PMID- 20943632
OWN - NLM
STAT- MEDLINE
DCOM- 20111017
LR  - 20200203
IS  - 1569-8041 (Electronic)
IS  - 0923-7534 (Linking)
VI  - 21 Suppl 7
DP  - 2010 Oct
TI  - Treatment of triple-negative metastatic breast cancer: toward individualized 
      targeted treatments or chemosensitization?
PG  - vii30-5
LID - 10.1093/annonc/mdq279 [doi]
AB  - Triple-negative [estrogen receptor (ER)-/progesterone receptor (PR)-/HER2-] 
      breast cancers account for ~15% of overall breast cancers. Triple-negative breast 
      cancers demonstrate a panel of specific molecular alterations including a high 
      rate of p53 mutations, frequent loss of function of BRCA1, phosphatase and tensin 
      homolog (PTEN) loss and a specific panel of tyrosine kinase activation 
      [fibroblast growth factor receptor 2 (FGFR2)]. This molecular entity is 
      considered as sensitive to chemotherapy in the adjuvant setting. When metastatic, 
      the disease is usually aggressive and drug resistant, leading to cancer death 
      within 18 months for the majority of patients. There is no evidence from 
      randomized trials that triple-negative breast cancers have a different 
      sensitivity to specific chemotherapy compared with other molecular classes. 
      Similar findings have been reported for bevacizumab. Several recent research 
      efforts have focused on this entity in the last few years. DNA alkylating agents 
      have shown promising activity in the neoadjuvant setting, but no evidence from a 
      phase III trial currently supports its use. Several targeted therapies are also 
      being successfully developed. Poly(ADP ribose) polymerase 1 (PARP1) inhibitors 
      induce tumor response as a single agent in BRCA1-mutated breast cancer, and could 
      sensitize cisplatin in the whole triple negative population. Several other 
      targeted agents are being developed in this setting, including epidermal growth 
      factor receptor (EGFR), FGFR2, mammalian target of rapamycin (mTOR) and NOTCH 
      inhibitors.
FAU - Berrada, N
AU  - Berrada N
AD  - Department of Medical Oncology and INSERM Unit U981, Institut Gustave Roussy, 
      Villejuif, France.
FAU - Delaloge, S
AU  - Delaloge S
FAU - Andre, F
AU  - Andre F
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Ann Oncol
JT  - Annals of oncology : official journal of the European Society for Medical 
      Oncology
JID - 9007735
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
SB  - IM
MH  - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use
MH  - Breast Neoplasms/metabolism/pathology/*therapy
MH  - Carcinoma/metabolism/pathology/*therapy
MH  - Chemotherapy, Adjuvant
MH  - Drug Resistance, Neoplasm/*drug effects/physiology
MH  - Drug Synergism
MH  - Female
MH  - Humans
MH  - Molecular Targeted Therapy/methods/*trends
MH  - Neoplasm Metastasis
MH  - Precision Medicine/*methods/trends
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
EDAT- 2010/10/15 06:00
MHDA- 2011/10/18 06:00
CRDT- 2010/10/15 06:00
PHST- 2010/10/15 06:00 [entrez]
PHST- 2010/10/15 06:00 [pubmed]
PHST- 2011/10/18 06:00 [medline]
AID - S0923-7534(19)39686-3 [pii]
AID - 10.1093/annonc/mdq279 [doi]
PST - ppublish
SO  - Ann Oncol. 2010 Oct;21 Suppl 7:vii30-5. doi: 10.1093/annonc/mdq279.