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Intragenic ERBB2 kinase mutations in tumours
Abstract
The protein-kinase family is the most frequently mutated gene family found in human cancer and faulty kinase enzymes are being investigated as promising targets for the design of antitumour therapies. We have sequenced the gene encoding the transmembrane protein tyrosine kinase ERBB2 (also known as HER2 or Neu) from 120 primary lung tumours and identified 4% that have mutations within the kinase domain; in the adenocarcinoma subtype of lung cancer, 10% of cases had mutations. ERBB2 inhibitors, which have so far proved to be ineffective in treating lung cancer, should now be clinically re-evaluated in the specific subset of patients with lung cancer whose tumours carry ERBB2 mutations.
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“with the A775_G776insYVMA mutation accounting for most of the mutations seen in NSCLC (17–21).”
From Response Heterogeneity of EGFR and HER2 Exon 20 Insertions to Covalent EGFR and HER2 Inhibitors (2017) · cites this paper as [17]
In the citing paper
“HER2 mutations have been found in a small proportion of lung, gastric, colorectal, breast and head and neck cancers (Lee et al., 2006; Ross et al., 2013; Stephens et al., 2004; Willmore-Payne et al., 2006).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Stephens et al., 2004
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Molecular Mechanisms of Trastuzumab-Based Treatment in HER2-Overexpressing Breast Cancer
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Genetic Alterations in the Tyrosine Kinase Transcriptome of Human Cancer Cell Lines
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Antitumor activity of HER-2 inhibitors
Rabindran, S. K. (2004) · Cancer Letters · doi:10.1016/j.canlet.2004.11.015 · Cited by 87
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“While EGFR and KRAS mutations are detected in ,10% and 20% of NSCLCs, respectively, somatic mutations have also been identified in HER2/ERBB2 (,2%; exons 19 and 20) [11,12] and HER4 (,2%, exons 20, 23) [13], the lipid kinase PIK3CA (,4%; exon 9) [14], and the serine/threonine kinase BRAF (,2%; exons 11 and 15) [15–17].”
BackgroundMethodTran, P. T., Fan, A. C., Bendapudi, P. K., Koh, S., Komatsubara, K. M., Chen, J., Horng, G., Bellovin, D. I., Giuriato, S., Wang, C. S., et al. (2008) · PLoS ONE · doi:10.1371/journal.pone.0002125 · Cited by 87
“studies of human lung tumors [53–62], some of these studies have implicated the EGFR/IL-6/Stat3 pathway in the pathogenesis of lung adenocarcinomas [43,49,50,61–63].”
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The force of HER2 – A druggable target in NSCLC?
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Krug, L. M., Miller, V. A., Patel, J. D., Crapanzano, J. P., Azzoli, C. G., Gomez, J. E., Kris, M. G., Heelan, R. T., Pizzo, B., Tyson, L. B., et al. (2005) · Cancer · doi:10.1002/cncr.21428 · Cited by 84
“described in 4% of patients with NSCLC, including 10% of patients with adenocarcinoma of the lung.(22)”
BackgroundAdvances in Target Therapy for Lung Cancer
Mitsudomi, T. (2009) · Japanese Journal of Clinical Oncology · doi:10.1093/jjco/hyp174 · Cited by 84
“The ERBB2 gene is mutated in a subset of patients with lung adenocarcinomas, although the frequency is low (28,29).”
BackgroundComprehensive molecular profiling of lung adenocarcinoma
Lander, E. S. (2014) · DSpace@MIT (Massachusetts Institute of Technology) · Cited by 84
Ross, J. S., Gay, L. M., Wang, K., Ali, S. M., Chumsri, S., Elvin, J. A., Bose, R., Vergilio, J., Suh, J. H., Yelensky, R., et al. (2016) · Cancer · doi:10.1002/cncr.30102 · Cited by 84
“In 2004, nonamplification alterations in the ERBB2 sequence were reported in patients with lung adenocarcinoma and shown to be associated with activation of HER2 signaling.(25) Mutations affecting the kinase domain of HER2 can drive downstream nuclear processes impacting proliferation, invasiveness, and resistance to…”
BackgroundAmplification of chromosomal segment 4q12 in non-small cell lung cancer
Ramos, A. H., Dutt, A., Mermel, C. H., Perner, S., Cho, J., Lafargue, C. J., Johnson, L. A., Stiedl, A., Tanaka, K., Bass, A. J., et al. (2009) · Cancer Biology & Therapy · doi:10.4161/cbt.8.21.9764 · Cited by 83
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“the presence of somatic mutations that alter the protein structure of the HER2 kinase domain has been recently reported in NSCLC patients”
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EGFR, ERBB2, and KRAS mutations in Korean non-small cell lung cancer patients
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Targeted therapies in development for non-small cell lung cancer
Dy, G. K., & Reungwetwattana, T. (2013) · Journal of Carcinogenesis · doi:10.4103/1477-3163.123972 · Cited by 80
“De novo mutations in HER2 occur in 2‐4% of NSCLC, up to approximately 10% in adenocarcinomas.[23,77] Majority (>95%) of these represent small insertions in exon 20, largely (>80%) represented by a 12 basepair in‐frame insertion causing a duplication of the amino acids YVMA that results in constitutive activation of HE…”
BackgroundPetrek, H. E., & Yu, A. (2019) · Pharmacology Research & Perspectives · doi:10.1002/prp2.528 · Cited by 82
Marchetti, A., Felicioni, L., Pelosi, G., Grammastro, M. D., Fumagalli, C., Sciarrotta, M., Malatesta, S., Chella, A., Barassi, F., Mucilli, F., et al. (2008) · Human Mutation · doi:10.1002/humu.20707 · Cited by 80
Heat Shock Protein 90 Inhibition in Lung Cancer
Shimamura, T., & Shapiro, G. I. (2008) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e318174ea3a · Cited by 79
NSCLC and HER2: between lights and shadows
Ricciardi, G. R. R., Russo, A., Franchina, T., Ferraro, G., Zanghì, M., Picone, A., Scimone, A., & Adamo, V. (2014) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000379 · Cited by 78
“In 2004, Stephens et al.79 first reported the presence of somatic mutations in the tyrosine kinase domain of HER2 in NSCLC. Sequencing the HER2 gene from 120 NSCLC samples, they detected in 4.2% of cases four in-frame mutations and one missense substitution, located in the kinase domain of HER2, that were analog of th…”
BackgroundInfluentialTargeted therapy in NSCLC driven by HER2 insertions.
Peters, S., & Zimmermann, S. (2014) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2218-6751.2014.02.06 · Cited by 77
Chung, A. P., Cui, X., Audeh, W., & Giuliano, A. E. (2013) · Clinical Breast Cancer · doi:10.1016/j.clbc.2013.04.001 · Cited by 77
Epidermal growth factor receptor mutations in lung cancers
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Chromosomes and Expression in Human Testicular Germ‐Cell Tumors
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High-Throughput Functional Evaluation of Variants of Unknown Significance in ERBB2
Nagano, M., Kohsaka, S., Ueno, T., Kojima, S., Saka, K., Iwase, H., Kawazu, M., & Mano, H. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-0991 · Cited by 79
“ERBB2mutations were first reported in 2% to 4% of lung adenocarcinomas (10), and cancer genome resequencing with next-generation sequencing technologies has identified many ERBB2 mutations across a variety of cancers, such as breast, lung, gastric, colorectal, liver, ovarian, and urothelial cancers (11–16).”
BackgroundYokoyama, T., Kondo, M., Gotô, Y., Fukui, T., Yoshioka, H., Yokoi, K., Osada, H., Imaizumi, K., Hasegawa, Y., Shimokata, K., et al. (2006) · Cancer Science · doi:10.1111/j.1349-7006.2006.00233.x · Cited by 76
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“To extend key aspects of these findings LB373-MEL primary melanoma cells homozygous for the PPP6C H114Y mutation were then compared to a control melanoma cell line LB2518MEL carrying wild-type PPP6C (Stephens et al., 2004; van Haaften et al., 2009).”
BackgroundResultMutations in the Kinase Domain of the HER2/ERBB2 Gene Identified in a Wide Variety of Human Cancers
Wen, W., Chen, W., Xiao, N., Bender, R. P., Ghazalpour, A., Tan, Z., Swensen, J. J., Millis, S. Z., Basu, G. D., Gatalica, Z., et al. (2015) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2015.04.003 · Cited by 76
Her2-Targeted Therapies in Non–Small Cell Lung Cancer
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“Only 5 missense mutations in the HER2 gene were previously found in exons 19 through 20.[2, 3, 8, 13, 16, 17, 32] We found that approximately half of the HER2-mutated tumors showed HER2 gene amplification.”
