study skbr 3 Search Results


study skbr3  (ATCC)
96
ATCC study skbr3
Study Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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skbr3  (DSMZ)
94
DSMZ skbr3
Percent inhibition of NRG1b CELx signal for <t>HER2+</t> cell lines versus HER2−/HSFs+ patient samples . Inhibition of NRG1-driven HER2 signaling by pertuzumab (10 mg/mL) or trastuzumab (10 mg/mL) alone or in combination in the CELx test. Percentages shown represent the average of four HER2+ HSFs+ cell lines <t>(SKBR3,</t> EFM192A, HCC1569, and ZR75-30) or 5 HER2−/HSFs+ primary tumor samples (C978, C133, C264, C309, and C371), performed with 2 technical replicates per biological sample
Skbr3, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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study skbr 3  (ATCC)
99
ATCC study skbr 3
Percent inhibition of NRG1b CELx signal for <t>HER2+</t> cell lines versus HER2−/HSFs+ patient samples . Inhibition of NRG1-driven HER2 signaling by pertuzumab (10 mg/mL) or trastuzumab (10 mg/mL) alone or in combination in the CELx test. Percentages shown represent the average of four HER2+ HSFs+ cell lines <t>(SKBR3,</t> EFM192A, HCC1569, and ZR75-30) or 5 HER2−/HSFs+ primary tumor samples (C978, C133, C264, C309, and C371), performed with 2 technical replicates per biological sample
Study Skbr 3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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skbr3  (ATCC)
90
ATCC skbr3
Validation of the binding affinity of targeted NPs to membrane receptors on cultured cells. (a, b) Flow cytometry validation. Fluorescence histograms are shown from cells stained with each NP flavor. (c) Comparison of the ratio of targeted versus untargeted NPs (based on flow cytometry) for NPs that were conjugated using one-step or two-step methods. For each condition, three batches of conjugated NPs were prepared to quantify the results. (d, e) Microscopic imaging (Renishaw InVia Raman microscope) of <t>SkBr3</t> cells stained with HER2-NPs (flow cytometry samples). The NP-stained cells were fixed in formalin and embedded in 1% agarose to immobilize them for imaging. The samples were imaged with a raster-scanned laser spot that measured 5 microns in diameter, with Raman signals collected through a high-NA (0.8) objective with a confocal pinhole applied, yielding an axial sectioning thickness of ∼ 5 μm. The scale bars represent 20 μm.
Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cell lines skbr3 atcc htb30 hek 293h atcc crl 1573 software  (ATCC)
99
ATCC cell lines skbr3 atcc htb30 hek 293h atcc crl 1573 software
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
Cell Lines Skbr3 Atcc Htb30 Hek 293h Atcc Crl 1573 Software, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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study t47d  (ATCC)
99
ATCC study t47d
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
Study T47d, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nci-h820  (ATCC)
94
ATCC nci-h820
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
Nci H820, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human bc cell lines  (ATCC)
96
ATCC human bc cell lines
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
Human Bc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mda361  (ATCC)
99
ATCC mda361
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
Mda361, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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u2os  (ATCC)
98
ATCC u2os
(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− <t>SKBr3</t> cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.
U2os, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Percent inhibition of NRG1b CELx signal for HER2+ cell lines versus HER2−/HSFs+ patient samples . Inhibition of NRG1-driven HER2 signaling by pertuzumab (10 mg/mL) or trastuzumab (10 mg/mL) alone or in combination in the CELx test. Percentages shown represent the average of four HER2+ HSFs+ cell lines (SKBR3, EFM192A, HCC1569, and ZR75-30) or 5 HER2−/HSFs+ primary tumor samples (C978, C133, C264, C309, and C371), performed with 2 technical replicates per biological sample

Journal: Journal of Cancer Research and Clinical Oncology

Article Title: New HER2-negative breast cancer subtype responsive to anti-HER2 therapy identified

doi: 10.1007/s00432-020-03144-7

Figure Lengend Snippet: Percent inhibition of NRG1b CELx signal for HER2+ cell lines versus HER2−/HSFs+ patient samples . Inhibition of NRG1-driven HER2 signaling by pertuzumab (10 mg/mL) or trastuzumab (10 mg/mL) alone or in combination in the CELx test. Percentages shown represent the average of four HER2+ HSFs+ cell lines (SKBR3, EFM192A, HCC1569, and ZR75-30) or 5 HER2−/HSFs+ primary tumor samples (C978, C133, C264, C309, and C371), performed with 2 technical replicates per biological sample

