title: The triple-negative subtype: new ideas for the poorest prognosis breast cancer.
abstract: Triple-negative breast cancer accounts for about 15%-20% of all breast cancers. Patients with triple-negative subtype have a significantly increased risk of relapse and death. A panel of specific molecular alterations like high rate of p53 mutations, frequent loss of function of BRCA1, and several tyrosine kinase activations has been shown in this specific phenotype. An optimal chemotherapy regimen for these cancers remains to be determined, representing a major challenge for patient management. DNA alkylating agents, as cisplatin, were shown to be particularly effective in the neoadjuvant setting for patients with the disease. Targeted therapies are being successfully developed. Poly (ADP-ribose) polymerase-1 inhibitors induce tumor response as a single agent in BRCA1-mutated breast cancer and might sensitize cancer cells to cisplatin in the triple-negative subpopulation. Chemotherapy is a cornerstone of current clinical practice for this type of disease. Progress might derive from refined biology-driven phase II trials that will also integrate targeted agents with chemotherapy.
authors: Department of Medicine, Division of Medical Oncology, Istituto Europeo di Oncologia, Milano 20141, Italy. giuseppe.curigliano@ieo.it
authors: Giuseppe
authors: G
authors: Curigliano
authors: Aron
authors: A
authors: Goldhirsch
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018906:Antineoplastic Agents, Alkylating / Q000627:therapeutic use; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000737:chemistry* / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000473:pathology; D017024:Chemotherapy, Adjuvant; D002986:Clinical Trials as Topic; D004260:DNA Repair / Q000187:drug effects; D005260:Female; D019398:Genes, BRCA1; D024522:Genes, BRCA2; D020022:Genetic Predisposition to Disease; D006801:Humans; D007150:Immunohistochemistry; D009154:Mutation; D020360:Neoadjuvant Therapy / Q000379:methods; D017671:Platinum Compounds / Q000494:pharmacology; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis
chemical_list: D020533:Angiogenesis Inhibitors; D000970:Antineoplastic Agents; D018906:Antineoplastic Agents, Alkylating; D014408:Biomarkers, Tumor; D017671:Platinum Compounds; D000071137:Poly (ADP-Ribose) Polymerase-1; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C499320:PARP1 protein, human