Vincent A. Miller
YOU?
Author Swipe
View article: Goserelin 3-month depot shows non-inferiority to the monthly formulation in U.S. patients with premenopausal breast cancer: a real-world evidence study
Goserelin 3-month depot shows non-inferiority to the monthly formulation in U.S. patients with premenopausal breast cancer: a real-world evidence study Open
Purpose Clinical trials demonstrated every 3-month goserelin 10.8 mg to be non-inferior to monthly goserelin 3.6 mg in premenopausal patients with ER-positive breast cancer. However, real-world studies comparing 3-month goserelin 10.8 mg w…
View article: Expanding the landscape of oncogenic drivers and treatment options in acral and mucosal melanomas by targeted genomic profiling
Expanding the landscape of oncogenic drivers and treatment options in acral and mucosal melanomas by targeted genomic profiling Open
Despite advancements in treating cutaneous melanoma, patients with acral and mucosal (A/M) melanomas still have limited therapeutic options and poor prognoses. We analyzed 156 melanomas (101 cutaneous, 28 acral, and 27 mucosal) using the F…
View article: Leveraging the Expertise of the CTSA Program to Increase the Impact and Efficiency of Clinical Trials
Leveraging the Expertise of the CTSA Program to Increase the Impact and Efficiency of Clinical Trials Open
Importance Multicenter clinical trials play a critical role in the translational processes that enable new treatments to reach all people and improve public health. However, conducting multicenter randomized clinical trials (mRCT) presents…
View article: Supplement Tables and Figures from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness
Supplement Tables and Figures from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness Open
Supplemental Tables 1-3 and Supplemental Figures 1-5
View article: Supplement Tables and Figures from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness
Supplement Tables and Figures from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness Open
Supplemental Tables 1-3 and Supplemental Figures 1-5
View article: Data from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness
Data from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness Open
Advanced and metastatic squamous cell carcinomas (SCC) are common and difficult-to-treat malignancies. We assessed 75 immunotherapy-treated patients with SCC from a clinically annotated database of 2,651 patients, as well as 9,407 patients…
View article: Data from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness
Data from Phenotypic and Genomic Determinants of Immunotherapy Response Associated with Squamousness Open
Advanced and metastatic squamous cell carcinomas (SCC) are common and difficult-to-treat malignancies. We assessed 75 immunotherapy-treated patients with SCC from a clinically annotated database of 2,651 patients, as well as 9,407 patients…
View article: Data from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics
Data from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics Open
TP53 tumor-suppressor gene mutations are among the most frequent abnormalities in cancer, affecting approximately 40% of patients. Yet, there is no accepted way to target these alterations in the clinic. At the same time, antagonists of VE…
View article: Data from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics
Data from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics Open
TP53 tumor-suppressor gene mutations are among the most frequent abnormalities in cancer, affecting approximately 40% of patients. Yet, there is no accepted way to target these alterations in the clinic. At the same time, antagonists of VE…
View article: Supplementary Figure S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes
Supplementary Figure S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes Open
Supplementary Fig. S3: Co-mutation across all PACC tumors.
View article: Data from <i>EGFR</i> Kinase Domain Duplication (<i>EGFR</i>-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
Data from <i>EGFR</i> Kinase Domain Duplication (<i>EGFR</i>-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib Open
Oncogenic EGFR mutations are found in 10% to 35% of lung adenocarcinomas. Such mutations, which present most commonly as small in-frame deletions in exon 19 or point mutations in exon 21 (L858R), confer sensitivity to EGFR tyrosine kinase …
View article: Supplementary Figures S1 - S2 from An Acquired <i>HER2</i> <sup>T798I</sup> Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant–Driven Breast Cancer
Supplementary Figures S1 - S2 from An Acquired <i>HER2</i> <sup>T798I</sup> Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant–Driven Breast Cancer Open
Supplementary Figure S1. HER2L869R and HER3E928G cooperate to drive ERBB signaling output. Supplementary Figure S2. MG132 treatment restores expression of HER2T798I.
