V. Craig Jordan
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View article: Progesterone from ovulatory menstrual cycles is an important cause of breast cancer
Progesterone from ovulatory menstrual cycles is an important cause of breast cancer Open
Many factors, including reproductive hormones, have been linked to a woman’s risk of developing breast cancer (BC). We reviewed the literature regarding the relationship between ovulatory menstrual cycles (MCs) and BC risk. Physiological v…
View article: Data from Paradoxical Clinical Effect of Estrogen on Breast Cancer Risk: A “New” Biology of Estrogen-induced Apoptosis
Data from Paradoxical Clinical Effect of Estrogen on Breast Cancer Risk: A “New” Biology of Estrogen-induced Apoptosis Open
Administration of estrogen replacement therapy (ERT) decreases the incidence of breast cancer, as shown in a double-blind, placebo-controlled randomized trial of the Women's Health Initiative (WHI) in 10,739 postmenopausal women wit…
View article: Supplementary Data from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer
Supplementary Data from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer Open
Table S5
View article: Supplementary Figure 2 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer
Supplementary Figure 2 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer Open
Supplementary Figure 2: (A) Reconstructed ion chromatogram for the MRM transition m/z 241 to 208 of standard BTC (100ng/mL); (B) Reconstructed ion chromatogram for the MRM transition m/z 709 to 171 of standard DansylBTC (100ng/ml).
View article: Supplementary Figure 1 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer
Supplementary Figure 1 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer Open
Supplementary Figure 1: Western blot showing ERalpha expression in T47D:A18/neo, T47D:A18/PKCalpha, T47D:A18, T47D:A18-TAM1, MCF-7:WS8 and MCF-7 5C cell lines.
View article: All Supplementary Figures from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer
All Supplementary Figures from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer Open
Supplementary figure/table materials except Table S1 and Table S5
View article: Supplementary Materials from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer
Supplementary Materials from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer Open
Supplementary written materials including Supplementary figure/table legends
View article: Supplementary Figure 4 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer
Supplementary Figure 4 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer Open
Supplementary Figure 4: The calibration standards were prepared by spiking working solution and IS (20ng/mL) into blank mouse plasma, giving final BTC concentrations of 5,10, 20, 30, 40, 50, and 100 ng/mL.
View article: Data from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer
Data from Rapid Induction of the Unfolded Protein Response and Apoptosis by Estrogen Mimic TTC-352 for the Treatment of Endocrine-Resistant Breast Cancer Open
Patients with long-term estrogen-deprived breast cancer, after resistance to tamoxifen or aromatase inhibitors develops, can experience tumor regression when treated with estrogens. Estrogen's antitumor effect is attributed to apoptosis vi…
View article: Supplementary Figure 3 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer
Supplementary Figure 3 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer Open
Supplementary Figure 3: Reagents and conditions: (a) N-Bromoacetamide, DCM, EtOH, rt; (b) BBr3, dry DCM, 0sup>; (c) Dansyl chloride, TEA, DCM, 60 sup>C.
View article: Supplementary Figure 1 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State
Supplementary Figure 1 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State Open
PDF file - 135K, Chemical structures of estrogens used in the experiments.(A) Steroidal estrogens (B) phytoestrogens.
View article: Supplementary Methods from Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein
Supplementary Methods from Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein Open
Details of Annexin V staining method
View article: Supplementary Figure S2 from Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells
Supplementary Figure S2 from Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells Open
(A) The JNK inhibitor effectively blocked phosphorylation of JNK. MCF-7:2A cells were treated with vehicle (0.1% DMSO) or SP600125 (10-5 mol/L) for 24 hours. p-JNK was examined by Western blot. Total JNK was measured as loading control. (B…
View article: Figure S7 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells
Figure S7 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells Open
Effects of GW9662 and T0070907 on two LTED breast cancer cells. A, DNA Growth assay of GW9662 in MCF-7:5C cells. Cells were treated with E2 (1 nM), GW9662 (10, 20 µM), or a combination of them for 7 days. Cells were harvested for DNA proli…
View article: Supplementary Figure 6 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer
Supplementary Figure 6 from Novel Selective Estrogen Mimics for the Treatment of Tamoxifen-Resistant Breast Cancer Open
Supplementary Figure 6: Plasma concentration-time profile of BTC following the administration of a single oral dose of 10 mg/Kg BTC to mice. Each data point represents the mean value {plus minus} SD (n = 3).