Article Snippet: Human breast cancer cell lines used in this study included SKBr3 (HER2+ /HSFs+), BT474 (HER2+ /HSFs−), BT483 (ER-/HER2−/HSFs+), ZR75-30 (HER2+ /HSFs+), HCC1569 (HER2+ /HSFs−), HCC1954 (ER-/HER2+ /HSFs−), HCC202 (HER2+ /HSFs+), MDA-MB361 (HER2+ /HSFs−), AU565 (HER2+ /HSFs−) (all from American Tissue Type Collection; ATCC, Manassas, VA), and EFM192A (HER2+ /HSFs+) (from Leibniz Institute DSMZ, Germany).

Techniques: Inhibition

Comparison of inhibition of NRG1-driven HER2 signaling by HER2 targeted therapeutics. Pertuzumab (10 μg/mL), lapatinib (200 nM), afatinib (120 nM), or neratinib (500 nM) inhibition of NRG1-driven HER2 signaling is shown as the average of 9 HER2+ cell lines (SKBR3, EFM192A, ZR75-30, HCC202, HCC1954, HCC1569, MDA-MB361, BT474, AU565) or 7 HER2−/HER2s+ primary tumors (R69, R20, R160, R82, R95, R25, R71) performed with 2 technical replicates per biological sample. Single dose concentrations were selected for relative comparator purposes only where a maximal amount of the signaling was inhibited in at least one of the samples. Variances from 100% inhibition likely arise from ligand generated signaling that was not directly related to HER activity or where a sample had some level of drug paradoxical response (Claus et al. )

Journal: Journal of Cancer Research and Clinical Oncology

Article Title: New HER2-negative breast cancer subtype responsive to anti-HER2 therapy identified

doi: 10.1007/s00432-020-03144-7

Figure Lengend Snippet: Comparison of inhibition of NRG1-driven HER2 signaling by HER2 targeted therapeutics. Pertuzumab (10 μg/mL), lapatinib (200 nM), afatinib (120 nM), or neratinib (500 nM) inhibition of NRG1-driven HER2 signaling is shown as the average of 9 HER2+ cell lines (SKBR3, EFM192A, ZR75-30, HCC202, HCC1954, HCC1569, MDA-MB361, BT474, AU565) or 7 HER2−/HER2s+ primary tumors (R69, R20, R160, R82, R95, R25, R71) performed with 2 technical replicates per biological sample. Single dose concentrations were selected for relative comparator purposes only where a maximal amount of the signaling was inhibited in at least one of the samples. Variances from 100% inhibition likely arise from ligand generated signaling that was not directly related to HER activity or where a sample had some level of drug paradoxical response (Claus et al. )

Article Snippet: Human breast cancer cell lines used in this study included SKBr3 (HER2+ /HSFs+), BT474 (HER2+ /HSFs−), BT483 (ER-/HER2−/HSFs+), ZR75-30 (HER2+ /HSFs+), HCC1569 (HER2+ /HSFs−), HCC1954 (ER-/HER2+ /HSFs−), HCC202 (HER2+ /HSFs+), MDA-MB361 (HER2+ /HSFs−), AU565 (HER2+ /HSFs−) (all from American Tissue Type Collection; ATCC, Manassas, VA), and EFM192A (HER2+ /HSFs+) (from Leibniz Institute DSMZ, Germany).

Techniques: Comparison, Inhibition, Generated, Activity Assay

Validation of the binding affinity of targeted NPs to membrane receptors on cultured cells. (a, b) Flow cytometry validation. Fluorescence histograms are shown from cells stained with each NP flavor. (c) Comparison of the ratio of targeted versus untargeted NPs (based on flow cytometry) for NPs that were conjugated using one-step or two-step methods. For each condition, three batches of conjugated NPs were prepared to quantify the results. (d, e) Microscopic imaging (Renishaw InVia Raman microscope) of SkBr3 cells stained with HER2-NPs (flow cytometry samples). The NP-stained cells were fixed in formalin and embedded in 1% agarose to immobilize them for imaging. The samples were imaged with a raster-scanned laser spot that measured 5 microns in diameter, with Raman signals collected through a high-NA (0.8) objective with a confocal pinhole applied, yielding an axial sectioning thickness of ∼ 5 μm. The scale bars represent 20 μm.

