Results-oriented Scientific Leader with 12 years of experience in drug discovery, translational medicine and clinical development. Proven track record managing matrix teams providing lead optimization, translational research and Phase 1/2 support for multiple programs. Known for flexibility, performing in a self-directed environment and as team member while managing junior scientists. Recognized as an effective communicator, drawing on broad knowledge base and employing team-oriented leadership to deliver results. [...]

Experience

• Merck - Senior Clinical Scientist

  • Employed Aug 2017 – Present

  • Employment Duration 2 yrs 9 mos

  • Location Greater Denver Area

• ExecuPharm - Senior Clinical Scientist on assignment to Merck

  • Employed May 2016 – Jul 2017

  • Employment Duration 1 yr 3 mos

  • Location Greater Denver Area

• Biodesix, Inc. - Senior Manager, Clinical Development/Translational Medicine

  • Employed Dec 2013 – Apr 2016

  • Employment Duration 2 yrs 5 mos

  • Location Boulder, CO

    • Collaborated with stakeholders on the design, execution and analysis of studies to elucidate the mechanism of action of VeriStrat®, a prognostic and predictive serum proteomics test for advanced non-small cell lung cancer patients

    • Wrote scientific proposals for nonclinical research projects, analyzed biomarker and clinical outcome data and prepared scientific reports for internal and external audiences.

• Array BioPharma (Total Duration 6 yrs 7 mos)

  • Research Investigator

    • Employed Oct 2012 – Aug 2013 ( 11 mos )

    • Location Boulder, Colorado

    • Developed Phase 2 strategies to identify nucleic acid and protein-based response biomarkers in plasma and bone marrow of patients with hematologic malignancies for two programs.

    • Managed Translational Operations group, enabling all aspects of clinical sample management for 8 concurrent clinical trials (e.g., creation of PK / biomarker sampling kits, generation of site training materials, sample tracking, and facilitating outsourcing activities).

    • Created biomarker sections of clinical protocols and clinical study reports.

    • Supervised scientific and operations staff.

  • Senior Research Scientist

    • Employed Oct 2009 – Sep 2012 ( 3 yrs )

    • Location Boulder, Colorado

    • Provided strategic, scientific and operational leadership of cross-functional teams supporting one IND-stage and 3 clinical stage programs.

    • Led biomarker team for CSF-1R inhibitor program demonstrating pharmacodynamic activity in blood / serum / urine in Ph 1 patients with solid tumors.

    • Coordinated predictive biomarker strategy and oversaw sample analyses (in house and outsourced) identifying protein-based plasma biomarkers related to disease, age or clinical benefit from treatment with p38 / Tie2 inhibitor in patients with MDS in Phase 1 study.

    • Supervised IHC / immunoassay PD biomarker assay development and clinical sample analyses demonstrating mechanistic and functional target inhibition by p38 / Tie2 inhibitor in MDS patient bone marrow and plasma samples from Phase 1 study.

    • Defined potential clinical development strategies for selective HER2 inhibitor.

    • Wrote biomarker sections of clinical protocols, Investigator’s brochures, informed consent forms and clinical study reports.

    • Prepared presentations and technical report sections of business development documents.

    • Supervised scientific staff.

  • Title Research Scientist

    • Employed Feb 2007 – Sep 2009 ( 2 yrs 8 mos )

    • Location Boulder, Colorado

    • Provided strategic, scientific and operational leadership for 2 clinical stage programs.

    • Developed Phase 1 biomarker strategy and coordinated outsourcing of tumor biopsy IHC analyses, demonstrating target inhibition and confirming possible sensitivity marker in breast cancer patients treated with HER2 inhibitor.

    • Performed and directed nonclinical research supporting development paths of small molecule ErbB inhibitors in solid tumor indications.

    • Generated / implemented biomarker strategies for Phase 1 clinical trials,

    • Created sample collection manuals, conducted clinical site training on laboratory procedures.

    • Supervised scientific staff.

• Myriad Genetics/Myriad Pharmaceuticals

  • Total Duration 3 yrs 9 mos

  • Title Scientist II

    • Employed May 2005 – Jan 2007 ( 1 yr 9 mos )

    • Served as Project Leader and managed multidisciplinary lead optimization effort delivering a small molecule HIV-1 maturation inhibitor IND candidate.

