objective To compare the efficacy of platinum and non-platinum-based regimens as first-line treatment for triple-negative breast cancer is advanced (TNBC) and analyze the relationship between their success and status of the BRCA genes.
method Retrospectively analyzed clinical data from 220 patients diagnosed with advanced pathological TNBC and treated in the Department of Breast Oncology, Peking University Cancer Hospital from 2013 to 2018 and evaluate the effectiveness of chemotherapy. A total of 114 patients had BRCA1 / 2 genes were tested by next generation sequencing (NGS) using peripheral blood, and we analyzed the correlation between efficacy and BRCA1 / 2 gene status.
result non-platinum-based chemotherapy (NPCT) was given to 129 and platinum-based chemotherapy (PBCT) to 91 study patients. The level of clinical benefit (CBR) and median progression-free survival (PFS) were not statistically different between groups NPCT and PBCT. Overall average life (OS) was 30.0 and 22.5 months for PBCT and NPCT groups, respectively [P = 0.090, hazard ratio (HR) = 0.703]. BRCA status assessed 114 patients, 14 of whom have a detrimental germline BRCA1 / 2 (gBRCA) mutation (seven in each group). In PBCT group, CBR was 85.7% and 35.1% for patients with and without mutations that destroy gBRCA, respectively (P = 0.039). Median PFS was 14.9 and 5.3 months and the median OS was 26.5 and 15.5 months for patients with and without mutations that destroy gBRCA, respectively (P = 0.001, P = 0.161, respectively). Patients in group PBCT have significantly greater levels of grade 3-4 anemia (5.5% vs. 0%) and thrombocytopenia (8.8% vs 0%), while the palmar-plantar erythrodysesthesia (12.4% vs 0% ) and peripheral neuropathy (8.6% vs. 1.1%) occurred more frequently in the group NPCT.
Efficacy of platinum in advanced triple-negative breast cancer with germline BRCA mutation determined by next generation sequencing.
conclusion platinum-based regimen was more effective in patients with mutations gBRCA damage, but there was no difference in patients without BRCA gene mutation, so that the non-platinum is an option in patients without BRCA gene mutation consider the toxicity and side effects. And we suggest that patients with advanced TNBC must have a BRCA gene test.
Description: Trimidox (hydrochloride) is a specific ribonucleotide reductase inhibitor [1][2][3]. Ribonucleotide reductase is the rate-limiting enzyme for de novo DNA synthesis.
Description: Trimidox (hydrochloride) is a specific ribonucleotide reductase inhibitor [1][2][3]. Ribonucleotide reductase is the rate-limiting enzyme for de novo DNA synthesis.
Description: Trimidox (hydrochloride) is a specific ribonucleotide reductase inhibitor [1][2][3]. Ribonucleotide reductase is the rate-limiting enzyme for de novo DNA synthesis.
Description: Trimidox (hydrochloride) is a specific ribonucleotide reductase inhibitor [1][2][3]. Ribonucleotide reductase is the rate-limiting enzyme for de novo DNA synthesis.
Description: S1RA hydrochloride is a potent and selective antagonist of ?1 receptor (?1R) with Ki value of 17nM [1].S1RA is the first ?1 receptor antagonist with potent antinociceptive activities in various pain models.
Description: S1RA hydrochloride is a potent and selective antagonist of ?1 receptor (?1R) with Ki value of 17nM [1].S1RA is the first ?1 receptor antagonist with potent antinociceptive activities in various pain models.
Description: S1RA hydrochloride is a potent and selective antagonist of ?1 receptor (?1R) with Ki value of 17nM [1].S1RA is the first ?1 receptor antagonist with potent antinociceptive activities in various pain models.
Description: S1RA hydrochloride is a potent and selective antagonist of ?1 receptor (?1R) with Ki value of 17nM [1].S1RA is the first ?1 receptor antagonist with potent antinociceptive activities in various pain models.