Journal: Journal of Biomedical Optics

Article Title: High-speed Raman-encoded molecular imaging of freshly excised tissue surfaces with topically applied SERRS nanoparticles

doi: 10.1117/1.JBO.23.4.046005

Figure Lengend Snippet: Validation of the binding affinity of targeted NPs to membrane receptors on cultured cells. (a, b) Flow cytometry validation. Fluorescence histograms are shown from cells stained with each NP flavor. (c) Comparison of the ratio of targeted versus untargeted NPs (based on flow cytometry) for NPs that were conjugated using one-step or two-step methods. For each condition, three batches of conjugated NPs were prepared to quantify the results. (d, e) Microscopic imaging (Renishaw InVia Raman microscope) of SkBr3 cells stained with HER2-NPs (flow cytometry samples). The NP-stained cells were fixed in formalin and embedded in 1% agarose to immobilize them for imaging. The samples were imaged with a raster-scanned laser spot that measured 5 microns in diameter, with Raman signals collected through a high-NA (0.8) objective with a confocal pinhole applied, yielding an axial sectioning thickness of ∼ 5 μm. The scale bars represent 20 μm.

Article Snippet: Cell Culture and Flow Cytometry The two cell lines employed in this study were SkBr3 (ATCC, HTB-30D) and ZR-75-1 (ATCC, CRL-1500), both of which overexpress HER2.

Techniques: Biomarker Discovery, Binding Assay, Membrane, Cell Culture, Flow Cytometry, Fluorescence, Staining, Comparison, Imaging, Microscopy

(A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− SKBr3 cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.

Journal: Cancer cell

Article Title: Widespread selection for oncogenic mutant allele imbalance in cancer

doi: 10.1016/j.ccell.2018.10.003

Figure Lengend Snippet: (A) As in the Figure 4A, but assessing the enrichment for loss of the WT allele as the mechanism of mutant allele imbalance. (B) In HR+ HER2− breast cancers, the rate of LOH spanning ESR1 in tumors with or without ESR1 gain-of-function mutations and those acquired before or after endocrine therapy (asterisk, p value = 0.00015, Chi-squared test; numbers in black bars represent the number of affected cases). (C) Luciferase reporter activity (RLU) in HR− SKBr3 cells ectopically expressing HA-ERα wild-type (WT) or the specified mutant in proportions equivalent to homozygous mutant (left) to heterozygosity (right) in hormone-depleted medium. Error bars are +/− SD from triplicate experiments. (D) Duration of time of patients with BRAF V600E-mutant metastatic melanomas on vemurafenib therapy as a function of allelic imbalance of V600E and the mechanisms thereof [median PFS is 31.7 months (95% CI, 6-not reached) for patients with loss of WT BRAF versus 6.5 months (4.8-12) in the rest; hazard ratio, 4.4; p value = 0.01]. Complete pathologic responses are indicated in dark blue (p value = 0.01 comparing patients whose tumors lost the WT allele to those whose tumors that do not, two-sided Fisher’s exact test). See also Figure S5.

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Rabbit polyclonal, Phospho-MEK (Ser217/221) Cell Signal Cat#9121; RRID: AB_331649 Rabbit polyclonal, Anti-MEK Cell Signal Cat#9122; RRID: AB_823567 Rabbit polyclonal, Phospho ERK (Thr202/Tyr204) Cell Signal Cat#9109; RRID: AB_331646 Rabbit polyclonal, Anti-ERK Cell Signal Cat#9102; RRID: AB_330744 Rabbit monoclonal, Anti-GFP Cell Signal Cat#2956; RRID: AB_1196615 Rabbit monoclonal, Anti-GAPDH Cell Signal Cat#2118; RRID: AB_561053 Biological Samples MSK-IMPACT Zehir et al. 2017 N/A Chemicals, Peptides, and Recombinant Proteins pEGPF-N1-MEK1 Addgene Cat#14746 3X-ERE-TATA-luciferase reporter Addgene Cat#11354 pRL-TK Renilla luciferase plasmid Promega Cat#E2231 HA-tagged WT ERα This study N/A pcDNA3.1 (EV) Thermo Fisher Cat#V79020 HA-tagged ERα Y537S This study N/A HA-tagged ERα D538G This study N/A Critical Commercial Assays QuikChange II XL Site-Directed Mutagenesis Kit Stratagene Cat#200521 SuperSignal West Pico Plus Chemiluminescent Thermo Fisher Cat#34577 Lipofectamine 2000 Transfection Reagent Invitrogen Cat#11668027 Dual-Luciferase Reporter Assay System Promega Cat#E1910 Deposited Data Prospective DNA sequencing This study Accession number for the prospective sequencing data reported in this study is EVA: PRJEB28874, https://www.ebi.ac.uk/eva/?eva-study=PRJEB28874 Experimental Models: Cell Lines SKBr3 ATCC HTB30 HEK-293H ATCC CRL-1573 Software and Algorithms R for Statistical Computing R Foundation http://www.r-project.org FACETS Shen, et al. 2016 http://github.com/mskcc/facets FACETS-suite This study http://github.com/mskcc/facets-suite Other BAM files for TCGA exomes TCGA https://cancergenome.nih.gov Open in a separate window KEY RESOURCES TABLE Mutant allele imbalance affects ~half of all oncogenic driver mutations in cancer Positive and negative selection shapes the allelic configuration of mutant oncogenes Mutant dosage gains and stoichiometric changes drive fitness and growth advantages Mutant oncogene zygosity dictates prognosis and enhanced therapeutic sensitivity Bielski et al. describe widespread allele imbalance in cancer, which is selected for via modest dosage increases of gain-of-fitness mutations and can be driven by antecedent oncogenic mutations.

