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sum149 tnbc cell line  (BioIVT Inc)

 
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    BioIVT Inc sum149 tnbc cell line
    Sum149 Tnbc Cell Line, supplied by BioIVT Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sum149+tnbc+cell+line/pm36253486-548-1-11?v=BioIVT+Inc
    Average 90 stars, based on 1 article reviews
    sum149 tnbc cell line - by Bioz Stars, 2026-08
    90/100 stars

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    sum149 tnbc cell line  (BioIVT Inc)
    90
    BioIVT Inc sum149 tnbc cell line
    Sum149 Tnbc Cell Line, supplied by BioIVT Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sum149+tnbc+cell+line/pm36253486-548-1-11?v=BioIVT+Inc
    Average 90 stars, based on 1 article reviews
    sum149 tnbc cell line - by Bioz Stars, 2026-08
    90/100 stars
    		  Buy from Supplier
    tnbc cell lines sum149  (Asterand Inc)
    90
    Asterand Inc tnbc cell lines sum149
    Potency, efficacy, and synergy of buparlisib, selumetinib, and pazopanib in four TNBC human-derived cancer cell lines in vitro. (A) Utilized cell lines, with their molecular classifications and relevant known mutational statuses. Drug response curves of <t>SUM149</t> (149), MDA-MB-231Br (231Br), MDA-MB-468 (468), and MDA-MB-436 (436) TNBC cells after 72 hours with (B) buparlisib, (C) selumetinib, or (D) pazopanib. Synergy fraction affected (FA) versus combination index (CI) curves quantification for combined (E) buparlisib+selumetinib or (F) selumetinib+pazopanib in 149, 231Br, 468, and 436. CI categories: synergistic: <0.1–0.9, additive: 0.9–1.1, antagonistic: >1.1.
    Tnbc Cell Lines Sum149, supplied by Asterand Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sum149+tnbc+cell+line/pmc05737524-77-4-8?v=Asterand+Inc
    Average 90 stars, based on 1 article reviews
    tnbc cell lines sum149 - by Bioz Stars, 2026-08
    90/100 stars
    		  Buy from Supplier

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    Potency, efficacy, and synergy of buparlisib, selumetinib, and pazopanib in four TNBC human-derived cancer cell lines in vitro. (A) Utilized cell lines, with their molecular classifications and relevant known mutational statuses. Drug response curves of SUM149 (149), MDA-MB-231Br (231Br), MDA-MB-468 (468), and MDA-MB-436 (436) TNBC cells after 72 hours with (B) buparlisib, (C) selumetinib, or (D) pazopanib. Synergy fraction affected (FA) versus combination index (CI) curves quantification for combined (E) buparlisib+selumetinib or (F) selumetinib+pazopanib in 149, 231Br, 468, and 436. CI categories: synergistic: <0.1–0.9, additive: 0.9–1.1, antagonistic: >1.1.

    Journal: Neuro-Oncology

    Article Title: Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

    doi: 10.1093/neuonc/nox052

    Figure Lengend Snippet: Potency, efficacy, and synergy of buparlisib, selumetinib, and pazopanib in four TNBC human-derived cancer cell lines in vitro. (A) Utilized cell lines, with their molecular classifications and relevant known mutational statuses. Drug response curves of SUM149 (149), MDA-MB-231Br (231Br), MDA-MB-468 (468), and MDA-MB-436 (436) TNBC cells after 72 hours with (B) buparlisib, (C) selumetinib, or (D) pazopanib. Synergy fraction affected (FA) versus combination index (CI) curves quantification for combined (E) buparlisib+selumetinib or (F) selumetinib+pazopanib in 149, 231Br, 468, and 436. CI categories: synergistic: <0.1–0.9, additive: 0.9–1.1, antagonistic: >1.1.

