Triple-negative breast cancer (TNBC), that is breast cancer which stains negatively at immunohistochemistry for estrogen receptor
(ER), progesterone receptor (PR) and human epidermal growth factor 2 (HER2), comprises a particularly aggressive subtype of
breast cancer, with high rate of early local and distant relapse. TNBC have demonstrated sensitivity to cytotoxic treatment regimens, but
in the absence of HER2, ER and PR there is no benefit from hormonal therapy or trastuzumab. The lack of known specific molecular targets
has promoted abundant research in order to find possible “vulnerabilities” in TNBC and the evaluation of novel biomarkers overcoming
the traditional approach based on hormonal receptors and HER2-targeted therapy is one of the priorities in breast cancer research.
Drugs under investigation can be broadly subdivided into four groups: (1) Agents that create DNA damage (i.e. cisplatin, cyclophosphamide);
(2) Agents that inhibit poly (ADP-ribose) polymerase (PARP); (3) Tyrosin-kinase inhibitors and monoclonal antibodies; (4)
Agents that inhibit downstream signals. Several preclinical and early phase clinical trials for the treatment or management of patients
with triple-negative breast tumors are underway. Nonetheless, so far the major issue to deal with when trying to provide evidence for
TNBC is the small numbers of the sample in the clinical studies and the retrospective nature of most of them. Future large studies could
help in defining optimal treatment strategies for TNBC, both in the advanced setting as well as in the (neo) adjuvant setting.
Keywords: Advanced breast cancer, targeted therapy, triple-negative, HER2, estrogen receptor, progesterone receptor, Triple-negative breast cancer(TNBC), immunohistochemistry, epidermal growth factor, (ADP-ribose) polymerase.
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