11 research outputs found
Supplementary Figures from Interaction Between MUC1 and STAT1 Drives IFITM1 Overexpression in Aromatase Inhibitor–Resistant Breast Cancer Cells and Mediates Estrogen-Induced Apoptosis
S1. E2 and GO-201 decrease IFITM1 expression. S2. Combination treatment with JAK/STAT inhibitor. S3. Alterations to IFITM1 expression upon MUC1 knockdown and Rux treatment. S4. Estrogen treatment reduces tumor size in Nude mice injected with MCF-7:5C AI-resistant cells in vivo. S5.Estrogen treatment reduces MUC 1, P-STAT1, and FITM 1 levels in Nude mice injected injected with MCF-7:5C AI-resistant cells in vivo. S6. TUNEL staining from AI-sensitive tumors. S7. MUC 1 staining intensities for ER+ breast cancer patients.</p
Supplementary data from Interferon-Stimulated Genes Are Transcriptionally Repressed by PR in Breast Cancer
Supplemental Figure 1: PR represses ISGs in multiple cell line models. Supplemental Figure 2: ISG repression is PR-dependent. Supplemental Figure 3. ISG repression not observed in PR-negative breast cancer cell lines. Supplemental Figure 4. PR is recruited to ISG enhancers.</p
Supplementary Table from Interferon-Stimulated Genes Are Transcriptionally Repressed by PR in Breast Cancer
Supplementary Table 1. Primer and si/shRNA sequences.</p
Supplementary Data from Effect of Bazedoxifene and Conjugated Estrogen (Duavee) on Breast Cancer Risk Biomarkers in High-Risk Women: A Pilot Study
Supplementary Tables 1-3</p
Supplementary Figure S2. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
NEMO is required for E+P induced expression of IL-6 and NFkB signaling in ER+PR+ overexpressing DCIS.com breast cancer cells.</p
Supplementary Table S1-S3 from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
S1:Differences in response to E+P were not correlated with any available patient data, including biomarker expression, age, or nuclear grade. S2:ER target genes with a role in NFkB pathway.S3:Relapse-free survival (RFS), distant metastasis-free survival (DMFS) and overall survival (OS) in all breast cancer patients or luminal A or B subtypes based on their expression levels of IKBKG and PML</p
Supplementary Figure S3 from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
NEMO KD results in increased cell survival and proliferation in MCF7 cells in vitro.</p
Supplementary Figure S4 from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
NEMO KD results in decreased IL-6, p-serine STAT3 and PML in vivo.</p
Supplementary Figure S5 from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Kaplan-Meier (KM) relapse-free and overall survival curves of breast cancer patients based on their expression levels of IKBKG, and PML.</p
Supplementary Figure S1. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Five ER+/PR+ DCIS patient samples were cultured under non adherent conditions and treated with E+P, E, P, and vehicle control. Only a subset of patient-derived ER+/PR+ DCIS cells responded to hormone treatment in vitro by increasing mammosphere formation efficiency.</p
