Triple negative tumours: a critical review

被引:703
作者
Reis-Filho, J. S. [1 ]
Tutt, A. N. J. [1 ]
机构
[1] Inst Canc Res, Breakthrough Breast Canc Res Ctr, Mol Pathol Lab, London SW3 6JB, England
关键词
adjuvant therapy; basal-like; BRCA1; breast cancer; triple negative;
D O I
10.1111/j.1365-2559.2007.02889.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Breast cancer is a heterogeneous disease that encompasses several distinct entities with remarkably different biological characteristics and clinical behaviour. Currently, breast cancer patients are managed according to algorithms based on a constellation of clinical and histopathological parameters in conjunction with assessment of hormone receptor (oestrogen and progesterone receptor) status and HER2 overexpression/gene amplification. Although effective tailored therapies have been developed for patients with hormone receptor-positive or HER2+ disease, chemotherapy is the only modality of systemic therapy for patients with breast cancers lacking the expression of these markers (triple-negative cancers). Recent microarray expression profiling analyses have demonstrated that breast cancers can be systematically characterized into biologically and clinically meaningful groups. These studies have led to the re-discovery of basal-like breast cancers, which preferentially show a triple-negative phenotype. Both triple-negative and basal-like cancers preferentially affect young and African-American women, are of high histological grade and have more aggressive clinical behaviour. Furthermore, a significant overlap between the biological and clinical characteristics of sporadic triple-negative and basal-like cancers and breast carcinomas arising in BRCA1 mutation carriers has been repeatedly demonstrated. In this review, we critically address the characteristics of basal-like and triple-negative cancers, their similarities and differences, their response to chemotherapy as well as strategies for the development of novel therapeutic targets for these aggressive types of breast cancer. In addition, the possible mechanisms are discussed leading to BRCA1 pathway dysfunction in sporadic triple-negative and basal-like cancers and animal models for these tumour types.
引用
收藏
页码:108 / 118
页数:11
相关论文
共 97 条
[1]   High-throughput protein expression analysis using tissue microarray technology of a large well-characterised series identifies biologically distinct classes of breast cancer confirming recent cDNA expression analyses [J].
Abd El-Rehim, DM ;
Ball, G ;
Pinder, SE ;
Rakha, E ;
Paish, C ;
Robertson, JFR ;
Macmillan, D ;
Blamey, RW ;
Ellis, IO .
INTERNATIONAL JOURNAL OF CANCER, 2005, 116 (03) :340-350
[2]   Topoisomerase II alpha amplification may predict benefit from adjuvant anthracyclines in HER2 positive early breast cancer [J].
Arriola, Edurne ;
Rodriguez-Pinilla, Socorro Maria ;
Lambros, Maryou B. K. ;
Jones, Robin L. ;
James, Michelle ;
Savage, Kay ;
Smith, Ian E. ;
Dowsett, Mitch ;
Reis-Filho, Jorge S. .
BREAST CANCER RESEARCH AND TREATMENT, 2007, 106 (02) :181-189
[3]   Small interfering RNA screens reveal enhanced cisplatin cytotoxicity in tumor cells having both BRCA network and TP53 disruptions [J].
Bartz, Steven R. ;
Zhang, Zhan ;
Burchard, Julja ;
Imakura, Maki ;
Martin, Melissa ;
Palmieri, Anthony ;
Needham, Rachel ;
Guo, Jie ;
Gordon, Marcia ;
Chung, Namjin ;
Warrener, Paul ;
Jackson, Aimee L. ;
Carleton, Michael ;
Oatley, Melissa ;
Locco, Louis ;
Santini, Francesca ;
Smith, Todd ;
Kunapuli, Priya ;
Ferrer, Marc ;
Strulovici, Berta ;
Friend, Stephen H. ;
Linsley, Peter S. .
MOLECULAR AND CELLULAR BIOLOGY, 2006, 26 (24) :9377-9386
[4]   Descriptive analysis of estrogen receptor (ER)negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype - A population-based study from the California Cancer Registry [J].
Bauer, Katrina R. ;
Brown, Monica ;
Cress, Rosemary D. ;
Parise, Carol A. ;
Caggiano, Vincent .
CANCER, 2007, 109 (09) :1721-1728
[5]   Identification of Id4 as a regulator of BRCA1 expression by using a ribozyme-library-based inverse genomics approach [J].
Beger, C ;
Pierce, LN ;
Krüger, M ;
Marcusson, EG ;
Robbins, JM ;
Welcsh, P ;
Welch, PJ ;
Welte, K ;
King, MC ;
Barber, JR ;
Wong-Staal, F .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (01) :130-135
[6]   Distinct patterns of DNA copy number alteration are associated with different clinicopathological features and gene-expression subtypes of breast cancer [J].
Bergamaschi, Anna ;
Kim, Young H. ;
Wang, Pei ;
Sorlie, Therese ;
Hernandez-Boussard, Tina ;
Lonning, Per E. ;
Tibshirani, Robert ;
Borresen-Dale, Anne-Lise ;
Pollack, Jonathan R. .
GENES CHROMOSOMES & CANCER, 2006, 45 (11) :1033-1040
[7]   EGFR gene amplification in breast cancer:: correlation with epidermal growth factor receptor mRNA and protein expression and HER-2 status and absence of EGFR-activating mutations [J].
Bhargava, R ;
Gerald, WL ;
Li, AR ;
Pan, QL ;
Lal, P ;
Ladanyi, M ;
Chen, BY .
MODERN PATHOLOGY, 2005, 18 (08) :1027-1033
[8]   Molecular classification and molecular forecasting of breast cancer: Ready for clinical application? [J].
Brenton, JD ;
Carey, LA ;
Ahmed, AA ;
Caldas, C .
JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (29) :7350-7360
[9]   Regulation, substrates and functions of src [J].
Brown, MT ;
Cooper, JA .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1996, 1287 (2-3) :121-149
[10]   Intrinsic molecular signature of breast cancer in a population-based cohort of 412 patients [J].
Calza, Stefano ;
Hall, Per ;
Auer, Gert ;
Bjohle, Judith ;
Klaar, Sigrid ;
Kronenwett, Ulrike ;
T Liu, Edison ;
Miller, Lance ;
Ploner, Alexander ;
Smeds, Johanna ;
Bergh, Jonas ;
Pawitan, Yudi .
BREAST CANCER RESEARCH, 2006, 8 (04)