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Mammalian two- hybrid assay of interactions of the wild type or mutant RARα LBD with a fragment of coactivator SRC2, b MED1, a component of the transcription pre-initiation complex and c fragment of corepressor NCOR, treated with increasing concentrations of RA. Left panel: Partially activatable mutants, Right panel: Non-activatable mutants. N = 3, Error bar = SD. d Binding affinities of WT or mutant RARα LBD with fragment of coactivator SRC1 (SRC1-NR2) in the presence of RA and <t>Am80.</t> N = 3, error bar = SE. **p < 0.01.
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Mammalian two- hybrid assay of interactions of the wild type or mutant RARα LBD with a fragment of coactivator SRC2, b MED1, a component of the transcription pre-initiation complex and c fragment of corepressor NCOR, treated with increasing concentrations of RA. Left panel: Partially activatable mutants, Right panel: Non-activatable mutants. N = 3, Error bar = SD. d Binding affinities of WT or mutant RARα LBD with fragment of coactivator SRC1 (SRC1-NR2) in the presence of RA and <t>Am80.</t> N = 3, error bar = SE. **p < 0.01.
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Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types
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AMS Biotechnology breast cancer tissue array
(A) Basal heparan sulfate expression was examined in the supernatants of TNBC cells and control immortal MCF-10A via ELISA analysis with MDA-MB 468 expressing the most. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed to determine the significance with * representing p<0.05 and ** representing p<0.01 the protein expression in MCF-10A to the protein expressions in the TNBC cell lines. (B) Baseline heparan sulfate cell surface expression levels were examined via flow cytometry analysis in nontumorigenic immortal mammary epithelial MCF-10A cells and TNBC MDA-MB 231, Hs 578t and MDA-MB 468 cells. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed with * representing p<0.05 and ** representing p<0.01 comparing expression levels in MCF-10A to those in the TNBC cell lines. (C) The AMSBIO BR1202B <t>breast</t> <t>cancer</t> <t>tissue</t> <t>array</t> (120 cores with 82 TNBC cores; key can be found in Supplemental Figure 8C and corresponding Supplemental Table 1 showing breast cancer sub-type distribution) was stained with heparan sulfate.
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Image Search Results


Mammalian two- hybrid assay of interactions of the wild type or mutant RARα LBD with a fragment of coactivator SRC2, b MED1, a component of the transcription pre-initiation complex and c fragment of corepressor NCOR, treated with increasing concentrations of RA. Left panel: Partially activatable mutants, Right panel: Non-activatable mutants. N = 3, Error bar = SD. d Binding affinities of WT or mutant RARα LBD with fragment of coactivator SRC1 (SRC1-NR2) in the presence of RA and Am80. N = 3, error bar = SE. **p < 0.01.

Journal: NPJ Breast Cancer

Article Title: Effects of RARα ligand binding domain mutations on breast fibroepithelial tumor function and signaling

doi: 10.1038/s41523-024-00716-5

Figure Lengend Snippet: Mammalian two- hybrid assay of interactions of the wild type or mutant RARα LBD with a fragment of coactivator SRC2, b MED1, a component of the transcription pre-initiation complex and c fragment of corepressor NCOR, treated with increasing concentrations of RA. Left panel: Partially activatable mutants, Right panel: Non-activatable mutants. N = 3, Error bar = SD. d Binding affinities of WT or mutant RARα LBD with fragment of coactivator SRC1 (SRC1-NR2) in the presence of RA and Am80. N = 3, error bar = SE. **p < 0.01.

Article Snippet: Compounds tested include all-trans retinoic acid (known as RA throughout the manuscript, Sigma R2625), Am80 (aka Tamibarotene, Tocris 3507), AM580 (Tocris 0760) and Ch55 (Tocris 2020).

Techniques: Two Hybrid Assay, Mutagenesis, Binding Assay

a Overexpression of Flag-tagged RARα WT and mutants in PT024 cells. b Cell viabilities of PT024 WT or mutant RARα expressing cells after treatment with increasing concentration of RA or Am80. N = 3, error bar = SD. *** p < 0.001, **** p < 0.0001. c Cell cycle distribution of PT024 WT or mutant RARα expressing cells when treated with either vehicle or 100 nM Am80. N = 2, error bar = SD. * p < 0.05, **** p < 0.0001. d GSEA analysis shows downregulation of retinoic acid signaling gene targets in mutant RARα-expressing cell lines. e Heatmap of genes associated with reactome retinoic acid signaling pathway. f Quantitative PCR of retinoic acid signaling associated genes. N = 3, error bar = SD. * p < 0.05 ** p < 0.01 *** p < 0.001 **** p < 0.0001.