View article: Data from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
Data from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade Open
Therapeutic antibodies blocking programmed death-1 and its ligand (PD-1/PD-L1) induce durable responses in a substantial fraction of melanoma patients. We sought to determine whether the number and/or type of mutations identified using a n…
View article: Supplementary Data Figure 2 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
Supplementary Data Figure 2 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets Open
PDF file 26K, Association of node status with RFS and OS, stratified by menopausal status
View article: Supplementary Table S4 from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics
Supplementary Table S4 from <i>TP53</i> Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics Open
Next generation sequencing gene list (Foundation Medicine) (N = 236 genes a)
View article: Supplementary Data Figure Legends from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
Supplementary Data Figure Legends from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets Open
PDF file 64K, Legends for all supplementary data figures (1-7)
View article: Data from An Acquired <i>HER2</i> <sup>T798I</sup> Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant–Driven Breast Cancer
Data from An Acquired <i>HER2</i> <sup>T798I</sup> Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant–Driven Breast Cancer Open
We report a HER2T798I gatekeeper mutation in a patient with HER2L869R-mutant breast cancer with acquired resistance to neratinib. Laboratory studies suggested that HER2L869R is a neratinib-sensitive, gain-of-function mutation that upon dim…
View article: Supplementary Data Figure 5 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
Supplementary Data Figure 5 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets Open
PDF file 62K, MCL1 overexpression enhances docetaxel resistance in non-amplified TNBC cell lines
View article: Data from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
Data from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets Open
Neoadjuvant chemotherapy (NAC) induces a pathologic complete response (pCR) in approximately 30% of patients with triple-negative breast cancers (TNBC). In patients lacking a pCR, NAC selects a subpopulation of chemotherapy-resistant tumor…
View article: Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors Open
Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility to targeted MET inhibitors. Recurrent somatic splice site alterations at MET exon 14 (METex14) that resul…
View article: Supplementary Table 1 from Inflammatory Myofibroblastic Tumors Harbor Multiple Potentially Actionable Kinase Fusions
Supplementary Table 1 from Inflammatory Myofibroblastic Tumors Harbor Multiple Potentially Actionable Kinase Fusions Open
PDF file - 87KB, Changes in the indicated laboratory parameters after 3 cycles of crizotinib. HgB: hemoglobin, Hct: hematocrit, MCV: mean corpuscular volume, ESR: erythrocyte sedimentation rate, LDH: lactate dehydrogenase.
View article: Supplementary Table 3 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
Supplementary Table 3 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer Open
PDF - 36K, Samples tested.
View article: Supplementary Figure 5 from <i>HER2</i> Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in <i>EGFR</i>-Mutant Lung Cancers That Lack the Second-Site <i>EGFR</i><sup>T790M</sup> Mutation
Supplementary Figure 5 from <i>HER2</i> Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in <i>EGFR</i>-Mutant Lung Cancers That Lack the Second-Site <i>EGFR</i><sup>T790M</sup> Mutation Open
PDF file - 92K, Effects of HER2 overexpression on the sensitivity of HCC827 cells to EGFR TKIs
View article: Supplementary Table 5 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
Supplementary Table 5 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer Open
PDF - 42K, Selected actionable alterations in patients.
View article: Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes
Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes Open
Supplementary Table S1A: Genes analyzed for base substitutions, short insertions/deletions, and copy number alterations (DNA). Supplementary Table S1B: Genes analyzed for rearrangements (DNA).
View article: Supplementary Data Figure 7 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
Supplementary Data Figure 7 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets Open
PDF 118K, TSC1 truncation in the RD of a TNBC after NAC
View article: Supplementary Table 2 from Inflammatory Myofibroblastic Tumors Harbor Multiple Potentially Actionable Kinase Fusions
Supplementary Table 2 from Inflammatory Myofibroblastic Tumors Harbor Multiple Potentially Actionable Kinase Fusions Open
PDF file - 53KB, FoundationOne panel. This targeted next generation sequencing platform evaluates for 3769 exons of 236 cancer genes and 47 introns of 19 commonly rearranged genes, including 8 tyrosine kinases.
View article: Supplementary Figure 1 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
Supplementary Figure 1 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer Open
PDF - 168K, Detailed analysis of matched primary and recurrent/metastatic breast tumors.
View article: Supplementary Figure S2 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes
Supplementary Figure S2 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent <i>RAF</i> Fusions and Frequent Inactivation of DNA Repair Genes Open
Supplementary Fig. S2: Loss of function mutations in select tumor suppressor genes.
View article: Supplementary Figure 4 from <i>HER2</i> Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in <i>EGFR</i>-Mutant Lung Cancers That Lack the Second-Site <i>EGFR</i><sup>T790M</sup> Mutation
Supplementary Figure 4 from <i>HER2</i> Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in <i>EGFR</i>-Mutant Lung Cancers That Lack the Second-Site <i>EGFR</i><sup>T790M</sup> Mutation Open
PDF file - 91K, Levels of HER2 affect the sensitivity of EGFR-mutant NSCLC cells to EGFR TKIs