99c3444279284575bbfdef9db628dc0e2025-08-20T03:09:20ZengNature PortfolioNature Communications2041-17232025-05-0116111510.1038/s41467-025-59588-3Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancerXueping Qu0Habib Hamidi1Radia M. Johnson2Ethan S. Sokol3Eva Lin4Cathy Eng5Tae Won Kim6Johanna Bendell7Smruthy Sivakumar8Benjamin Kaplan9Felipe de Sousa e Melo10Andrew Mancini11Matthew Wongchenko12Yi Shi13David Shames14Yibing Yan15Fortunato Ciardiello16Carlos Bais17Genentech, IncGenentech, IncGenentech, IncFoundation Medicine, IncGenentech, IncMD Anderson Cancer CenterAsan Medical Center, University of UlsanSarah Cannon Research Institute/Tennessee OncologyFoundation Medicine, IncFoundation Medicine, IncGenentech, IncGenentech, IncGenentech, IncGenentech, IncGenentech, IncGenentech, IncUniversità degli Studi della Campania Luigi VanvitelliGenentech, IncAbstract Understanding mechanisms of resistance to active therapies is crucial for developing more effective treatments. Here, we investigate resistance to anti-EGFR and anti-VEGF plus chemotherapy treatment in colorectal cancer (CRC) patients from the IMblaze370 trial (NCT02788279). While anti-VEGF does not select for secondary mutations, anti-EGFR leads to simultaneous mutations in EGFR and MAPK, but not PI3K pathway genes. Notably, we observe frequent acquired mutations in the EGFR extracellular but not intracellular domain and that patients with higher baseline expression of EGFR-ligands are prone to acquire resistant mutations. This data reveals a ligand-activated EGFR/MAPK-signaling dependency in CRC. We also observe enrichment for 8q gains in anti-EGFR treated patients, potentially linked to MYC amplification, a finding further supported by baseline expression analysis. This work adds to the evidence supporting broader evaluation of EGFR and pan-KRAS inhibitor combinations in CRC patients. It also underscores the utility of EGFR ligands as anti-EGFR efficacy biomarkers and provides a rationale for developing ligand blockers to complement and/or improve conventional anti-EGFR therapies in CRC.https://doi.org/10.1038/s41467-025-59588-3
spellingShingle Xueping Qu
Habib Hamidi
Radia M. Johnson
Ethan S. Sokol
Eva Lin
Cathy Eng
Tae Won Kim
Johanna Bendell
Smruthy Sivakumar
Benjamin Kaplan
Felipe de Sousa e Melo
Andrew Mancini
Matthew Wongchenko
Yi Shi
David Shames
Yibing Yan
Fortunato Ciardiello
Carlos Bais
Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
Nature Communications
title Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
title_full Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
title_fullStr Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
title_full_unstemmed Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
title_short Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer
title_sort ligand activated egfr mapk signaling but not pi3k are key resistance mechanisms to egfr therapy in colorectal cancer
url https://doi.org/10.1038/s41467-025-59588-3
work_keys_str_mv AT xuepingqu ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT habibhamidi ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT radiamjohnson ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT ethanssokol ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT evalin ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT cathyeng ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT taewonkim ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT johannabendell ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT smruthysivakumar ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT benjaminkaplan ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT felipedesousaemelo ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT andrewmancini ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT matthewwongchenko ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT yishi ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT davidshames ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT yibingyan ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT fortunatociardiello ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer
AT carlosbais ligandactivatedegfrmapksignalingbutnotpi3karekeyresistancemechanismstoegfrtherapyincolorectalcancer