View article: Supplementary Figure S3 from Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells
Supplementary Figure S3 from Integration of Downstream Signals of Insulin-like Growth Factor-1 Receptor by Endoplasmic Reticulum Stress for Estrogen-Induced Growth or Apoptosis in Breast Cancer Cells Open
MCF-7:5C cells were treated with vehicle (0.1% DMSO; con), E2 (10-9 mol/L), SP600125 (10-5 mol/L), and E2 (10-9 mol/L) plus SP600125 (10-5 mol/L) for 72 hours. Cells were harvested in TRIzol. Genes were quantitated by real-time RT-PCR. (A)…
View article: Figure S6 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells
Figure S6 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells Open
Effective knockdown of PPARγ at RNA levels in LTED breast cancer cell lines. A, MCF-7:5C cells were transfected with scrambled siRNA or specific PPARγ siRNA for 72 hours. Next, cells were treated with a vehicle control (0.1% EtOH) or E2 (1…
View article: Supplementary Figure S5 from Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein
Supplementary Figure S5 from Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein Open
Fulvestrant potentiates the apoptotic effect of salubrinal in MCF7:5C and LCC9 cells.
View article: Supplementary Fig. S1 from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
Supplementary Fig. S1 from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen Open
Supplementary Fig. S1 from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
View article: Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen Open
Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
View article: Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen Open
Supplementary Text from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
View article: Supplementary Tables from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
Supplementary Tables from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen Open
Supplementary Tables from Exemestane's 17-hydroxylated metabolite exerts biological effects as an androgen
View article: Supplementary Table 1, Figures 1-2 from Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells
Supplementary Table 1, Figures 1-2 from Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells Open
Supplementary Table 1, Figures 1-2 from Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells
View article: Supplementary Figure 1 from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study
Supplementary Figure 1 from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study Open
Supplementary Figure 1. A. MCF-7:WS8 and MCF-7:5C cells were treated with either vehicle for 72 hours or 1nM E2 for 24 or 72 hours. Cells were then harvested, and ERα, PR, and GR proteins were measured by Western blot. MCF-7:WS8 cells were…
View article: Data from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study
Data from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study Open
Hormone replacement therapy (HRT) is widely used to manage menopausal symptoms in women and can be comprised of an estrogen alone or an estrogen combined with a progestin. The Women's Health Initiative demonstrated in their randomized tria…
View article: Supplementary Figure 7. Effects of progestin, MPA, and Dex on E2-stimulated growth in MCF-7:WS8 cells. from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study
Supplementary Figure 7. Effects of progestin, MPA, and Dex on E2-stimulated growth in MCF-7:WS8 cells. from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study Open
Supplementary Figure 6. MCF-8:WS8 cells were transferred to estrogen-free medium for 3 days. The, cells were loaded in 24-well plates. A. MCF-7:WS8 cells were treated with vehicle, 0.01µM R5020, 1nM E2, and 0.01µM R5020+1nM E2. Cells were …
View article: Data from Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells
Data from Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells Open
Dysadherin, a cancer-associated membrane glycoprotein, down-regulates E-cadherin and promotes cancer metastasis. This study examined the role of dysadherin in breast cancer progression. Expression of dysadherin was found to be highest in b…
View article: Supplementary Figure 6 from c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells
Supplementary Figure 6 from c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells Open
PDF file - 82K, 6A, The c-Src inhibitor blocked tumor necrosis factor (TNF) super family genes induced by E2. MCF-7:5C cells were treated with vehicle (0.1% DMSO), E2 (10-9 mol/L), 4-OHT (10-6 mol/L), E2 (10-9 mol/L) plus 4-OHT (10-6 mol/L…
View article: Supplementary Figure Legends from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study
Supplementary Figure Legends from Molecular Modulation of Estrogen-Induced Apoptosis by Synthetic Progestins in Hormone Replacement Therapy: An Insight into the Women's Health Initiative Study Open
Supplementary Figure Legends. Supplementary Figure Legends
View article: Supplementary Figure 1 from The G Protein–Coupled Receptor GPR30 Inhibits Proliferation of Estrogen Receptor–Positive Breast Cancer Cells
Supplementary Figure 1 from The G Protein–Coupled Receptor GPR30 Inhibits Proliferation of Estrogen Receptor–Positive Breast Cancer Cells Open
Supplementary Figure 1 from The G Protein–Coupled Receptor GPR30 Inhibits Proliferation of Estrogen Receptor–Positive Breast Cancer Cells