BackgroundMethodResultInfluentialRon Kinase Transphosphorylation Sustains MET Oncogene Addiction
Benvenuti, S., Lazzari, L., Arnesano, A., Chiavi, G. L., Gentile, A., & Comoglio, P. M. (2011) · Cancer Research · doi:10.1158/0008-5472.can-10-2100 · Cited by 79
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Somatic point mutations occurring early in development: a monozygotic twin study
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“Activating mutations in EGFRs and downstream effectors in the PI3K/AKT and MAPK signaling pathways have been recognized as driver mutations in human cancer (Paez et al. 2004; Stephens et al. 2004; Citri and Yarden 2006; Sibilia et al. 2007).”
BackgroundGenetic and epigenetic changes in lung carcinoma and their clinical implications
Wen, J., Fu, J., Zhang, W., & Guo, M. (2011) · Modern Pathology · doi:10.1038/modpathol.2011.46 · Cited by 77
The ErbB2 Signaling Network as a Target for Breast Cancer Therapy
Badache, A., & Gonçalvès, A. (2006) · Journal of Mammary Gland Biology and Neoplasia · doi:10.1007/s10911-006-9009-1 · Cited by 78
“Of note, mutations in the kinase domain of ErbB2 were recently identified in a small subset of non-small cell lung cancer [59], and subsequently in other tumor types including head and neck, ovarian, brain and gastric cancers, even though with a low prevalence.”
BackgroundBiomarkers in Lung Adenocarcinoma: A Decade of Progress
Sholl, L. M. (2014) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2014-0128-ra · Cited by 75
“The best-defined mechanism of ERBB2 activation in lung ACA is in the form of small exon 20 in-frame insertion mutations occurring at or around codon 775 and leading to duplications of some or all of the YVMA amino acid sequence.(128) Copy number changes have not been a component of regular mutation screening in lung A…”
BackgroundRexer, B. N., Ghosh, R., Narasanna, A., Estrada, M. V., Chakrabarty, A., Song, Y., Engelman, J. A., & Arteaga, C. L. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-13-1038 · Cited by 73
“Mutations in the tyrosine kinase domain of HER2 have been identified in head and neck, lung, gastric and breast carcinomas (19-23).”
BackgroundALK-rearrangements and testing methods in non-small cell lung cancer: a review
Shackelford, R. E., Vora, M., Mayhall, K., & Cotelingam, J. D. (2014) · Genes & Cancer · doi:10.18632/genesandcancer.3 · Cited by 72
“Presently, at least eighteen different driver mutations have been identified in NSCLC [8-38].”
BackgroundTargeting HER2 alterations in non-small cell lung cancer: Therapeutic breakthrough and challenges
Yu, Y., Yang, Y., Li, H., & Fan, Y. (2023) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2023.102520 · Cited by 75
Bronchioloalveolar Carcinoma: A Review
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Chronic myeloproliferative disorders: a tyrosine kinase tale
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Mutational Analysis of AKT1, AKT2 and AKT3 Genes in Common Human Carcinomas
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“6 %) of lung cancers mainly in exon 19–20 [26,31].”
BackgroundUncommon V599E BRAF Mutations in Japanese Patients with Lung Cancer
Sasaki, H., Kawano, O., Endo, K., Suzuki, E., Haneda, H., Yukiue, H., Kobayashi, Y., Yano, M., & Fujii, Y. (2005) · Journal of Surgical Research · doi:10.1016/j.jss.2005.10.022 · Cited by 68
Cretella, D., Saccani, F., Quaini, F., Frati, C., Lagrasta, C. A., Bonelli, M. A., Caffarra, C., Cavazzoni, A., Fumarola, C., Galetti, M., et al. (2014) · Molecular Cancer · doi:10.1186/1476-4598-13-143 · Cited by 66
“HER-2 mutations are present in about 2-4% of NSCLC, especially in women, never-smokers, Asian patients and in adenocarcinomas without EGFR or K-RAS mutations [34-38].”
