Thomas J. Rogers
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View article: An alternative route for β-hydroxybutyrate metabolism supports cytosolic acetyl-CoA synthesis in cancer cells
An alternative route for β-hydroxybutyrate metabolism supports cytosolic acetyl-CoA synthesis in cancer cells Open
View article: An alternative route for β-hydroxybutyrate metabolism supports fatty acid synthesis in cancer cells
An alternative route for β-hydroxybutyrate metabolism supports fatty acid synthesis in cancer cells Open
Cancer cells are exposed to diverse metabolites in the tumor microenvironment that are used to support the synthesis of nucleotides, amino acids, and lipids needed for rapid cell proliferation 1–3 . Recent work has shown that ketone bodies…
View article: Lipid availability influences ferroptosis sensitivity in cancer cells by regulating polyunsaturated fatty acid trafficking
Lipid availability influences ferroptosis sensitivity in cancer cells by regulating polyunsaturated fatty acid trafficking Open
Ferroptosis is a form of cell death caused by lipid peroxidation that is emerging as a target for cancer therapy, highlighting the need to identify factors that govern ferroptosis susceptibility. Lipid peroxidation occurs primarily on phos…
View article: Frontmatter
Frontmatter Open
View article: EP07.01-16 The Relationship of FDG PET-SUVm and Glucose Metabolism and Contribution to Early-Stage Non-Small Cell Lung Cancer Survival
EP07.01-16 The Relationship of FDG PET-SUVm and Glucose Metabolism and Contribution to Early-Stage Non-Small Cell Lung Cancer Survival Open
View article: Tumor lipid metabolism: a mechanistic link between diet and cancer progression
Tumor lipid metabolism: a mechanistic link between diet and cancer progression Open
View article: Frontmatter
Frontmatter Open
View article: Table S2. Top 10 Enriched Pathways Upregulated Following miR-200c Restoration from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Table S2. Top 10 Enriched Pathways Upregulated Following miR-200c Restoration from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression Open
Extended list of genes associated with top 10 enriched pathways following GSEA analysis in BT549-TripZ-200c cells following miR-200c restoration.
View article: Supplementary Figure 1 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Supplementary Figure 1 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression Open
Comparison of Gene Signatures following miR-200c Restoration in TNBC Cells.
View article: Supplementary Figure 2 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Supplementary Figure 2 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression Open
Expanded GSEA results following miR-200c restoration in TNBC cells.
View article: Data from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Data from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
Androgen receptor (AR) is expressed in 90% of estrogen receptor alpha–positive (ER+) breast tumors, but its role in tumor growth and progression remains controversial. Use of two anti-androgens that inhibit AR nuclear localizati…
View article: Supplementary Figure Legends from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Figure Legends from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
Supplementary Figure Legends
View article: Supplementary Tables 1-3 from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Tables 1-3 from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
S1. E2 induces AR binding at sites that overlap with ER binding. S2. Enza alters expression of E2-regulated genes in PT12 xenograft tumors. S3. Pathway analysis of Enza-regulated genes in PT12 xenograft tumors.
View article: Supplementary Figures 1-6 from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Figures 1-6 from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
S1. Enza or AR knockdown decrease baseline and E2-induced proliferation of breast cancer cells in vitro. S2. E2 induces and Enza inhibits AR nuclear localization. S3. AR and ER binding in MCF7 cells. S4. Enza synergizes with anti-estrogens…
View article: Supplementary Tables 1-3 from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Tables 1-3 from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
S1. E2 induces AR binding at sites that overlap with ER binding. S2. Enza alters expression of E2-regulated genes in PT12 xenograft tumors. S3. Pathway analysis of Enza-regulated genes in PT12 xenograft tumors.
View article: Supplementary Figure 2 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Supplementary Figure 2 from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression Open
Expanded GSEA results following miR-200c restoration in TNBC cells.
View article: Supplementary Figure Legends from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Figure Legends from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
Supplementary Figure Legends
View article: Supplementary Figures 1-6 from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Supplementary Figures 1-6 from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
S1. Enza or AR knockdown decrease baseline and E2-induced proliferation of breast cancer cells in vitro. S2. E2 induces and Enza inhibits AR nuclear localization. S3. AR and ER binding in MCF7 cells. S4. Enza synergizes with anti-estrogens…
View article: Data from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression
Data from Reversal of Triple-Negative Breast Cancer EMT by miR-200c Decreases Tryptophan Catabolism and a Program of Immunosuppression Open
Tryptophan-2,3-dioxygenase (TDO2), a rate-limiting enzyme in the tryptophan catabolism pathway, is induced in triple-negative breast cancer (TNBC) by inflammatory signals and anchorage-independent conditions. TNBCs express extremely low le…
View article: Data from Cooperative Dynamics of AR and ER Activity in Breast Cancer
Data from Cooperative Dynamics of AR and ER Activity in Breast Cancer Open
Androgen receptor (AR) is expressed in 90% of estrogen receptor alpha–positive (ER+) breast tumors, but its role in tumor growth and progression remains controversial. Use of two anti-androgens that inhibit AR nuclear localizati…
View article: Supplemental Figure Legends from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure Legends from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Supplemental Figure Legends
View article: Data from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Data from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Preclinical and early clinical trials indicate that up to 50% of triple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially responsive to antiandrogens. However, the function of AR in TNBC and the mechanisms b…
View article: Supplemental Figure 1 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure 1 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Immunohistochemistry for AR in BT549 cells cultured in attached or forced suspension culture conditions.
View article: Supplemental Figure Legends from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure Legends from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Supplemental Figure Legends
View article: Supplemental Figure 3 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure 3 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Paclitaxel and enzalutamide combination treatment.
View article: Supplemental Figure 1 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure 1 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Immunohistochemistry for AR in BT549 cells cultured in attached or forced suspension culture conditions.
View article: Supplemental Figure 3 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Supplemental Figure 3 from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Paclitaxel and enzalutamide combination treatment.
View article: Data from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer
Data from Androgen Receptor Supports an Anchorage-Independent, Cancer Stem Cell-like Population in Triple-Negative Breast Cancer Open
Preclinical and early clinical trials indicate that up to 50% of triple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially responsive to antiandrogens. However, the function of AR in TNBC and the mechanisms b…
View article: Supplemental Figure Legends from A TDO2-AhR Signaling Axis Facilitates Anoikis Resistance and Metastasis in Triple-Negative Breast Cancer
Supplemental Figure Legends from A TDO2-AhR Signaling Axis Facilitates Anoikis Resistance and Metastasis in Triple-Negative Breast Cancer Open
Legends for Supplemental Figures S1-S7.
View article: 3D Printing Center of Excellence (Dept. 2479).
3D Printing Center of Excellence (Dept. 2479). Open