Javascript must be enabled to continue!
Abstract 2994: Co-targeting the HER family and mutant KRAS is efficacious in colorectal cancer
View through CrossRef
We are investigating the role of naturally co-occurring HER3 and KRAS mutations in colorectal cancer, as about 6% of all colorectal cancers contain a HER3 mutation and 41% contain a KRAS mutation. After investigating the frequency of co-occurring mutations in publicly available data sets, we observed that there is a statistically significant co-occurrence of HER3 in KRAS mutations while there is mutual exclusivity with mutations in the other members of the HER family (EGFR, HER2, HER4) and mutant KRAS. We have found that there is a striking increase in total HER3 levels in SNU-407, LS180, LS513 cells and 572918-348-R and 172845-121-B patient derived organoids (PDOs) when treated with the KRASG12D inhibitorsMRTX1133 and RMC9805, creating an adaptive response that could limit the efficacy of a KRAS inhibitor as a single agent. We next aimed to determine if this was biologically meaningful by genetically knocked down HER3, KRAS or the combination in SNU-407 and LS-513 cells. We have found that genetic knockdown of both KRAS and HER3 with siRNA targeting KRAS and HER3 in the CRC cell lines SNU-407 (HER3V104M,KRASG12D) and LS513 (HER3WT, KRASG12D) results in a statistical reduction in cell proliferation in comparison to genetic knockdown with only KRAS or HER3. Next, we examined HER3 binding partners in a panel of CRC and observed HER3 bound to EGFR in SNU-407 cells and HER3 bound to MET in LS513 cells. Co-targeting EGFR and mutant KRAS resulted in a slight synergistic effect in KRASG12D mutant cell lines usingMRTX1133 in combination with sapitinib, afatinib or peltinib. Currently, we are assessing if there is a synergistic effect directly targeting HER3 with a HER3 antibody-drug-conjugate in combination with a KRAS inhibitor in CRC cells. Our findings may present a new paradigm for targeted combination therapies in colorectal cancer with the eventual goal of increased overall patient survival.
Citation Format:
Mary Kate Kilroy, Cecilia Wischmeier, Briley SoYoung Park, Rosalin Mishra, Wasim Feroz, Joan T. Garrett. Co-targeting the HER family and mutant KRAS is efficacious in colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2994.
American Association for Cancer Research (AACR)
Title: Abstract 2994: Co-targeting the HER family and mutant KRAS is efficacious in colorectal cancer
Description:
We are investigating the role of naturally co-occurring HER3 and KRAS mutations in colorectal cancer, as about 6% of all colorectal cancers contain a HER3 mutation and 41% contain a KRAS mutation.
After investigating the frequency of co-occurring mutations in publicly available data sets, we observed that there is a statistically significant co-occurrence of HER3 in KRAS mutations while there is mutual exclusivity with mutations in the other members of the HER family (EGFR, HER2, HER4) and mutant KRAS.
We have found that there is a striking increase in total HER3 levels in SNU-407, LS180, LS513 cells and 572918-348-R and 172845-121-B patient derived organoids (PDOs) when treated with the KRASG12D inhibitorsMRTX1133 and RMC9805, creating an adaptive response that could limit the efficacy of a KRAS inhibitor as a single agent.
We next aimed to determine if this was biologically meaningful by genetically knocked down HER3, KRAS or the combination in SNU-407 and LS-513 cells.
We have found that genetic knockdown of both KRAS and HER3 with siRNA targeting KRAS and HER3 in the CRC cell lines SNU-407 (HER3V104M,KRASG12D) and LS513 (HER3WT, KRASG12D) results in a statistical reduction in cell proliferation in comparison to genetic knockdown with only KRAS or HER3.
Next, we examined HER3 binding partners in a panel of CRC and observed HER3 bound to EGFR in SNU-407 cells and HER3 bound to MET in LS513 cells.