Journal: NPJ Breast Cancer

Article Title: Effects of RARα ligand binding domain mutations on breast fibroepithelial tumor function and signaling

doi: 10.1038/s41523-024-00716-5

Figure Lengend Snippet: a Overexpression of Flag-tagged RARα WT and mutants in PT024 cells. b Cell viabilities of PT024 WT or mutant RARα expressing cells after treatment with increasing concentration of RA or Am80. N = 3, error bar = SD. *** p < 0.001, **** p < 0.0001. c Cell cycle distribution of PT024 WT or mutant RARα expressing cells when treated with either vehicle or 100 nM Am80. N = 2, error bar = SD. * p < 0.05, **** p < 0.0001. d GSEA analysis shows downregulation of retinoic acid signaling gene targets in mutant RARα-expressing cell lines. e Heatmap of genes associated with reactome retinoic acid signaling pathway. f Quantitative PCR of retinoic acid signaling associated genes. N = 3, error bar = SD. * p < 0.05 ** p < 0.01 *** p < 0.001 **** p < 0.0001.

Article Snippet: Compounds tested include all-trans retinoic acid (known as RA throughout the manuscript, Sigma R2625), Am80 (aka Tamibarotene, Tocris 3507), AM580 (Tocris 0760) and Ch55 (Tocris 2020).

Techniques: Over Expression, Mutagenesis, Expressing, Concentration Assay, Real-time Polymerase Chain Reaction

Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Journal: Journal for Immunotherapy of Cancer

Article Title: BTN1A1 is a novel immune checkpoint mutually exclusive to PD-L1

doi: 10.1136/jitc-2023-008303

Figure Lengend Snippet: Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Article Snippet: Pancreatic cancer , AMSBIO PA804b , 30% , 18% , 52%.

Techniques: Staining, Microarray

Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Journal: Journal for Immunotherapy of Cancer

Article Title: BTN1A1 is a novel immune checkpoint mutually exclusive to PD-L1

doi: 10.1136/jitc-2023-008303

Figure Lengend Snippet: Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Article Snippet: Colon cancer , AMSBIO CO802d , 40% , 20% , 40%.

Techniques: Staining, Microarray

Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Journal: Journal for Immunotherapy of Cancer

Article Title: BTN1A1 is a novel immune checkpoint mutually exclusive to PD-L1

doi: 10.1136/jitc-2023-008303

Figure Lengend Snippet: Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Article Snippet: Pancreatic cancer , AMSBIO PA804b , 30% , 18% , 52%.

Techniques: Staining, Microarray

Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Journal: Journal for Immunotherapy of Cancer

Article Title: BTN1A1 is a novel immune checkpoint mutually exclusive to PD-L1

doi: 10.1136/jitc-2023-008303

Figure Lengend Snippet: Summary of butyrophilin 1A1 staining results in tissue microarray scores for patients with different solid and hematological tumor types

Article Snippet: Colon cancer , AMSBIO CO802d , 40% , 20% , 40%.

Techniques: Staining, Microarray

(A) Basal heparan sulfate expression was examined in the supernatants of TNBC cells and control immortal MCF-10A via ELISA analysis with MDA-MB 468 expressing the most. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed to determine the significance with * representing p<0.05 and ** representing p<0.01 the protein expression in MCF-10A to the protein expressions in the TNBC cell lines. (B) Baseline heparan sulfate cell surface expression levels were examined via flow cytometry analysis in nontumorigenic immortal mammary epithelial MCF-10A cells and TNBC MDA-MB 231, Hs 578t and MDA-MB 468 cells. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed with * representing p<0.05 and ** representing p<0.01 comparing expression levels in MCF-10A to those in the TNBC cell lines. (C) The AMSBIO BR1202B breast cancer tissue array (120 cores with 82 TNBC cores; key can be found in Supplemental Figure 8C and corresponding Supplemental Table 1 showing breast cancer sub-type distribution) was stained with heparan sulfate.

