Donna, what a mind link! I didn't see you'd put this up here and just did the same thing over in the Talk section. There's some interesting trials right now and I'm always thankful when I see the long list now compared to what was available just a few short years ago.
Triple-negative breast cancer (TNBC) is defined as the absence of staining for estrogen receptor, progesterone receptor, and HER2/neu. TNBC is insensitive to some of the most effective therapies available for breast cancer treatment including HER2-directed
therapy such as trastuzumab and endocrine therapies such as tamoxifen
or the aromatase inhibitors. Combination cytotoxic chemotherapy
administered in a dose-dense or metronomic schedule remains the standard
therapy for early-stage TNBC.[1]
A prospective analysis of 1,118 patients who received neoadjuvant
chemotherapy at a single institution, of whom 255 (23%) had TNBC, found
that patients with TNBC had higher pathologic complete response (pCR)
rates compared with non-TNBC patients (22% vs. 11%; P = 0.034).[2][Level of evidence: 3iiDiv] Improved pCR rates may be important since in some studies, pCR is associated with improved long-term outcomes.
Platinum
agents have recently emerged as drugs of interest for the treatment of
TNBC. One trial that treated 28 women with stage II or stage III TNBC
with four cycles of neoadjuvant cisplatin resulted in a 22% pCR rate.[3][Level of evidence: 3iiiDiv] An ongoing randomized clinical trial, CALGB-40603
(NCT00861705), is evaluating the benefit of carboplatin added to
paclitaxel and adriamycin plus cyclophosphamide chemotherapy in the
neoadjuvant setting. Another trial, entitled the Triple Negative Trial
(NCT00532727), is evaluating carboplatin against docetaxel in the
metastatic setting. These trials will help to define the role of
platinum agents for the treatment of TNBC. Currently, there is no
established role for adding platinum agents to the treatment of
early-stage TNBC outside of a clinical trial.
The poly (ADP-ribose) polymerase (PARP) inhibitors are emerging as promising therapeutics for the treatment of TNBC.[4]
PARPs are a family of enzymes involved in multiple cellular processes,
including DNA repair. Because TNBC shares multiple clinicopathologic
features with BRCA-mutated breast
cancers, which harbor dysfunctional DNA repair mechanisms, it is
possible that PARP inhibition, in conjunction with the loss of DNA
repair via BRCA-dependent mechanisms, would result in synthetic
lethality and augmented cell death. PARP inhibitors are currently being
evaluated in clinical trials for patients with BRCA mutations and in TNBC.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with triple-negative breast cancer. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
References
Mehta
RS: Dose-dense and/or metronomic schedules of specific chemotherapies
consolidate the chemosensitivity of triple-negative breast cancer: a
step toward reversing triple-negative paradox. J Clin Oncol 26 (19):
3286-8; author reply 3288, 2008. [PUBMED Abstract]
Liedtke
C, Mazouni C, Hess KR, et al.: Response to neoadjuvant therapy and
long-term survival in patients with triple-negative breast cancer. J
Clin Oncol 26 (8): 1275-81, 2008. [PUBMED Abstract]
Silver
DP, Richardson AL, Eklund AC, et al.: Efficacy of neoadjuvant Cisplatin
in triple-negative breast cancer. J Clin Oncol 28 (7): 1145-53, 2010. [PUBMED Abstract]
Anders
CK, Winer EP, Ford JM, et al.: Poly(ADP-Ribose) polymerase inhibition:
"targeted" therapy for triple-negative breast cancer. Clin Cancer Res 16
(19): 4702-10, 2010. [PUBMED Abstract]
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