    Article Snippet: Cell Lines The human-derived TNBC cell lines SUM149 (Asterand; basal-like BRCA1 -mutant, PTEN− ), MDA-MB-231Br (Dr Toshiyuki Yoneda; claudin-low BRCA1 -wildtype, PTEN -wildtype, KRAS -mutant, BRAF -mutant), MDA-MB-468 (American Type Culture Collection [ATCC]; basal-like BRCA1 -wildtype, PTEN −), and MDA-MB-436 (ATCC; claudin-low BRCA1 -mutant, PTEN −) ( ) were transfected with luciferase vector under control of a cytomegalovirus promoter as described, 31 , 32 were confirmed mycoplasma free (September 2015), and were verified by gene expression (September 2010 31 , 32 ).

    Techniques: Derivative Assay, In Vitro

    Synthetically lethal genes in the siRNA screens in SUM149 and MDA-MB-231Br TNBC cells with PI3K or MEK inhibition*

    Journal: Neuro-Oncology

    Article Title: Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

    doi: 10.1093/neuonc/nox052

    Figure Lengend Snippet: Synthetically lethal genes in the siRNA screens in SUM149 and MDA-MB-231Br TNBC cells with PI3K or MEK inhibition*

    Article Snippet: Cell Lines The human-derived TNBC cell lines SUM149 (Asterand; basal-like BRCA1 -mutant, PTEN− ), MDA-MB-231Br (Dr Toshiyuki Yoneda; claudin-low BRCA1 -wildtype, PTEN -wildtype, KRAS -mutant, BRAF -mutant), MDA-MB-468 (American Type Culture Collection [ATCC]; basal-like BRCA1 -wildtype, PTEN −), and MDA-MB-436 (ATCC; claudin-low BRCA1 -mutant, PTEN −) ( ) were transfected with luciferase vector under control of a cytomegalovirus promoter as described, 31 , 32 were confirmed mycoplasma free (September 2015), and were verified by gene expression (September 2010 31 , 32 ).

    Techniques: Inhibition

    In vivo efficacy of PI3K ± MEK inhibition in established intracranial TNBC. (A) Experimental schedule. (B) The median survival (MS) and number of mice alive at the end of the study for mice with intracranial SUM149, MDA-MB-231Br, MDA-MB-468, or MDA-MB-436 tumors. Median survival (MS) for treatment groups statistically different from control (*) or buparlisib (^). Kaplan–Meier curves by treatment group for the (C) SUM149, (D) MDA-MB-231Br, (E) MDA-MB-468, and (F) MDA-MB-436 models. Vertical dotted lines indicate the study’s end.

    Journal: Neuro-Oncology

    Article Title: Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

    doi: 10.1093/neuonc/nox052

    Figure Lengend Snippet: In vivo efficacy of PI3K ± MEK inhibition in established intracranial TNBC. (A) Experimental schedule. (B) The median survival (MS) and number of mice alive at the end of the study for mice with intracranial SUM149, MDA-MB-231Br, MDA-MB-468, or MDA-MB-436 tumors. Median survival (MS) for treatment groups statistically different from control (*) or buparlisib (^). Kaplan–Meier curves by treatment group for the (C) SUM149, (D) MDA-MB-231Br, (E) MDA-MB-468, and (F) MDA-MB-436 models. Vertical dotted lines indicate the study’s end.

    Article Snippet: Cell Lines The human-derived TNBC cell lines SUM149 (Asterand; basal-like BRCA1 -mutant, PTEN− ), MDA-MB-231Br (Dr Toshiyuki Yoneda; claudin-low BRCA1 -wildtype, PTEN -wildtype, KRAS -mutant, BRAF -mutant), MDA-MB-468 (American Type Culture Collection [ATCC]; basal-like BRCA1 -wildtype, PTEN −), and MDA-MB-436 (ATCC; claudin-low BRCA1 -mutant, PTEN −) ( ) were transfected with luciferase vector under control of a cytomegalovirus promoter as described, 31 , 32 were confirmed mycoplasma free (September 2015), and were verified by gene expression (September 2010 31 , 32 ).