BackgroundUnique prevalence of oncogenic genetic alterations in young patients with lung adenocarcinoma
Tanaka, K., Hida, T., Oya, Y., Yoshida, T., Shimizu, J., Mizuno, T., Kuroda, H., Sakakura, N., Yoshimura, K., Horio, Y., et al. (2017) · Cancer · doi:10.1002/cncr.30539 · Cited by 68
“Age: Median [range], y 65 [26-93] 36 [26-40] 66 [41-93]”
Biomarkers for prediction of sensitivity to EGFR inhibitors in non-small cell lung cancer
Hirsch, F. R., & Witta, S. E. (2005) · Current Opinion in Oncology · doi:10.1097/01.cco.0000155059.39733.9d · Cited by 68
The FGFR4 Y367C mutant is a dominant oncogene in MDA-MB453 breast cancer cells
Roidl, A., Foo, P., Wong, W., Mann, C., Bechtold, P. D. S., Berger, H.-J., Streit, S., Ruhe, J. E., Hart, S., Ullrich, A., et al. (2009) · Oncogene · doi:10.1038/onc.2009.432 · Cited by 67
“…in cell signalling molecules such as the tyrosine kinase superfamily to better understand the pathophysiology of cancers and to identify new drug targets (Bardelli et al., 2003; Stephens et al., 2004, 2005; Bignell et al., 2006; Greenman et al., 2007; Ruhe et al., 2007; Thomas et al., 2007).”
BackgroundOncogenic drivers, targeted therapies, and acquired resistance in non-small-cell lung cancer
Gower, A., Wang, Y., & Giaccone, G. (2014) · Journal of Molecular Medicine · doi:10.1007/s00109-014-1165-y · Cited by 68
Novel drugs targeting EGFR and HER2 exon 20 mutations in metastatic NSCLC
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Linking somatic genetic alterations in cancer to therapeutics
Stuart, D. D., & Sellers, W. R. (2009) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2009.02.001 · Cited by 66
Mutational profiling of kinases in glioblastoma
Bleeker, F. E., Lamba, S., Zanon, C., Molenaar, R. J., Hulsebos, T. J. M., Troost, D., van Tilborg, A. A., Vandertop, W. P., Leenstra, S., Noorden, C. J. F. V., et al. (2014) · BMC Cancer · doi:10.1186/1471-2407-14-718 · Cited by 67
“Characteristic Mean or number Age (years) 53 (27-80) KPS 76 (50-90) Irradiation dosage (Gy) 41 (0-78) Gender M 53 (54%) F 45 (46%) Surgical procedure Biopsy or irradical resection 41 (42%) Gross total removal 57 (59%) Other therapy No additional therapy 61 (62%) Additional therapy 37 (38%) Tumor occurrence Primary gli…”
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“2, insertion mutations in ErbB2 are focused in the same highly conserved region of exon 20 as insertion mutations in EGFR [97,98].”
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Analysis of different HER ‐2 mutations in breast cancer progression and drug resistance
Sun, Z., Shi, Y., Shen, Y., Cao, L., Zhang, W., & Guan, X. (2015) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12662 · Cited by 64
“Though HER-2 point or insertion mutations were first described in 2004, researches efforts about them are not exhaustive compared with his family EGFR to date [5].”
BackgroundPrevalence of driver mutations in non-small-cell lung cancers in the People’s Republic of China
Wu, Y.-L. L. C., & Gou, L.-Y. (2014) · Lung Cancer Targets and Therapy · doi:10.2147/lctt.s40817 · Cited by 63
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Epidermal growth factor receptor expression status in lung cancer correlates with its mutation
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“On the other hand, no correlation was found between HER2 overexpression and HER2 mutation, consistent with previous research [17].”
BackgroundResultMutational landscape and characteristics of ERBB2 in non‐small cell lung cancer
Wei, X., Gao, X., Zhang, X., Yang, J., Chen, Z., Wu, Y.-L. L. C., & Zhou, Q. H. (2020) · Thoracic Cancer · doi:10.1111/1759-7714.13419 · Cited by 62
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“Her2, a receptor tyrosine kinase and a member of the EGFR family is overexpressed in 20% of the advanced NSCLC and mutated in less than 2%.(30,31) In ES-NSCLC, studies suggest that overexpression of Her2 mRNA or protein is associated with an unfavorable prognosis.”
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Targeted Therapy: Wave of the Future
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Role of Consolidation Durvalumab in Patients With EGFR- and HER2-Mutant Unresectable Stage III NSCLC
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The HER2 inhibitor lapatinib potentiates doxorubicin-induced cardiotoxicity through iNOS signaling
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“In recent years, HER2 has attracted great attention as a drug discovery target for breast and lung cancers due to the association of its overexpression with progression of malignancy and poor prognosis [1,2].”
BackgroundInherited lung cancer syndromes targeting never smokers
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“Interestingly, an analogous mutation was reported in glioblastoma in the Erb-B2 receptor tyrosine kinase gene (ERBB2) [39].”