    • Developed cellular assays and performed compound characterization, including resistance selection and mechanism of action studies.

    • Created IND-enabling documents.

    • Supervised scientific staff.

  • Title Scientist I

    • Employed May 2003 – Apr 2005 ( 2 yrs )

    • Provided scientific leadership and laboratory support for 2 antiviral lead optimization projects.

    • Developed and optimized cell-based assays and tested compounds, supporting structure-activity relationship studies of small molecule compounds for antiviral and oncology programs.

    • Managed Biosafety Level 3 (BSL3) laboratory.

    • Supervised scientific staff.

[...] Jennifer will be remembered for being highly intelligent, down to earth, gracious, kind, fun-loving, and for her huge, heart-warming smile – with her eyes always twinkling. She was very humble, despite being extremely accomplished in her personal and professional life. She was a devoted mother, a loving daughter and sister, a loyal friend, and a giving member of her community.

She and her family moved to Colorado when she was three years old. She lived there most of her life, aside from the 10 years she spent in Utah pursuing her PhD and working as a scientist.

As a young girl, Jennifer was precocious, and she remained curious, driven and ambitious throughout her life. She was a member of the National Honor Society at Arapahoe High School. She studied ballet, played competitive soccer, and enjoyed water sports throughout her childhood and teen years.

While earning her degree in Biochemistry from Colorado State University, she received numerous awards and certificates of recognition, as well as the distinguished Colorado Scholars Scholarship from the College of Natural Sciences.

After completing her PhD in Biochemistry, she was a Senior Clinical researcher, most recently at Merck. She was a tenacious leader and worker, managing teams who conducted critical research on cures for cancer and viruses.

She dedicated her personal time to raising her children with warmth and generosity; although she enjoyed gardening, hiking, and time with family and friends, her kids were her primary source of joy, meaning and purpose. [...] .

Ebola (above) is a killer virus that may commandeer cellular protein-sorting pathways through TSG101.

Viruses can't do much without a host. They propagate by usurping cellular machinery, and much of an infection's misery is due to the immune response. But conventional therapies, without much luck, essentially have targeted one-half of the infection equation: the foreign invader. Now, researchers increasingly are setting their sights on the host's role.

Investigators recently attempted to mitigate the host immune response and the associated collateral damage (see sidebar). Some explore a complementary approach: to cut off access to the cellular pathway that a virus commandeers to mass-produce, specifically, the route used to bud from the cell. Doing so, without impairing the host, could provide a powerful new broad-spectrum antiviral agent. "Conventional antivirals are highly specific, and pathogens can mutate to insensitivity," says Stanley Cohen, professor of genetics and medicine at Stanford University. "But if one can attack host genes required for pathogens to be pathogenic, resistance is less likely. One can affect the pathogenicity of the virus."

DUBIOUS BEGINNINGS

Cohen, who with Herbert W. Boyer in the early 1970s essentially founded recombinant DNA technology, says he might have zeroed in on what may become the first such "host-oriented" therapeutic target: Tumor Susceptibility Gene 101. Despite its moniker, TSG101 may have less to do with cancer than first thought, and everything to do with the vacuolar protein-sorting pathway that ferries excess cell-surface receptors to lysosomes, the enzyme-filled sacs that dismantle debris. Certain killer viruses, including HIV, Ebola, and Marburg, hijack this transport system using TSG101 protein to cloak themselves in membranous escape pods. At least three biotech companies are developing drugs to target TSG101, which Cohen dubs "the getaway driver for viral release." But a clinical future awaits clarification of its obfuscated origins as a tumor suppressor.

Discovering TSG101 in 1996 was the first fruit of random homozygous knockout (RHKO) technology, an antisense technique that identifies genes by a particular function, in this case, cellular transformation.1 Dampening TSG101 expression transformed murine 3T3 fibroblasts, which caused metastatic tumors in nude mice. The encoded protein bore the hallmarks of a transcription factor, but the links to carcinogenesis turned out to be indirect.

