C. Elizabeth Caldon
YOU?
Author Swipe
View article: Unmatched Cell Line Collections Are Not Optimal for Identification of <scp>PARP</scp> Inhibitor Response and Drug Synergies
Unmatched Cell Line Collections Are Not Optimal for Identification of <span>PARP</span> Inhibitor Response and Drug Synergies Open
PARP inhibitors show great efficacy in BRCA1 / 2‐ mutated patients, but many preclinical studies, including combination therapies, fail to translate clinically, likely due to the limitations of preclinical models. This brief report aimed t…
View article: JNK pathway suppression mediates insensitivity to combination endocrine therapy and CDK4/6 inhibition in ER+ breast cancer
JNK pathway suppression mediates insensitivity to combination endocrine therapy and CDK4/6 inhibition in ER+ breast cancer Open
CDK4/6 inhibitors in combination with endocrine therapy are now used as front-line treatment for patients with estrogen-receptor positive (ER+) breast cancer. While this combination improves overall survival, the mechanisms of disease prog…
View article: ROCK2 inhibition has a dual role in reducing ECM remodelling and cell growth, while impairing migration and invasion
ROCK2 inhibition has a dual role in reducing ECM remodelling and cell growth, while impairing migration and invasion Open
Summary The Rho-associated coiled-coil containing protein kinases 1/2 (ROCK1/2) are key signalling proteins involved in the regulation of the actin cytoskeleton and control a variety of cellular processes. This includes cell proliferation,…
View article: JNK pathway suppression drives resistance to combination endocrine therapy and CDK4/6 inhibition in ER+ breast cancer
JNK pathway suppression drives resistance to combination endocrine therapy and CDK4/6 inhibition in ER+ breast cancer Open
Endocrine therapy in combination with CDK4/6 inhibition doubles the progression-free survival of patients with advanced ER + breast cancer, but resistance is inevitable, leaving patients with limited treatment options. Here, we performed u…
View article: SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers
SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers Open
DNA methylation is an epigenetic mark that plays a critical role in regulating gene expression. DNA methyltransferase (DNMT) inhibitors, inhibit global DNA methylation and have been a key tool in studies of DNA methylation. A major bottlen…
View article: miR-99b-5p, miR-380-3p, and miR-485-3p are novel chemosensitizing miRNAs in high-risk neuroblastoma
miR-99b-5p, miR-380-3p, and miR-485-3p are novel chemosensitizing miRNAs in high-risk neuroblastoma Open
View article: SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers
SAM-DNMT3A, a strategy for induction of genome-wide DNA methylation, identifies DNA methylation as a vulnerability in ER-positive breast cancers Open
DNA methylation is an epigenetic mark that plays a critical role in regulation of gene expression. DNA methylase (DNMT) inhibitors, inhibit global DNA methylation, and have been a key tool in studies of DNA methylation in healthy or diseas…
View article: The potential of epigenetic therapy to target the 3D epigenome in endocrine-resistant breast cancer
The potential of epigenetic therapy to target the 3D epigenome in endocrine-resistant breast cancer Open
Three-dimensional (3D) epigenome remodeling is an important mechanism of gene deregulation in cancer. However, its potential as a target to counteract therapy resistance remains largely unaddressed. Here, we show that epigenetic therapy wi…
View article: DNA repair biomarkers to guide usage of combined PARP inhibitors and chemotherapy: A meta-analysis and systematic review
DNA repair biomarkers to guide usage of combined PARP inhibitors and chemotherapy: A meta-analysis and systematic review Open
Combination therapy only improves PFS in patients with identifiable DNA repair biomarkers. This indicates that PARP inhibitors do not sensitise patients to chemotherapy treatment, except where their cancer has a homologous recombination de…
View article: DNA repair biomarkers to guide usage of combined PARP inhibitors and chemotherapy: a meta-analysis and systematic review
DNA repair biomarkers to guide usage of combined PARP inhibitors and chemotherapy: a meta-analysis and systematic review Open
Purpose The addition of PARP inhibitors to chemotherapy has been assessed in ∼80 clinical trials across multiple malignancies, on the premise that PARP inhibitors will increase chemotherapy effectiveness regardless of whether cancers have …
View article: Supplementary Figure 2 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 2 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 664KB, BCL-2 Gene expression vs methylation status.
