Angel E Dago Rodriguez Email & Phone Number

California, United States

Madison, Wisconsin, Us

Madison, Wisconsin, Us

Madison, Wisconsin, Us

San Diego, California, Us

i. Genomic lead for the strategic development of a portfolio of breast cancer liquid biopsy products utilizing circulating tumor cell & cfDNA-based liquid biopsy tests. Responsible for scientific diligence, evidentiary build planning and execution to demonstrate biomarker clinical utility. ii. The intellectual author responsible for the analytical validation and incorporation of cfDNA CNV analysis in our company. This work enables the comprehensive patient’s tumor profiling by complementing CTCs and cfDNA information from a single blood draw, constituting our company’s new mission statement and the strategic framework for future clinical product developments.iii. Under my leadership the Epic Sciences single-cell genomics research group has maintained consistent and robust performance during the last five years, resulting so far in more than 6,000 single CTCs profiled for CNVs from patient’s clinical samples, the majority in late-stage prostate and breast cancers.

i. Team leader responsible for providing technical expertise and scientific input to complete key project milestones for internal teams, Biopharma clients, and academic KOL.ii. Co-lead the design, execution, data analysis and scientific publication of a retrospective clinical study (257 individual CTC sequenced from 47 patients), showing that high genomic instability measured in patient’s CTCs constitutes a poor prognostic biomarker and a distinct feature of patients with aggressive prostate cancer (Paymaneh DM, et al. Clinical Cancer Research. 2020).iii. Co-lead the design, execution, and data analysis (585 individual CTC sequenced from 58 mCRPC patients) of a retrospective clinical study that demonstrated high genomic concordance between patient’s CTCs and their matched tumor tissue biopsy-based on CNV analysis. Our single CTC CNV assay showed superior sensitivity to detect tumor-suppressing genes (e.g. pTEN, TP53, RB1 and BRAC2) deletions and genomic heterogeneity compared to tissue (ASCO 2019, poster presentation). iv. Lead the execution and genomic analysis (172 CTCs sequenced from 13 patients) from a small clinical cohort, confirming the distinct genomic landscape between adenocarcinoma and neuroendocrine prostate cancer (NEPC) based on the non-invasive CNV characterization of patient’s derived CTCs (ESMO 2019, Poster).v. Responsible for the design of customized cancer gene panels, as well as proof of concept and clinical feasibility studies aimed to profile and catalog somatic SNVs mutations using patient-derived CTCs resulting in the execution of a business contract with different Biopharma clients and publications.

i. Built and established from its inception, the Epic Sciences Single CTC Isolation System, enabling the genomic characterization of single CTCs.ii. Lead efforts in the protocol and workflow optimization of our single-cell CNV assay (e.g. single-cell lysis, optimization in whole genome amplification and NGS library prep methods), resulting in the analytical validation of Epic Sciences single CTC low pass whole genome sequencing, to infer genome-wide CNV events (Greene S, Dago AE, et al. PLOS ONE. 2016).iii. Lead the design and execution of analytical and clinical feasibility studies to profile SNVs at the single-cell level based on custom-designed targeted gene panel.iv. Designed and developed assays using Cast-PCR (qPCR) for profiling single locus or point SNVs mutations predictive of clinical responses such as EGFR activation mutations (L858F or T790M) in NSCLC at the single-cell level.v. Lead collaborations with academic centers (MD Anderson, UCSF) and cancer diagnostic companies (e.g. Sequenom, Asuragen, Foundation Medicine) to demonstrate analytical feasibility for the detection of clinically actionable single nucleotide variations in single tumor cells.

Developed a platform for single-cell genomic analysis based on low pass whole genome sequencing, to infer genome-wide copy number variations (CNVs) in single circulating tumor cells (CTCs) as well as in cfDNA isolated from the blood of cancer patients. The method proved effective to delineate and characterize patient’s tumor genomic heterogeneity and clinical potential for the non-invasive monitoring of the patient’s response to treatment (Dago AE, et al. PLOS ONE 2014).

La Jolla, California, Us

Genomics analysis, protein molecular dynamics and site directed mutagenesis were integrated to deduce and generated a molecular model of the autophosphorylation and transient active state of KinA bacterial Sensor Histidine kinsase. Publications1) Steiner E, Dago AE, Young D, Heap JT, Minton NP, Hoch JA and Young M. 2011. Multiple orphan histidine kinase interact directly with Spo0A to control the initiation of endospore formation in Clostridium acetobutylicum. Molecular Microbiology. Vol.32) Dago AE, Schug A, Procaccini A, Hoch JA, Weight M and Szurmant H (2012). The Structural Basis of Histidine Kinase Autophosphorylation deduced by integrating genomics, molecular Dynamics and mutagenesis. PNAS. Vol.109

Involved in the comprehensive characterization and mapping of transcriptional start sites (TSS) from all the genes expressed in the Escherichia coli K-12 genome. The method used to accomplish this goal was based on the pyrosequencing-454 of cDNA amplified libraries obtained under different growth conditions

Goal: To gain molecular insights into the mechanism of transcriptional activation of the genes controlled by the bacterial sigma 54-RNA polymerase.Publications1) Dago AE, Wigneshweraraj SR, Buck M and Morett E (2007). A role for the conserved GAFTGA motif of AAA+ transcription activators in sensing promoter DNA conformation. J Biol Chem.2) Bordes P, Wigneshwerarj SR, Chaney M, Dago AE, Morett E and Buck M. (2004). Communication between Esigma54, promoter DNA and the conserved threonine residue in the GAFTGA motif of the PspF sigma-dependent activator during transcription activation. Molecular Microbiology.

Identification and characterization of the molecular determinants that mediated the interaction between the transcriptional activator and its cognate sigma 54 transcriptional factor (Esigma54) required for the formation of an open promoter complex.PublicationChaney M, Grande R, Wigneshweraraj SR, Cannon W, Casaz P, Gallegos MT, Schumacher J, jones S, Dago AE, Morett E, Buck M. (2001). Binding of trnascriptional activators to sigma 54 in the presence of the transition state analog ADP-aluminum fluoride:insights into activator mechanochemical action. Genes and Development.

I designed, developed and implemented a DNA plasmid based on the replicate machinery of theSemliki Forest virus encoding the GP120 HIV protein aimed for DNA immunization.

Phd, Biochemistry

Master Degree, Biochemistry