Co-targeting EGFR and mutant KRAS resulted in a slight synergistic effect in KRASG12D mutant cell lines usingMRTX1133 in combination with sapitinib, afatinib or peltinib.
Currently, we are assessing if there is a synergistic effect directly targeting HER3 with a HER3 antibody-drug-conjugate in combination with a KRAS inhibitor in CRC cells.
Our findings may present a new paradigm for targeted combination therapies in colorectal cancer with the eventual goal of increased overall patient survival.
Citation Format:
Mary Kate Kilroy, Cecilia Wischmeier, Briley SoYoung Park, Rosalin Mishra, Wasim Feroz, Joan T.
Garrett.
Co-targeting the HER family and mutant KRAS is efficacious in colorectal cancer [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL.
Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2994.
Related Results
Increased life expectancy of heart failure patients in a rural center by a multidisciplinary program
Increased life expectancy of heart failure patients in a rural center by a multidisciplinary program
Abstract
Funding Acknowledgements
Type of funding sources: None.
INTRODUCTION Patients with heart failure (HF)...
Hubungan Perilaku Pola Makan dengan Kejadian Anak Obesitas
Hubungan Perilaku Pola Makan dengan Kejadian Anak Obesitas
<p><em><span style="font-size: 11.0pt; font-family: 'Times New Roman',serif; mso-fareast-font-family: 'Times New Roman'; mso-ansi-language: EN-US; mso-fareast-langua...
Primary PCI: a reasonable treatment for STEMI care during the COVID-19 pandemic
Primary PCI: a reasonable treatment for STEMI care during the COVID-19 pandemic
Abstract
Funding Acknowledgements
Type of funding sources: None.
Introduction
...
On Flores Island, do "ape-men" still exist? https://www.sapiens.org/biology/flores-island-ape-men/
On Flores Island, do "ape-men" still exist? https://www.sapiens.org/biology/flores-island-ape-men/
<span style="font-size:11pt"><span style="background:#f9f9f4"><span style="line-height:normal"><span style="font-family:Calibri,sans-serif"><b><spa...
Abstract 2441: The myCAF and ECM landscape in KRAS-mutated cancer: Utilizing liquid biomarkers to track KRAS-induced fibrosis and KRAS inhibitor efficacy
Abstract 2441: The myCAF and ECM landscape in KRAS-mutated cancer: Utilizing liquid biomarkers to track KRAS-induced fibrosis and KRAS inhibitor efficacy
Abstract
Background:
KRAS-driven cancer represents ∼25% of cancers, with high rates in pancreatic cancer (PDAC), colorect...
Abstract 5735: Novel KRAS G12D degrader ASP3082 demonstrates in vivo, dose-dependent KRAS degradation, KRAS pathway inhibition, and antitumor efficacy in multiple KRAS G12D-mutated cancer models
Abstract 5735: Novel KRAS G12D degrader ASP3082 demonstrates in vivo, dose-dependent KRAS degradation, KRAS pathway inhibition, and antitumor efficacy in multiple KRAS G12D-mutated cancer models
Abstract
KRAS is one of the most frequently mutated oncogenes in various cancers. Among KRAS mutations, KRAS G12D is the most frequent driver mutation and is found i...
Clinical outcome in patients with metastatic colorectal cancer harboring KRAS p.G13D mutation treated with cetuximab.
Clinical outcome in patients with metastatic colorectal cancer harboring KRAS p.G13D mutation treated with cetuximab.
448 Background: Metastatic colorectal cancer patients with KRAS codon 12 or 13 mutated tumors are presently excluded from treatment with cetuximab (Cmab). On the other hand, a few...
Abstract IA07: Molecular characterization of acquired resistance to KRASG12C-EGFR inhibition in colorectal cancer
Abstract IA07: Molecular characterization of acquired resistance to KRASG12C-EGFR inhibition in colorectal cancer
Abstract
Until recently, efforts to pharmacologically target KRAS have been unsuccessful due to its small binding pocket, high affinity for GTP, and redundant mechan...

