Breast Cancer

, Volume 14, Issue 2, pp 156–162

Does lapatinib, a small-molecule tyrosine kinase inhibitor, constitute a breakthrough in the treatment of breast cancer?

Authors

    • Department of Medical OncologyCancer Institute Hospital, Japanese Foundation for Cancer Research
  • Nahomi Tokudome
    • Department of Medical OncologyCancer Institute Hospital, Japanese Foundation for Cancer Research
  • Tsutomu Sugihara
    • Department of Medical OncologyCancer Institute Hospital, Japanese Foundation for Cancer Research
  • Shunji Takahashi
    • Department of Medical OncologyCancer Institute Hospital, Japanese Foundation for Cancer Research
  • Kiyohiko Hatake
    • Department of Medical OncologyCancer Institute Hospital, Japanese Foundation for Cancer Research
Review Article

DOI: 10.2325/jbcs.971

Cite this article as:
Ito, Y., Tokudome, N., Sugihara, T. et al. Breast Cancer (2007) 14: 156. doi:10.2325/jbcs.971

Abstract

ErbB/HER receptor or its signal transduction pathway is an attractive therapeutic target for breast cancer. Lapatinib, an orally administered dual inhibitor of ErbB1 (EGFR) and ErbB2 (HER2) receptor tyrosine kinases has shown promising results for metastatic breast cancer (MBC). Lapatinib exhibited activity against trastuzumab-refractory MBC and showed an acceptable adverse event profile such as tran-sient mild rash, diarrhea and nausea. The addition of lapatinib to capecitabine resulted in significantly pro-longed time to progression. Large randomized trials using lapatinib following chemotherapy and surgery are ongoing for early stage HER2-overexpressing breast cancer. Various combinations with agents such as paclitaxel, aromatase inhibitors, or other molecular targeted agents are currently being investigated in clinical trials. If these approaches overcome the limitations of trastuzumab, lapatinib will become an effec-tive treatment option for breast cancer in the near future.

Keywords

Breast cancerErbBHERLapatinib

Abbreviations

MBC

Metastatic breast cancer

EGFR

Epidermal growth factor receptor

MAPK

Mitogen-activated protein kinase

PI3K

Phatidylinositol 3 kinase

IGF-IR

Insulin-like growth factor-l receptor

Cdk

Cyclin-dependent kinase

ER

Estrogen receptor

Al

Aromatase inhibitor

TAM

Tamoxifen

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Copyright information

© The Japanese Breast Cancer Society 2007