Cited by 240Immunotherapy and Immune ResponsesCAR-T cell therapy researchCancer Immunotherapy and Biomarkers

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Identification of T-cell Receptors Targeting KRAS-Mutated Human Tumors

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Wang, Qiong J., Yu, Zhiya, Griffith, Kayla, Hanada, Ken-ichi, Restifo, Nicholas P., Yang, James C.·2016·Cancer Immunology Research

DOI 10.1158/2326-6066.cir-15-0188PMC PMC4775432

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Abstract

KRAS is one of the most frequently mutated proto-oncogenes in human cancers. The dominant oncogenic mutations of KRAS are single amino acid substitutions at codon 12, in particular G12D and G12V present in 60% to 70% of pancreatic cancers and 20% to 30% of colorectal cancers. The consistency, frequency, and tumor specificity of these “neoantigens” make them attractive therapeutic targets. Recent data associate T cells that target mutated antigens with clinical immunotherapy responses in patients with metastatic melanoma, lung cancer, or cholangiocarcinoma. Using HLA-peptide prediction algorithms, we noted that HLA-A*11:01 could potentially present mutated KRAS variants. By immunizing HLA-A*11:01 transgenic mice, we generated murine T cells and subsequently isolated T-cell receptors (TCR) highly reactive to the mutated KRAS variants G12V and G12D. Peripheral blood lymphocytes (PBL) transduced with these TCRs could recognize multiple HLA-A*11:01+ tumor lines bearing the appropriate KRAS mutations. In a xenograft model of large established tumor, adoptive transfer of these transduced PBLs reactive with an HLA-A*11:01, G12D-mutated pancreatic cell line could significantly reduce its growth in NSG mice (P = 0.002). The success of adoptive transfer of TCR-engineered T cells against melanoma and other cancers supports clinical trials with these T cells that recognize mutated KRAS in patients with a variety of common cancer types. Cancer Immunol Res; 4(3); 204–14. ©2015 AACR.

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Retracted

Authors: Wang, Q. J., Yu, Z., Griffith, K., Hanada, K.-I., Restifo, N. P., & Yang, J. C.
Affiliations: National Institutes of Health (US)
Corresponding author: Wang, Qiong J.
Yang, James C.
ORCID: Wang, Qiong J.
Yu, Zhiya
Hanada, Ken-ichi
Restifo, Nicholas P.
Yang, James C.
Venue: Cancer Immunology Research
Publisher: American Association for Cancer Research (AACR)
Published: 2016-02-29
Volume: 4
Issue: 3
Pages: 204-214
ISSN: 2326-6066 (ISSN-L)
2326-6074
DOI: 10.1158/2326-6066.cir-15-0188
PMC: PMC4775432
OpenAlex: W2239878160
Cited by: 240
References: 37
Citations by year: 2026: 17 · 2025: 27 · 2024: 27 · 2023: 30 · 2022: 36 · 2021: 29 · 2020: 24 · 2019: 19 · 2018: 11 · 2017: 13 · 2016: 7
FWCI: 10.11
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Cancer Immunology Research (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (Z99 CA999999)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Health Sciences › Medicine › Oncology › CAR-T cell therapy research
Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Keywords: KRAS mutation, T cell receptor engineering, neoantigens, HLA-A*11:01, pancreatic cancer, adoptive T cell therapy, xenograft tumor growth, cancer immunotherapy
MeSH terms: Amino Acid Sequence, Animals, Humans, Lymph Nodes, Mice, Transgenic, Neoplasm Transplantation, Pancreatic Neoplasms, Receptors, Antigen, T-Cell, Spleen, Proto-Oncogene Proteins p21(ras), Mice, SCID, Mice, Inbred NOD, Adoptive Transfer, Mutation, Missense, Cell Line, Tumor, HLA-A11 Antigen

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Identification of T-cell Receptors Targeting KRAS-Mutated Human Tumors

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