Mechanisms of lapatinib resistance in HER2-driven breast cancer

被引：123

作者：

D'Amato, Valentina ^{[1
]}

Raimondo, Lucia ^{[1
]}

Formisano, Luigi ^{[1
]}

Giuliano, Mario ^{[1
]}

De Placido, Sabino ^{[1
]}

Rosa, Roberta ^{[1
]}

Bianco, Roberto ^{[1
]}

机构：

[1] Univ Naples Federico II, Dipartimento Med Clin & Chirurg, I-80131 Naples, Italy

来源：

CANCER TREATMENT REVIEWS | 2015年 / 41卷 / 10期

关键词：

Lapatinib; Resistance; ErbB2/HER2; Breast cancer; GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITOR; NEOPLASTIC TRANSFORMATION; TRASTUZUMAB RESISTANCE; MEDIATES RESISTANCE; ESTROGEN-RECEPTOR; DRIVEN RESISTANCE; GENE-EXPRESSION; PHASE-II; CELLS;

D O I：

10.1016/j.ctrv.2015.08.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Targeted therapies have been approved for various malignancies but the acquisition of resistance remains a substantial challenge in the clinical management of advanced cancers. Twenty-five per cent of breast cancers overexpress ErbB2/HER2, which confers a more aggressive phenotype and is associated with a poor prognosis. HER2-targeting therapies (trastuzumab, pertuzumab, TDM1 and lapatinib) are available, but a significant fraction of HER2-positive breast cancers eventually relapse or progress. This suggests that acquired or intrinsic resistance enables escape from HER2 inhibition. This review focuses on mechanisms of intrinsic/acquired resistance to lapatinib identified in preclinical and clinical studies. A better understanding of these mechanisms could lead to novel predictive markers of lapatinib response and to novel therapeutic strategies for breast cancer patients. (C) 2015 Elsevier Ltd. All rights reserved.

引用

页码：877 / 883

页数：7

共 57 条

[1]

ALIMANDI M, 1995, ONCOGENE, V10, P1813

[2]

BERGER MS, 1988, CANCER RES, V48, P1238

[3] PI3K-independent mTOR activation promotes lapatinib resistance and IAP expression that can be effectively reversed by mTOR and Hsp90 inhibition [J].

Brady, Samuel W. ;

Zhang, Jian ;

Tsai, Ming-Horng ;

Yu, Dihua .

CANCER BIOLOGY & THERAPY, 2015, 16 (03) :402-411

[4]

Brown Kristin K, 2015, F1000Prime Rep, V7, P13, DOI 10.12703/P7-13

[5] BREAST CANCER HER2-a good addiction [J].

Carey, Lisa A. .

NATURE REVIEWS CLINICAL ONCOLOGY, 2012, 9 (04) :196-197

[6] MET Activation Mediates Resistance to Lapatinib Inhibition of HER2-Amplified Gastric Cancer Cells [J].

Chen, Chin-Tung ;

Kim, Hyaehwan ;

Liska, David ;

Gao, Sizhi ;

Christensen, James G. ;

Weiser, Martin R. .

MOLECULAR CANCER THERAPEUTICS, 2012, 11 (03) :660-669

[7] Response of some head and neck cancers to epidermal growth factor receptor tyrosine kinase inhibitors may be linked to mutation of ERBB2 rather than EGFR [J].

Cohen, EEW ;

Lingen, MW ;

Martin, LE ;

Harris, PL ;

Brannigan, BW ;

Haserlat, SM ;

Okimoto, RA ;

Sgroi, DC ;

Dahiya, S ;

Muir, B ;

Clark, JR ;

Rocco, JW ;

Vokes, EE ;

Haber, DA ;

Bell, DW .

CLINICAL CANCER RESEARCH, 2005, 11 (22) :8105-8108

[8] Drug development of MET inhibitors: targeting oncogene addiction and expedience [J].

Comoglio, Paolo M. ;

Giordano, Silvia ;

Trusolino, Livio .

NATURE REVIEWS DRUG DISCOVERY, 2008, 7 (06) :504-516

[9] Cell-Autonomous and Non-Cell-Autonomous Mechanisms of HGF/MET-Driven Resistance to Targeted Therapies: From Basic Research to a Clinical Perspective [J].

Corso, Simona ;

Giordano, Silvia .

CANCER DISCOVERY, 2013, 3 (09) :978-992

[10] Translational evidence on the role of Src kinase and activated Src kinase in invasive breast cancer [J].

Elsberger, Beatrix .

CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY, 2014, 89 (03) :343-351

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