Triple-negative breast cancer.
Recent advances in biological characterization of breast cancer have eventually increased our understanding of underlying tumour biology. While for endocrine responsive and Her2-positive disease different molecular targeted therapies are available, up to now no specific targeted approach for triple-negative breast cancer has been developed. Patients with triple-negative disease are at high risk for tumour recurrence. Preclinical and limited clinical data suggest that platinum-based regimens may be the most active conventional chemotherapy, but prospective randomized trials are missing. Bevacizumab and other agents targeting tumour vessel growth have potential activity in all subtypes of breast cancer, and therefore are not considered a targeted approach for triple-negative tumours alone. Due to specific defects in DNA-damage repair, basal-like cancers depend on alternative, more error-prone repair pathways. Currently, scientific interest is focussing on drugs blocking those mechanisms. PARP-1 inhibitors, in conjunction with platinum derivatives, were found to exhibit significant survival benefit over chemotherapy alone even in a relatively small phase II study. For the first time, this approach offers the chance of highly active, specific therapy for triple-negative disease.
Bartsch
Rupert
R
Clinical Division of Oncology, Department of Medicine 1 and Cancer Centre, Medical University of Vienna, Vienna, Austria. rupert.bartsch@meduniwien.ac.at
Ziebermayr
Reinhard
R
Zielinski
Christoph C
CC
Steger
Guenther G
GG
D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000235:genetics* / Q000401:mortality / Q000473:pathology / Q000628:therapy; D017024:Chemotherapy, Adjuvant; D003131:Combined Modality Therapy; D004249:DNA Damage / Q000235:genetics*; D004260:DNA Repair / Q000235:genetics*; D018572:Disease-Free Survival; D005260:Female; D020869:Gene Expression Profiling; D005819:Genetic Markers / Q000235:genetics; D006801:Humans; D008408:Mastectomy; D009364:Neoplasm Recurrence, Local / Q000235:genetics* / Q000401:mortality / Q000517:prevention & control; D009376:Neoplasms, Hormone-Dependent / Q000235:genetics* / Q000401:mortality / Q000628:therapy; D020411:Oligonucleotide Array Sequence Analysis; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D011065:Poly(ADP-ribose) Polymerases / Q000235:genetics*; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics*; D011960:Receptors, Estrogen / Q000235:genetics*; D011980:Receptors, Progesterone / Q000235:genetics*; D012307:Risk Factors
D005819:Genetic Markers; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D011065:Poly(ADP-ribose) Polymerases; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C499320:PARP1 protein, human; C508053:ERBB2 protein, human
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