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Triple-negative breast cancer (TNBC)
内容
Triple-negative breast cancer (TNBC) is a subtype of breast tumor that is negative for estrogen receptors (ER) and progesterone receptors (PR) and does not show over-expression of Her-2/neu (HER2). Higher occurrences of TNBC have been noted in younger and African-American women. Few drug choices with the exception of chemotherapy such as anthracycline, taxane and platinum are currently available for the treatment of TNBC. Patients with TNBC have a poor prognosis [1] because of the tendency for early relapse and visceral metastasis [2, 3]. TNBC is also insensitive to some of the effective therapies for breast cancer, including HER2-directed therapies, such as trastuzumab, and endocrine therapies, such as tamoxifen or aromatase inhibitors. Hence, treatment of TNBC remains a great challenge. Gene expression analysis has revealed six subtypes of TNBC [4], including two basal-like subtypes (BL1 and BL2) and immunomodulatory, mesenchymal (M), mesenchymal stem-like (MSL), and luminal androgen receptor (LAR) subtypes. Current and future treatment options include modulation of the DNA repair machinery, p53 family signaling, androgen receptor and MAPK/MEK signaling and PI3K/AKT/mTOR signaling. PI3K/AKT/mTOR inhibitors are one of these therapeutic regimens [5], and some of these inhibitors, such as GDC-0941, BKM120 and Everolimus, have been used as the therapeutic choice in recent clinical trials of TNBC (https://clinicaltrials.gov). It was recently reported that a PI3K inhibitor sensitized tumors to PARP inhibition by impairing BRCA1/2 expression [6].
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