THE VIRAL PIRATE

In 2000, experimental roads converged to flesh out the role of TSG101. Beth Agresta, a graduate student working with molecular geneticist Carol Carter, State University of New York, Stony Brook, was screening for cellular proteins that interact with HIV proteins. "She got several hits and wrote her thesis on one, but continued to check the database to see if there was any more information. One day, there was," recalls Carter. That was TSG101. Carter and Cohen collaborated to get at protein function.

Soon, another graduate student in Carter's group, Lynn Ver-Plank, identified the major viral core protein Gag as HIV's binding site for TSG101.2 Gag lets mature viruses bud from cells. At about the same time, Jennifer Garrus, a graduate student with biochemist [Dr. Wesley Ian Sundquist (born 1959)], University of Utah School of Medicine, Salt Lake City, blocked TSG101 with small interfering RNA, halting HIV budding. When she restored gene function, budding resumed.3

Gag and TSG101 attach by ubiquitin tags, and the host protein then escorts the viral emissary into the vacuolar protein-sorting pathway. But instead of being carted away to digestive doom in the lysosome, Gag proteins attach by their bound TSG101s to bits of cell membrane, ultimately becoming packaged into mature virions.

Yeast provided another connection. Also in 2000, University of Utah biologist Markus Babst and Scott Emr, a Howard Hughes Medical Institute investigator at the University of California, San Diego, found that TSG101 has a yeast counterpart, Vps23.4 Vps23/TSG101 is a subunit of a complex, called ESCRT-I, which binds and sorts ubiquitin-tagged molecules. They tested Cohen's TSG101 mutant cell line for protein transport defects and found trafficking phenotypes, says Babst.

The solid link to intracellular protein transport may explain the dual role of TSG101 in carcinogenesis and viral infection. The pathway normally recycles cell-surface receptors, including growth-factor receptors. Silence TSG101, and these receptors aren't sent to the lysosomal garbage dumps; instead they accumulate at the cell surface like uncollected trash. There, the receptors transduce too many signals to divide, and runaway mitosis results.

But the cancer connection still is not as clear as some researchers would like. "The role of TSG101 in cancer has been quite elusive," says [Dr. Wesley Ian Sundquist (born 1959)], citing a retracted report on TSG101 mutations in cancer patients.5 And Kay-Uwe Wagner, at the Eppley Institute for Research in Cancer and Allied Diseases at the University of Nebraska Medical Center, Omaha, used knockout mice to show that TSG101 is essential for embryo implantation but not tumor suppression.6 She also reexamined the original 1996 tumorigenic cell line and found "whopping levels" of TSG101.7 She blames Cohen's use of an immortal cell line. "Nobody was able to repeat these transformation studies in other cell lines," she says.

DRUG DEVELOPMENT

Still, Cohen maintains that TSG101 makes a good antiviral target. He and former postdoctoral researcher Limin Li cofounded the company Functional Genetics, which is developing a viral budding inhibitor based on TSG101's action.

But the jump from promising target in cell culture to antiviral development will not be easy. Such a drug probably would block normal ESCRT function as well, says Babst. "This could result in a tumorigenic phenotype." Effects could be wide-ranging. "I'm worried about the potential that a TSG101 inhibitor would exhibit general cytotoxicity," suggests Sundquist, who also works with Myriad Pharmaceuticals in Salt Lake City.

Even if TSG101 never overcomes its tainted beginnings, it may still pioneer host-oriented therapeutics, for there may be unknown aspects of the viral subversion of TSG101 to exploit. Concludes Carter: "That's what one goes after – to understand the process, what the virus does to divert the machinery – and target that."

Ricki Lewis rickilewis@nasw.org is a freelance writer in Scotia, NY.

Fight the Flu, Ignore the Bug

At the start of this year's particularly worrisome flu sea-son, researchers at London Imperial college in the United Kingdom posed a comforting thought. Suppose the bug's nasty symptoms could be avoided without vaccination or antiviral drugs by targeting the immune responses responsible for influenza's misery. Their tests on mice showed positive results, they say. Maybe so, say the skeptics, but that doesn't prove how humans would respond.

The Imperial College researchers have found that a receptor molecule called OX40 is overexpressed in T cells responding to a viral infection, but not in the remaining T-cell population.1 The receptor can be blocked using an OX40-immunoglobulin fusion protein called OX40:Ig. This, the researchers say, should temper overzealous immune responses in the lungs.

