Cited by 252HER2/EGFR in Cancer ResearchPI3K/AKT/mTOR signaling in cancerLung Cancer Treatments and Mutations

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Loss of phosphatase and tensin homolog or phosphoinositol-3 kinase activation and response to trastuzumab or lapatinib in human epidermal growth factor receptor 2-overexpressing locally advanced breast cancers

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Dave, Bhuvanesh, Migliaccio, Ilenia, Gutierrez, M. Carolina, Wu, Meng-Fen, Chamness, Gary C., Wong, Helen, Narasanna, Archana, Chakrabarty, Anindita, Hilsenbeck, Susan G., Huang, Jian, Rimawi, Mothaffar, Schiff, Rachel, Arteaga, Carlos, Osborne, C. Kent, Chang, Jenny C.·2011·Journal of Clinical Oncology

DOI 10.1200/jco.2009.27.7814PMC PMC3058274

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Abstract

PURPOSE: Phosphatase and tensin homolog (PTEN) loss or activating mutations of phosphoinositol-3 (PI3) kinase (PIK3CA) may be associated with trastuzumab resistance. Trastuzumab, the humanized human epidermal growth factor receptor 2 (HER2) monoclonal antibody, and lapatinib, an epidermal growth factor receptor/HER2 tyrosine kinase inhibitor, are both established treatments for HER2-overexpressing breast cancers. Understanding of the cellular response to HER2-targeted therapies is needed to tailor treatments and to identify patients less likely to benefit. METHODS: We evaluated the effect of trastuzumab or lapatinib in three HER2-overexpressing cell lines. We confirmed the in vitro observations in two neoadjuvant clinical trials in patients with HER2 overexpression; 35 patients received trastuzumab as a single agent for the first 3 weeks, then docetaxel every 3 weeks for 12 weeks (trastuzumab regimen), whereas 49 patients received lapatinib as a single agent for 6 weeks, followed by trastuzumab/docetaxel for 12 weeks before primary surgery (lapatinib regimen). Apoptosis, Ki67, p-MAPK, p-AKT, and PTEN were assessed by immunohistochemistry. Genomic DNA was sequenced for PIK3CA mutations. RESULTS: Under low PTEN conditions, in vitro data indicate that lapatinib alone and in combination with trastuzumab was effective in decreasing p-MAPK and p-AKT levels, whereas trastuzumab was ineffective. In the clinical trials, we confirmed that low PTEN or activating mutation in PIK3CA conferred resistance to the trastuzumab regimen (P = .015), whereas low PTEN tumors were associated with a high pathologic complete response rate (P = .007). CONCLUSION: Activation of PI3 kinase pathway is associated with trastuzumab resistance, whereas low PTEN predicted for response to lapatinib. These observations support clinical trials with the combination of both agents.

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Authors: Dave, B., Migliaccio, I., Gutierrez, M. C., Wu, M.-F., Chamness, G. C., Wong, H., Narasanna, A., Chakrabarty, A., Hilsenbeck, S. G., Huang, J., Rimawi, M., Schiff, R., Arteaga, C., Osborne, C. K., & Chang, J. C.
Affiliations: Houston Methodist (US)
ORCID: Migliaccio, Ilenia
Wu, Meng-Fen
Wong, Helen
Chakrabarty, Anindita
Hilsenbeck, Susan G.
Huang, Jian
Rimawi, Mothaffar
Schiff, Rachel
Arteaga, Carlos
Osborne, C. Kent
Chang, Jenny C.
Venue: Journal of Clinical Oncology
Publisher: American Society of Clinical Oncology (ASCO)
Published: 2011-01-10
Volume: 29
Issue: 2
Pages: 166-173
ISSN: 0732-183X (ISSN-L)
1527-7755
DOI: 10.1200/jco.2009.27.7814
PMC: PMC3058274
OpenAlex: W2109189228
Cited by: 252
References: 28
Citations by year: 2026: 1 · 2025: 10 · 2024: 7 · 2023: 15 · 2022: 10 · 2021: 7 · 2020: 12 · 2019: 14 · 2018: 10 · 2017: 17 · 2016: 15 · 2015: 32 · 2014: 21 · 2013: 34 · 2012: 21
FWCI: 12.66
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Clinical Oncology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Breast Cancer Research Foundation
GlaxoSmithKline
National Cancer Institute (P50 CA 50183, R01CA112305)
Medical Research and Materiel Command
Topics: Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Keywords: PTEN loss, PIK3CA mutation, trastuzumab resistance, lapatinib, HER2-positive breast cancer, locally advanced breast cancer, PI3 kinase pathway, MAPK signaling, Akt phosphorylation, pathological complete response, neoadjuvant therapy
MeSH terms: Trastuzumab, Docetaxel, Lapatinib, Adult, Aged, Antibodies, Monoclonal, Antineoplastic Combined Chemotherapy Protocols, Breast Neoplasms, Enzyme Activation, Female, Humans, Middle Aged, Mutation, Quinazolines, Transfection, Clinical Trials, Phase II as Topic, Receptor, ErbB-2, Erb-b2 Receptor Tyrosine Kinases, Phosphatidylinositol 3-Kinases, Neoadjuvant Therapy, RNA, Small Interfering, Taxoids, Cell Line, Tumor, PTEN Phosphohydrolase, Class I Phosphatidylinositol 3-Kinases, Antibodies, Monoclonal, Humanized

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Loss of phosphatase and tensin homolog or phosphoinositol-3 kinase activation and response to trastuzumab or lapatinib in human epidermal growth factor receptor 2-overexpressing locally advanced breast cancers

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