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Paul, I., Chacko, A., Stasik, I., Busacca, S., Crawford, N., McCoy, F. P. G., McTavish, N., Wilson, B. G., Barr, M. P., O'Byrne, K. J., et al. (2012) · Cell Death and Disease · doi:10.1038/cddis.2012.186 · Cited by 56
“Additional molecular subclasses with associated somatic gene alterations have been discovered, predominantly in lung adenocarcinomas and include mutations of BRAF,(13) human epidermal growth factor receptor 2(14) and phosphoinositide-3-kinase, catalytic, alpha polypeptide.(15) Despite these advances the majority of”
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“[4] Stephens P, Hunter C, Bignell G, Edkins S, Davies H, Teague J, Stevens C,”
BackgroundPotential role of LMP2 as tumor-suppressor defines new targets for uterine leiomyosarcoma therapy
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Morphological and molecular characteristics of HER2 amplified urothelial bladder cancer
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“Finally, we tested all UBC for activating HER2 mutations which have been reported in a small subset of lung and breast cancer [19, 31, 32].”
Method
Metadata
- Authors
- Stephens, P., Hunter, C., Bignell, G., Edkins, S., Davies, H., Teague, J., Stevens, C., O'Meara, S., Smith, R., Parker, A., Barthorpe, A., Blow, M., Brackenbury, L., Butler, A., Clarke, O., Cole, J., Dicks, E., Dike, A., Drozd, A., Edwards, K., Forbes, S., Foster, R., Gray, K., Greenman, C., Halliday, K., Hills, K., Kosmidou, V., Lugg, R., Menzies, A., Perry, J., Petty, R., Raine, K., Ratford, L., Shepherd, R., Small, A., Stephens, Y., Tofts, C., Varian, J., West, S., Widaa, S., Yates, A., Brasseur, F., Cooper, C. S., Flanagan, A. M., Knowles, M., Leung, S. Y., Louis, D. N., Looijenga, L. H. J., Malkowicz, B., Pierotti, M. A., Teh, B., Chenevix-Trench, G., Weber, B. L., Yuen, S. T., Harris, G., Goldstraw, P., Nicholson, A. G., Futreal, P. A., Wooster, R., & Stratton, M. R.
- Affiliations
- Wellcome Sanger Institute (GB)
- Ludwig Cancer Research (BE)
- Institute of Cancer Research (GB)
- University College London (GB)
- Cancer Research UK (GB)
- Queen Mary Hospital (CN)
- Massachusetts General Hospital (US)
- Erasmus MC (NL)
- University of Pennsylvania (US)
- IFOM (IT)
- Van Andel Institute (US)
- Royal Brompton Hospital (GB)
- Corresponding author
- Futreal, P. Andrew
- ORCID
- Hunter, Chris
- Edkins, Sarah
- Davies, Helen
- Teague, Jon
- Blow, Matthew
- Clarke, Oliver
- Dicks, Ed
- Foster, Rebecca
- Gray, Kristian
- Greenman, Chris
- Raine, Keiran
- Shepherd, Rebecca
- Widaa, Sara
- Yates, Andrew
- Flanagan, Adrienne M.
- Knowles, Margaret
- Louis, David N.
- Looijenga, Leendert H. J.
- Pierotti, Marco A.
- Teh, Bin
- Yuen, Siu T.
- Nicholson, Andrew G.
- Futreal, P. Andrew
- Stratton, Michael R.
- Venue
- Nature
- Published
- 2004-09
- Volume
- 431
- Issue
- 7008
- Pages
- 525-526
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2049449785
- Cited by
- 802
- References
- 7
- Citations by year
- 2026: 14 · 2025: 25 · 2024: 19 · 2023: 20 · 2022: 31 · 2021: 41 · 2020: 26 · 2019: 26 · 2018: 34 · 2017: 30 · 2016: 20 · 2015: 45 · 2014: 61 · 2013: 46 · 2012: 40
- FWCI
- 48.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- UEA Digital Repository (University of East Anglia) (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- ERBB2, HER2, c-erbB-2, kinase domain mutations, intragenic mutations, lung cancer, lung adenocarcinoma
- MeSH terms
- Gefitinib, Carcinoma, Non-Small-Cell Lung, DNA Mutational Analysis, Enzyme Activation, Humans, Lung Neoplasms, Models, Molecular, Mutation, Neoplasms, Quinazolines, Protein Structure, Tertiary, Receptor, ErbB-2, Erb-b2 Receptor Tyrosine Kinases, ErbB Receptors
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