Journal: bioRxiv

Article Title: The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer

doi: 10.1101/2023.09.08.556819

Figure Lengend Snippet: (A) Basal heparan sulfate expression was examined in the supernatants of TNBC cells and control immortal MCF-10A via ELISA analysis with MDA-MB 468 expressing the most. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed to determine the significance with * representing p<0.05 and ** representing p<0.01 the protein expression in MCF-10A to the protein expressions in the TNBC cell lines. (B) Baseline heparan sulfate cell surface expression levels were examined via flow cytometry analysis in nontumorigenic immortal mammary epithelial MCF-10A cells and TNBC MDA-MB 231, Hs 578t and MDA-MB 468 cells. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed with * representing p<0.05 and ** representing p<0.01 comparing expression levels in MCF-10A to those in the TNBC cell lines. (C) The AMSBIO BR1202B breast cancer tissue array (120 cores with 82 TNBC cores; key can be found in Supplemental Figure 8C and corresponding Supplemental Table 1 showing breast cancer sub-type distribution) was stained with heparan sulfate.

Article Snippet: An AMSBIO breast cancer tissue array (120 cores specifically with 82 TNBC cores), two normal breast tissue slides and three ductal carcinoma in situ DCIS tissue slides were stained with heparanase. ( ) and statistical analysis was performed ( ).

Techniques: Expressing, Control, Enzyme-linked Immunosorbent Assay, Standard Deviation, Flow Cytometry, Staining

(A) Pairwise comparisons using Dunn’s test indicated that there was a significant difference between TNBC and normal breast (p = 0.0040), TNBC and DCIS (p = 0.0359), ER+/PR+ and normal (p = 0.0209), and HER2+ and normal (p = 0.0403), in the percentage of heparan sulfate positively stained cells in the tissue sections. No other differences were significantly different. (B) Pairwise comparisons using Dunn’s test showed that there was a significant difference between TNBC and normal (p = 0.0048), TNBC and DCIS (p = 0.0416), ER+/PR+ and normal (p = 0.0131), and HER2+ and normal (p = 0.0321), in the percentage of heparan sulfate weakly stained cells. No other differences were significantly different. (C) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and normal (p = 0.0003), TNBC and DCIS (p = 0.0064), ER+/PR+ and normal (p = 0.0127), HER2+ and normal (p = 0.0041), and HER2+ and DCIS (p = 0.0305), in the percentage of heparan sulfate moderately stained cells. No other differences were significantly different. (D) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and Normal (p = 0.0001), TNBC and DCIS (p = 0.0020), ER+/PR+ and normal (p = 0.0002), ER+/PR+ and DCIS (p = 0.0087), HER2+ and normal (p = 0.0003), and HER2+ and DCIS (p = 0.0109), in the percentage of heparan sulfate strongly stained cells. No other differences were significantly different. (E) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and normal (p = 0.0040), TNBC and DCIS (p = 0.0359), ER+/PR+ and normal (p = 0.0209), HER2+ and normal (p = 0.0003), and HER2+ and normal (p = 0.0403), in the percentage of cells negative for heparan sulfate staining. No other differences were significantly different. (F) Kruskal-Wallis test indicated that there was no significant difference in the percentage of heparan sulfate positively stained cells in the tumor amongst the TNBC breast cancer stages.