Description: S1RA hydrochloride is a potent and selective antagonist of ?1 receptor (?1R) with Ki value of 17nM [1].S1RA is the first ?1 receptor antagonist with potent antinociceptive activities in various pain models.
Description: THZ1 is a covalent inhibitor of CDK7 with IC50 value of 3.2nM [1].THZ1 covalently modifies CDK7 by targeting C312 residue outside of the kinase domain, providing an unanticipated means of achieving covalent selectivity.
Description: THZ1 is a covalent inhibitor of CDK7 with IC50 value of 3.2nM [1].THZ1 covalently modifies CDK7 by targeting C312 residue outside of the kinase domain, providing an unanticipated means of achieving covalent selectivity.
Description: THZ1 is a covalent inhibitor of CDK7 with IC50 value of 3.2nM [1].THZ1 covalently modifies CDK7 by targeting C312 residue outside of the kinase domain, providing an unanticipated means of achieving covalent selectivity.
Description: THZ1 is a covalent inhibitor of CDK7 with IC50 value of 3.2nM [1].THZ1 covalently modifies CDK7 by targeting C312 residue outside of the kinase domain, providing an unanticipated means of achieving covalent selectivity.
Description: IC50: 36 nMMPEP is a potent, selective and systemically active mGlu5 receptor antagonist. Metabotropic glutamate (mGlu) receptors are a of G-protein-coupled receptor family linked to multiple second messengers and modulation of ion channel functions in the nervous system.
Description: IC50: 36 nMMPEP is a potent, selective and systemically active mGlu5 receptor antagonist. Metabotropic glutamate (mGlu) receptors are a of G-protein-coupled receptor family linked to multiple second messengers and modulation of ion channel functions in the nervous system.
Description: IC50 Value: 53uM?inhibited the nerve-evoked twitches of phrenic nerve-hemidiaphragm preparations from ICR mice? . MPTP HCl (Sigma-Chem.) induced reduction in the DOPAC HVA/dopamine (DA) ratio and increase in striatal ascorbate (AS) oxidation in rats [1].
Description: IC50 Value: 53uM?inhibited the nerve-evoked twitches of phrenic nerve-hemidiaphragm preparations from ICR mice? . MPTP HCl (Sigma-Chem.) induced reduction in the DOPAC HVA/dopamine (DA) ratio and increase in striatal ascorbate (AS) oxidation in rats [1].
Description: IC50: 5 nMMTEP is a selective metabotropic glutamate receptor subtype 5 (mGluR5) antagonist.The mGluRs are classified into three groups: group I (mGluR1 and 5), group II (mGluR2 and 3) and group III (mGluR4, 6, 7 and 8).
Description: IC50: 5 nMMTEP is a selective metabotropic glutamate receptor subtype 5 (mGluR5) antagonist.The mGluRs are classified into three groups: group I (mGluR1 and 5), group II (mGluR2 and 3) and group III (mGluR4, 6, 7 and 8).
Description: IC50: 5 nMMTEP is a selective metabotropic glutamate receptor subtype 5 (mGluR5) antagonist.The mGluRs are classified into three groups: group I (mGluR1 and 5), group II (mGluR2 and 3) and group III (mGluR4, 6, 7 and 8).
Description: PJ34 is a novel and potent inhibitor of poly(ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair and cell proliferation, that dose-dependently inhibits purified PARP enzyme in a cell-free assay with half maximal effective concentration EC50 value of 20 nM.
Description: PJ34 is a novel and potent inhibitor of poly(ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair and cell proliferation, that dose-dependently inhibits purified PARP enzyme in a cell-free assay with half maximal effective concentration EC50 value of 20 nM.
Description: PJ34 is a novel and potent inhibitor of poly(ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair and cell proliferation, that dose-dependently inhibits purified PARP enzyme in a cell-free assay with half maximal effective concentration EC50 value of 20 nM.
Description: PJ34 is a novel and potent inhibitor of poly(ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair and cell proliferation, that dose-dependently inhibits purified PARP enzyme in a cell-free assay with half maximal effective concentration EC50 value of 20 nM.