Techniques: Mutagenesis, Luciferase, Activity Assay, Expressing

KEY RESOURCES TABLE

Journal: Cancer cell

Article Title: Widespread selection for oncogenic mutant allele imbalance in cancer

doi: 10.1016/j.ccell.2018.10.003

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Rabbit polyclonal, Phospho-MEK (Ser217/221) Cell Signal Cat#9121; RRID: AB_331649 Rabbit polyclonal, Anti-MEK Cell Signal Cat#9122; RRID: AB_823567 Rabbit polyclonal, Phospho ERK (Thr202/Tyr204) Cell Signal Cat#9109; RRID: AB_331646 Rabbit polyclonal, Anti-ERK Cell Signal Cat#9102; RRID: AB_330744 Rabbit monoclonal, Anti-GFP Cell Signal Cat#2956; RRID: AB_1196615 Rabbit monoclonal, Anti-GAPDH Cell Signal Cat#2118; RRID: AB_561053 Biological Samples MSK-IMPACT Zehir et al. 2017 N/A Chemicals, Peptides, and Recombinant Proteins pEGPF-N1-MEK1 Addgene Cat#14746 3X-ERE-TATA-luciferase reporter Addgene Cat#11354 pRL-TK Renilla luciferase plasmid Promega Cat#E2231 HA-tagged WT ERα This study N/A pcDNA3.1 (EV) Thermo Fisher Cat#V79020 HA-tagged ERα Y537S This study N/A HA-tagged ERα D538G This study N/A Critical Commercial Assays QuikChange II XL Site-Directed Mutagenesis Kit Stratagene Cat#200521 SuperSignal West Pico Plus Chemiluminescent Thermo Fisher Cat#34577 Lipofectamine 2000 Transfection Reagent Invitrogen Cat#11668027 Dual-Luciferase Reporter Assay System Promega Cat#E1910 Deposited Data Prospective DNA sequencing This study Accession number for the prospective sequencing data reported in this study is EVA: PRJEB28874, https://www.ebi.ac.uk/eva/?eva-study=PRJEB28874 Experimental Models: Cell Lines SKBr3 ATCC HTB30 HEK-293H ATCC CRL-1573 Software and Algorithms R for Statistical Computing R Foundation http://www.r-project.org FACETS Shen, et al. 2016 http://github.com/mskcc/facets FACETS-suite This study http://github.com/mskcc/facets-suite Other BAM files for TCGA exomes TCGA https://cancergenome.nih.gov Open in a separate window KEY RESOURCES TABLE Mutant allele imbalance affects ~half of all oncogenic driver mutations in cancer Positive and negative selection shapes the allelic configuration of mutant oncogenes Mutant dosage gains and stoichiometric changes drive fitness and growth advantages Mutant oncogene zygosity dictates prognosis and enhanced therapeutic sensitivity Bielski et al. describe widespread allele imbalance in cancer, which is selected for via modest dosage increases of gain-of-fitness mutations and can be driven by antecedent oncogenic mutations.

Techniques: Recombinant, Luciferase, Plasmid Preparation, Mutagenesis, Transfection, Reporter Assay, DNA Sequencing, Sequencing, Software