Journal: bioRxiv

Article Title: The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer

doi: 10.1101/2023.09.08.556819

Figure Lengend Snippet: (A) Pairwise comparisons using Dunn’s test indicated that there was a significant difference between TNBC and normal breast (p = 0.0040), TNBC and DCIS (p = 0.0359), ER+/PR+ and normal (p = 0.0209), and HER2+ and normal (p = 0.0403), in the percentage of heparan sulfate positively stained cells in the tissue sections. No other differences were significantly different. (B) Pairwise comparisons using Dunn’s test showed that there was a significant difference between TNBC and normal (p = 0.0048), TNBC and DCIS (p = 0.0416), ER+/PR+ and normal (p = 0.0131), and HER2+ and normal (p = 0.0321), in the percentage of heparan sulfate weakly stained cells. No other differences were significantly different. (C) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and normal (p = 0.0003), TNBC and DCIS (p = 0.0064), ER+/PR+ and normal (p = 0.0127), HER2+ and normal (p = 0.0041), and HER2+ and DCIS (p = 0.0305), in the percentage of heparan sulfate moderately stained cells. No other differences were significantly different. (D) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and Normal (p = 0.0001), TNBC and DCIS (p = 0.0020), ER+/PR+ and normal (p = 0.0002), ER+/PR+ and DCIS (p = 0.0087), HER2+ and normal (p = 0.0003), and HER2+ and DCIS (p = 0.0109), in the percentage of heparan sulfate strongly stained cells. No other differences were significantly different. (E) Pairwise comparisons using Dunn’s test demonstrated that there was a significant difference between TNBC and normal (p = 0.0040), TNBC and DCIS (p = 0.0359), ER+/PR+ and normal (p = 0.0209), HER2+ and normal (p = 0.0003), and HER2+ and normal (p = 0.0403), in the percentage of cells negative for heparan sulfate staining. No other differences were significantly different. (F) Kruskal-Wallis test indicated that there was no significant difference in the percentage of heparan sulfate positively stained cells in the tumor amongst the TNBC breast cancer stages.

Article Snippet: An AMSBIO breast cancer tissue array (120 cores specifically with 82 TNBC cores), two normal breast tissue slides and three ductal carcinoma in situ DCIS tissue slides were stained with heparanase. ( ) and statistical analysis was performed ( ).

Techniques: Staining

(A) Baseline extracellular heparanase expression was determined in nontumorigenic immortal mammary epithelial MCF-10A cells and TNBC MDA-MB 231, Hs 578t and MDA-MB 468 cells by ELISAs. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed with * representing p<0.05 and ** representing p<0.01, comparing expression levels in MCF-10A to those in the TNBC cell lines. (B) The AMSBIO BR1202B breast cancer tissue array (120 cores with 82 TNBC cores; key can be found in Supplemental Figure 8C and corresponding Excel worksheet showing breast cancer sub-type distribution) was stained with heparanase.

Journal: bioRxiv

Article Title: The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer

doi: 10.1101/2023.09.08.556819

Figure Lengend Snippet: (A) Baseline extracellular heparanase expression was determined in nontumorigenic immortal mammary epithelial MCF-10A cells and TNBC MDA-MB 231, Hs 578t and MDA-MB 468 cells by ELISAs. The standard deviation was calculated from three independent experiments performed in triplicate. The student’s t-test was performed with * representing p<0.05 and ** representing p<0.01, comparing expression levels in MCF-10A to those in the TNBC cell lines. (B) The AMSBIO BR1202B breast cancer tissue array (120 cores with 82 TNBC cores; key can be found in Supplemental Figure 8C and corresponding Excel worksheet showing breast cancer sub-type distribution) was stained with heparanase.

Article Snippet: An AMSBIO breast cancer tissue array (120 cores specifically with 82 TNBC cores), two normal breast tissue slides and three ductal carcinoma in situ DCIS tissue slides were stained with heparanase. ( ) and statistical analysis was performed ( ).

Techniques: Expressing, Standard Deviation, Staining

Kruskal-Wallis test indicated that there was no significant difference: (A) in the percentage of heparanase positively stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (B) in the percentage of heparanase weakly stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (C) in the percentage of heparanase moderately stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (D) in the percentage of heparanase strongly stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (E) in the percentage of negative heparanase stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes and (F) in the percentage of heparanase positively stained cells in the tissue sections of different TNBC breast cancer stages.

Journal: bioRxiv

Article Title: The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer

doi: 10.1101/2023.09.08.556819

Figure Lengend Snippet: Kruskal-Wallis test indicated that there was no significant difference: (A) in the percentage of heparanase positively stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (B) in the percentage of heparanase weakly stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (C) in the percentage of heparanase moderately stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (D) in the percentage of heparanase strongly stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes, (E) in the percentage of negative heparanase stained cells in the tissue sections of normal breast tissue, DCIS and invasive breast cancer subtypes and (F) in the percentage of heparanase positively stained cells in the tissue sections of different TNBC breast cancer stages.

Article Snippet: An AMSBIO breast cancer tissue array (120 cores specifically with 82 TNBC cores), two normal breast tissue slides and three ductal carcinoma in situ DCIS tissue slides were stained with heparanase. ( ) and statistical analysis was performed ( ).

Techniques: Staining