View article: Supplementary Figure 4 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 4 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 4365KB, BCL-2 Methylation vs disease free survival.
View article: Supplementary Figure 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Figure 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 78KB, Supplementary Figure 2: Deregulation of cyclin E in tamoxifen-resistant cells. MCF-7C and TAMR cells were treated with vehicle, OH-Tam (100 nM) or fulvestrant (10 nM). A: S phase percentage derived from flow cytometry of pr…
View article: Supplementary Figure 2 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 2 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 664KB, BCL-2 Gene expression vs methylation status.
View article: Data from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Data from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
Overexpression of the antiapoptotic factor BCL-2 is a frequent feature of malignant disease and is commonly associated with poor prognosis and resistance to conventional chemotherapy. In breast cancer, however, high BCL-2 expression is ass…
View article: Supplementary Figure 5 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 5 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 221KB, A. Plk1 Expression vs relapse-free survival in endocrine treated ER-positive breast cancer patients (n=287). B. Correlative analysis of ER, BCL-2 and PLK1 gene expression in TCGA breast cohort (n=774).
View article: Supplementary Figure 3 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Figure 3 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 41KB, Supplementary Figure 3: Effect of overexpression of cyclins E1 and E2 on antiestrogen-induced growth arrest. T-47D cells overexpressing cyclin E1, cyclin E2 or vector control were treated with fulvestrant or vehicle. Densit…
View article: Supplementary Methods, Figure Legends and Tables 1 - 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Methods, Figure Legends and Tables 1 - 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 56KB.
View article: Supplementary Figure 3 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 3 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 459KB, BCL-2 Methylation status in cancer vs normal tissue.
View article: Supplementary Materials and Methods from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Materials and Methods from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 51KB, PLK1 gene expression/survival analysis.
View article: Supplementary Figure 1 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Figure 1 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 929KB, Supplementary Figure 1: Cyclin E2 association with breast cancer subtype, grade, and outcome. A: Relationship between a second cyclin E2 probeset and breast cancer subtype, or histological grade. Box: upper and lower quart…
View article: Supplementary Figure 1 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Figure 1 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 929KB, Supplementary Figure 1: Cyclin E2 association with breast cancer subtype, grade, and outcome. A: Relationship between a second cyclin E2 probeset and breast cancer subtype, or histological grade. Box: upper and lower quart…
View article: Supplementary Figure 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Figure 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 78KB, Supplementary Figure 2: Deregulation of cyclin E in tamoxifen-resistant cells. MCF-7C and TAMR cells were treated with vehicle, OH-Tam (100 nM) or fulvestrant (10 nM). A: S phase percentage derived from flow cytometry of pr…
View article: Supplementary Figure 4 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 4 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 4365KB, BCL-2 Methylation vs disease free survival.
View article: Supplementary Figure 3 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 3 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 459KB, BCL-2 Methylation status in cancer vs normal tissue.
View article: Supplementary Figure 1 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 1 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 289KB, BCL-2 450K Methylation array probes (n=42).
View article: Supplementary Methods, Figure Legends and Tables 1 - 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Supplementary Methods, Figure Legends and Tables 1 - 2 from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
PDF file, 56KB.
View article: Data from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells
Data from Cyclin E2 Overexpression Is Associated with Endocrine Resistance but not Insensitivity to CDK2 Inhibition in Human Breast Cancer Cells Open
Cyclin E2, but not cyclin E1, is included in several gene signatures that predict disease progression in either tamoxifen-resistant or metastatic breast cancer. We therefore examined the role of cyclin E2 in antiestrogen resistance in v…
View article: Data from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Data from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
Overexpression of the antiapoptotic factor BCL-2 is a frequent feature of malignant disease and is commonly associated with poor prognosis and resistance to conventional chemotherapy. In breast cancer, however, high BCL-2 expression is ass…
View article: Supplementary Figure 6 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer
Supplementary Figure 6 from BCL-2 Hypermethylation Is a Potential Biomarker of Sensitivity to Antimitotic Chemotherapy in Endocrine-Resistant Breast Cancer Open
PDF - 80KB, The effect of BI2536 in endocrine-sensitive and endocrine-resistant breast cancer cells.