    Techniques: In Vivo, Inhibition, Control

    Efficacy of PDGFR+MEK inhibition. (A) Median survival (MS) and number of mice alive at the study’s end for intracranial SUM149 and MDA-MB-231Br tumors, statistically different from control (*), pazopanib (^), selumetinib (~). SUM149 (B) MS and (C) in vivo intracranial tumor burden by treatment group. MDA-MB-231Br (D) MS and (E) tumor burden by treatment group. Vertical dotted lines indicate study’s end per IACUC-approved protocols. N/D = not determined.

    Journal: Neuro-Oncology

    Article Title: Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

    doi: 10.1093/neuonc/nox052

    Figure Lengend Snippet: Efficacy of PDGFR+MEK inhibition. (A) Median survival (MS) and number of mice alive at the study’s end for intracranial SUM149 and MDA-MB-231Br tumors, statistically different from control (*), pazopanib (^), selumetinib (~). SUM149 (B) MS and (C) in vivo intracranial tumor burden by treatment group. MDA-MB-231Br (D) MS and (E) tumor burden by treatment group. Vertical dotted lines indicate study’s end per IACUC-approved protocols. N/D = not determined.

    Article Snippet: Cell Lines The human-derived TNBC cell lines SUM149 (Asterand; basal-like BRCA1 -mutant, PTEN− ), MDA-MB-231Br (Dr Toshiyuki Yoneda; claudin-low BRCA1 -wildtype, PTEN -wildtype, KRAS -mutant, BRAF -mutant), MDA-MB-468 (American Type Culture Collection [ATCC]; basal-like BRCA1 -wildtype, PTEN −), and MDA-MB-436 (ATCC; claudin-low BRCA1 -mutant, PTEN −) ( ) were transfected with luciferase vector under control of a cytomegalovirus promoter as described, 31 , 32 were confirmed mycoplasma free (September 2015), and were verified by gene expression (September 2010 31 , 32 ).

    Techniques: Inhibition, Control, In Vivo

    Kinome alteration following 2 weeks of treatment with buparlisib, selumetinib, or combination in intracranial SUM149 TNBC tumors. (A) Fold change of kinases comparing buparlisib (green), selumetinib (blue), or combination (red) relative to controls. Only kinases with a Log2 fold change of >0.5 or <−0.5 in any treatment group relative to controls are shown. B‒D. Kinome tree diagrams of altered kinases following (B) buparlisib, (C) selumetinib, and (D) combination, colored by fold change relative to controls: ≥2x (red), 1.5x–2x (pink), ≤0.5x (blue), unchanged (black), detected only in treatment (gray).

    Journal: Neuro-Oncology

    Article Title: Combined kinase inhibitors of MEK1/2 and either PI3K or PDGFR are efficacious in intracranial triple-negative breast cancer

    doi: 10.1093/neuonc/nox052

    Figure Lengend Snippet: Kinome alteration following 2 weeks of treatment with buparlisib, selumetinib, or combination in intracranial SUM149 TNBC tumors. (A) Fold change of kinases comparing buparlisib (green), selumetinib (blue), or combination (red) relative to controls. Only kinases with a Log2 fold change of >0.5 or <−0.5 in any treatment group relative to controls are shown. B‒D. Kinome tree diagrams of altered kinases following (B) buparlisib, (C) selumetinib, and (D) combination, colored by fold change relative to controls: ≥2x (red), 1.5x–2x (pink), ≤0.5x (blue), unchanged (black), detected only in treatment (gray).

    Article Snippet: Cell Lines The human-derived TNBC cell lines SUM149 (Asterand; basal-like BRCA1 -mutant, PTEN− ), MDA-MB-231Br (Dr Toshiyuki Yoneda; claudin-low BRCA1 -wildtype, PTEN -wildtype, KRAS -mutant, BRAF -mutant), MDA-MB-468 (American Type Culture Collection [ATCC]; basal-like BRCA1 -wildtype, PTEN −), and MDA-MB-436 (ATCC; claudin-low BRCA1 -mutant, PTEN −) ( ) were transfected with luciferase vector under control of a cytomegalovirus promoter as described, 31 , 32 were confirmed mycoplasma free (September 2015), and were verified by gene expression (September 2010 31 , 32 ).

    Techniques: