Triple-Negative Breast Cancer: What Is Known About It?

Ferguson, Lisa; Curran, Britne; Martinez, M.T.; Mancuso, Peggy

doi:10.1188/14.cjon.e6-e11

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…Triple negative breast cancer (TNBC) is defined by the absence of detectable estrogen and progesterone receptors and the lack of amplification in the human epidermal growth factor receptor 2 gene [ 34 ]. Triple negative breast cancer accounts for 15-20% of all breast cancers, is generally more aggressive, and patients have decreased overall survival [ 35 ]. TNBC does not represent a single type of breast cancer, but rather a heterogeneous group of tumors with distinct molecular subtypes.…”

Section: Discussionmentioning

confidence: 99%

Computational identification of multi-omic correlates of anticancer therapeutic response

Pearl

Chen²,

Barnholtz‐Sloan

2014

BMC Genomics

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BackgroundA challenge in precision medicine is the transformation of genomic data into knowledge that can be used to stratify patients into treatment groups based on predicted clinical response. Although clinical trials remain the only way to truly measure drug toxicities and effectiveness, as a scientific community we lack the resources to clinically assess all drugs presently under development. Therefore, an effective preclinical model system that enables prediction of anticancer drug response could significantly speed the broader adoption of personalized medicine.ResultsThree large-scale pharmacogenomic studies have screened anticancer compounds in greater than 1000 distinct human cancer cell lines. We combined these datasets to generate and validate multi-omic predictors of drug response. We compared drug response signatures built using a penalized linear regression model and two non-linear machine learning techniques, random forest and support vector machine. The precision and robustness of each drug response signature was assessed using cross-validation across three independent datasets. Fifteen drugs were common among the datasets. We validated prediction signatures for eleven out of fifteen tested drugs (17-AAG, AZD0530, AZD6244, Erlotinib, Lapatinib, Nultin-3, Paclitaxel, PD0325901, PD0332991, PF02341066, and PLX4720).ConclusionsMulti-omic predictors of drug response can be generated and validated for many drugs. Specifically, the random forest algorithm generated more precise and robust prediction signatures when compared to support vector machines and the more commonly used elastic net regression. The resulting drug response signatures can be used to stratify patients into treatment groups based on their individual tumor biology, with two major benefits: speeding the process of bringing preclinical drugs to market, and the repurposing and repositioning of existing anticancer therapies.

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Section: Discussionmentioning

confidence: 99%

Computational identification of multi-omic correlates of anticancer therapeutic response

Pearl

Chen²,

Barnholtz‐Sloan

2014

BMC Genomics

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“…TNBC (triple-negative breast cancer) is an aggressive subclass of breast cancer (BC), representing around 10-20% of all invasive BCs [1,2]. As TNBC does not respond to endocrine treatment and always shows low effectiveness to targeted therapy, chemotherapy is still the most effective method of preventing cancer cell growth along with metastasis [3]. Nevertheless, because of the adverse side effects of chemotherapy, research into new safe and effective drugs or methods for TNBC is continuing.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐129‐1‐3p Represses the Progression of Triple‐Negative Breast Cancer by Targeting the GRIN2D Gene

Tan

et al. 2022

BioMed Research International

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The aberrant expression of miRNA is strongly linked to numerous stages of triple-negative breast cancer (TNBC) progression, and it plays an indispensable role in the process from tumor onset and progress to invasion and metastasis. In this study, we first transfected miR-129-1-3p mimics and inhibitor into MDA-MB-231 TNBC cells, respectively. Then, we assessed the pathological role of miR-129-1-3p in MDA-MB-231 cells. The results showed that miR-129-1-3p were successfully inserted into MDA-MB-231 cells. Besides, miR-129-1-3p could distinctively repress the growth, migration along with infiltration of MDA-MB-231 cells, which might be related to the inhibition of GRIN2D expression. Our results indicate that miR-129-1-3p was illustrated to serve as a tumor repressor via targeting GRIN2D in TNBC cells and highlight that the restoration of miR-129-1-3p might be a new treatment target for TNBC.

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“…TNBC tumors are characterized by the absence of estrogen receptor (ER) and progesterone receptor (PR) expression as well as human epidermal growth factor receptor 2 (HER-2) amplification. Therefore, patients with TNBCs do not benefit from commonly used antiestrogen and herceptin-based therapies (4,5). Although chemotherapy is currently the mainstay of systemic treatment for breast cancer, patients with TNBC disease have a worse outcome after chemotherapy than patients with other subtypes of breast cancer (6,7).…”

Section: Introductionmentioning

confidence: 99%

Lentiviral vector-mediated doxycycline-inducible USP39 shRNA or cDNA expression in triple-negative breast cancer cells

Liu

Wang

et al. 2015

Oncology Reports

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Abstract. Triple-negative breast cancer (TNBC), characterized by distinct biological and clinicopathological features, has a poor prognosis due to lack of effective therapeutic targets. Our previous data revealed that high levels of USP39 were selectively present in TNBC samples compared with their normal breast tissue samples and USP39 was also expressed at different levels in cultured TNBC cells and normal breast cells. Yet, the underlying cellular and molecular mechanisms of USP39 remain unclear. In the present study, we describe a doxycycline (DOX)-regulated lentiviral vector system expressing shRNA or cDNA of the USP39 gene in the TNBC cell line MDA-MB-231. USP39 expression was knocked down by the miR-30-based inducible lentiviral short hairpin RNA (shRNA) delivery system or overexpressed by the inducible cDNA system. The inducible shRNA-mediated downregulation of USP39 expression markedly reduced the proliferation and colony-forming ability of MDA-MB-231 cells, while overexpression of USP39 by the inducible system did not promote cancer cell proliferation. The lentiviral vector-mediated Tet-on system demonstrated efficient and inducible knockdown of USP39 or overexpression of USP39 in TNBC cells, facilitating a wide variety of applications for gene knockdown and overexpression experiments in gene functional studies in vitro and in vivo.

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Triple-Negative Breast Cancer: What Is Known About It?

Cited by 5 publications

References 28 publications

Computational identification of multi-omic correlates of anticancer therapeutic response

Computational identification of multi-omic correlates of anticancer therapeutic response

MicroRNA‐129‐1‐3p Represses the Progression of Triple‐Negative Breast Cancer by Targeting the GRIN2D Gene

Lentiviral vector-mediated doxycycline-inducible USP39 shRNA or cDNA expression in triple-negative breast cancer cells

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