Description: PJ34 is a novel and potent inhibitor of poly(ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair and cell proliferation, that dose-dependently inhibits purified PARP enzyme in a cell-free assay with half maximal effective concentration EC50 value of 20 nM.
Description: Tris(2-carboxyethyl)phosphine hydrochloride (TCEP HCL) is a water soluble strong reducing agent that cleave disulfide bonds. It is a non-thiol and non-volatile solid.
Description: Tris(2-carboxyethyl)phosphine hydrochloride (TCEP HCL) is a water soluble strong reducing agent that cleave disulfide bonds. It is a non-thiol and non-volatile solid.
Description: Tris(2-carboxyethyl)phosphine hydrochloride (TCEP HCL) is a water soluble strong reducing agent that cleave disulfide bonds. It is a non-thiol and non-volatile solid.
Description: IC50: 2 nM: blocks the receptor tyrosine kinase RET in Drosophila.AD57, as a polypharmacological cancer therapeutic, is designed to regulate multiple targets related to cancer.
Description: IC50: 2 nM: blocks the receptor tyrosine kinase RET in Drosophila.AD57, as a polypharmacological cancer therapeutic, is designed to regulate multiple targets related to cancer.
Description: IC50: 2 nM: blocks the receptor tyrosine kinase RET in Drosophila.AD57, as a polypharmacological cancer therapeutic, is designed to regulate multiple targets related to cancer.
Description: XL413 is a potent and selective Cdc7 inhibitor with an IC50 of 3.7 nM, >60-fold selectivity against CK2, >10-fold selectivity against PIM, and >300-fold selectivity against a panel of over 100 protein kinases. Phase 1
Description: XL413 is a potent and selective Cdc7 inhibitor with an IC50 of 3.7 nM, >60-fold selectivity against CK2, >10-fold selectivity against PIM, and >300-fold selectivity against a panel of over 100 protein kinases. Phase 1
Description: XL413 is a potent and selective Cdc7 inhibitor with an IC50 of 3.7 nM, >60-fold selectivity against CK2, >10-fold selectivity against PIM, and >300-fold selectivity against a panel of over 100 protein kinases. Phase 1
Description: XL413 is a potent and selective Cdc7 inhibitor with an IC50 of 3.7 nM, >60-fold selectivity against CK2, >10-fold selectivity against PIM, and >300-fold selectivity against a panel of over 100 protein kinases. Phase 1
Description: IC50: 20, 119, 83, 8, and 8 nM for PRMT1, 3, 4, 6, and 8, respectivelyMS023 is a type I PRMT inhibitor. Protein arginine methyltransferases (PRMTs) play a critical role in various biological processes.
Description: IC50: 20, 119, 83, 8, and 8 nM for PRMT1, 3, 4, 6, and 8, respectivelyMS023 is a type I PRMT inhibitor. Protein arginine methyltransferases (PRMTs) play a critical role in various biological processes.
Description: IC50: 20, 119, 83, 8, and 8 nM for PRMT1, 3, 4, 6, and 8, respectivelyMS023 is a type I PRMT inhibitor. Protein arginine methyltransferases (PRMTs) play a critical role in various biological processes.
Description: IC50: 20, 119, 83, 8, and 8 nM for PRMT1, 3, 4, 6, and 8, respectivelyMS023 is a type I PRMT inhibitor. Protein arginine methyltransferases (PRMTs) play a critical role in various biological processes.
Description: IC50: Inhibit tumor cells growth with an IC50of about 4 M.Being defective for the tumor-suppressor function, mutant p53, a major contributor to malignancy, exerts oncogenic activity also by blocking another tumor-suppressing protein - p73.
Description: IC50: Inhibit tumor cells growth with an IC50of about 4 M.Being defective for the tumor-suppressor function, mutant p53, a major contributor to malignancy, exerts oncogenic activity also by blocking another tumor-suppressing protein - p73.
