|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, our study provided a rationale for the clinical application of CDK4/6 inhibitor combinatorial regimens for patients with TNBC.
|
31253784 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, this study provides important clues about the cyclin D1-CDK4-RB1 pathway as a potential target for proton beam therapy in TNBC.
|
31591311 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
We defined a new association of three biomarkers (MT4-MMP/EGFR/RB) expressed together in 50% of TNBC and demonstrated its usefulness to predict the TNBC response to anti-EGFR and anti-CDK4/6 drugs used in single or combined therapy.
|
30504427 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
While Retinoblastoma protein (pRb), a major substrate of CDK4/6, is a potential target in triple negative breast cancer (TNBC), the usefulness of CDK4/6 inhibitors in this cancer has not been established.
|
30607633 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although the mechanisms by which the CDK4/6 complex is involved in the control of cell growth in triple negative breast cancer (TNBC) are still unclear, some TNBCs might be sensitive to CDK4/6 inhibitors.<b>Areas covered</b>: The authors provide an overview of the treatments that target cell cycle machinery in breast cancer and provide their perspectives for the future.<b>Expert opinion</b>: CDK 4/6 inhibitors are active drugs in HR+ MBC, but some unresolved issues remain.
|
31610139 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Addition of the CDK4/6 inhibitor LEE011 to BYL719 caused a simultaneous reduction of p-RB and p-S6, and a more complete inhibition of p-S6, leading to decreased expression of the pro-survival protein MCL-1, an induction of apoptosis, and an enhanced reduction of tumor growth in a PDX model of TNBC.
|
31101835 |
2019 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pharmacological or genetic inhibition of CDC25 suppressed growth of RB1-deficient TNBC cells that are resistant to combined CDK4/6 plus CDK2 inhibition.
|
29617654 |
2018 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Notably, combined PI3Kα and CDK4/6 inhibition, along with inhibition of immune checkpoints PD-1 and CTLA-4, induced complete and durable regressions (>1 year) of established TNBC tumors <i>in vivo</i> Overall, our results illustrate convergent mechanisms of PI3Kα and CDK4/6 blockade on cell-cycle progression, DNA damage response, and immune-modulation and may provide a novel therapeutic approach for TNBC.<i></i>.
|
28947417 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we demonstrate that inhibition of CDK4/6 blocks breast tumour metastasis in the triple-negative breast cancer model, without affecting tumour growth.
|
28067227 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
CDK4/6 inhibitors, alone and in combination, are a novel therapeutic strategy for specific subgroups of TNBC.<i></i>.
|
28606920 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Retinoblastoma (RB, a known substrate of CDK4/6) pathway deregulation is a frequent occurrence in TNBC and studies have revealed that pharmacological CDK4/6 inhibition induces a cooperative cytostatic effect with doxorubicin in RB-proficient TNBC models.
|
29261702 |
2017 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Finally, blocking CDK4 activity efficiently eliminated both normal and chemotherapy-resistant cancer cells in triple negative breast cancers, highlighting CDK4 as a promising novel therapeutic target for these aggressive breast tumors.
|
27759034 |
2016 |
|
Triple Negative Breast Neoplasms
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Herein, we investigated how repression of E2F activity via CDK4/6 inhibition and RB activation impacts the response of triple negative breast cancer (TNBC) to frequently used therapeutic agents.
|
22733811 |
2012 |
|
Triple Negative Breast Neoplasms
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, the ability of CDK4/6 inhibition to protect TNBC cells from doxorubicin-mediated cytotoxicity resulted in recurrent populations of cells specifically in RB-proficient cell models, indicating that CDK4/6 inhibition can preserve cell viability in the presence of genotoxic agents.
|
22751436 |
2012 |