Tracy Hussell and colleagues, who tested the drug on mice injected with influenza type A, found that clinical symptoms such as congestion and high body temperature were virtually eliminated. Hussell says there's no reason why the treatment could not be extended to humans, after symptoms have emerged. "Mice could show signs of illness for three days, and as soon as you administer this reagent, it stops clinical symptoms in their tracks."

In the future, humans could experience similar remission of symptoms, according to Alan Hay, director of the WHO Collaborating Centre for Reference and Research on Influenza at the UK National Institute for Medical Research. "It's interesting work, but it's early stages and needs further development," says Hay.

Brad Magor, assistant professor, Department of Biological Sciences (Immunogenetics), University of Alberta, is more dubious. "Mice are not natural hosts to influenza A, so their response to the pathogen is less likely to reflect that of a natural host such as a chicken, swine, or human." Magor says he's concerned that the body might permanently lose influenza-specific memory cells as a result of the treatment. He conceded, however, that blocking OX40 molecules showed significant promise for modulating immunity and inducing tolerance to engrafted organs.

Hussell says the group is focusing on the influenza treatment for now and is applying to the UK Medical Research Council and the Wellcome Trust for funding to begin human clinical trials. The Imperial College group collaborates with Xenova, a UK-based biotech that explores various therapeutic uses of OX40, including autoimmune disease and cancer.

17^th Judicial District Attorney Dave Young announced Wednesday that Michael Arthur Ellison has been charged with first-degree murder after deliberation in the stabbing death of his wife in Thornton.

Thornton police found Jennifer Ellison, 45, dead at the couple’s home at 13154 Uinta Street in Thornton on October 17 after receiving a 911 call from Michael Ellison.

Ellison (DOB 02/25/72) was advised of the charges Wednesday in Adams County District Court. A preliminary hearing is set for December 31 in Division E of Adams County District Court.

The filing of a criminal charge is merely a formal accusation that an individual committed a crime under Colorado Laws. A defendant is presumed innocent until and unless proven guilty.

Research Scientist

• Greater Denver Area

• Contact info

• University of Colorado Denver

• University of Utah

About

Results-oriented scientist with 15 years of experience in lab management, design and execution of experiments and publication. Track record of leading laboratory personnel in multiple projects. Known for independent hypothesis creation and testing. An effective communicator with a broad knowledge base.

• Molecular Biology

• Biochemistry

• Cell Biology

• Scientific leadership

• Publication of peer reviewed studies

Experience

• University of Colorado Denver - Senior Research Associate

  • Dates Employed 2013 – Present (7 yrs)

  • Location Aurora Colorado

  • Characterization of neutrophils from individuals treated with interferon gamma or cannabis

  • Analysis of neutrophils from patients with immune deficiency

  • Guidance, training and leadership for medical fellows and junior lab personnel

  • Preparation and submission of scientific manuscripts

  • Clinical study design

  • Development and use of myeloid cell function assays

  • Coordination of a bioinformatics group and a genomics core facility to measure drug induced changes in mRNA profiles in myeloid cells

  • Design/use of colorimetric, luminescent and fluorescent-96 well assays

  • Review of microarray data to derive biological insights

  • Correlation of mRNA and protein expression changes

• Bonfills Blood Center - Post Doctoral Fellow

  • Dates Employed 2008 – 2013 ( 5 years )

  • Location Denver Colorado

  • Characterization of the role of peroxiredoxin 6 (Prdx6) in modulating the oxidative burst of neutrophils.

  • Analysis of neutrophils from patients with immune deficiency

  • Genetic manipulation of model cell lines to achieve depletion of Prdx6

  • Re-expression of wild type and mutant Prdx6 in knockdown cell lines

  • Luminescence and colorimetric based assays of oxidase activity

  • Over-expression and purification of wild type and mutant Prdx6

  • In vitro enzyme assays to characterize recombinant Prdx6 molecules

  • Training of undergraduate summer rotation students

  • Preparation and submission of scientific manuscripts

• University of Utah - Postdoctoral Associate

  • Dates Employed 2002 – 2007

  • Characterization of novel peptide inhibitors of nicotinic acetylcholine receptors (nAChRs)

  • Lecturer, undergraduate biochemistry

  • RT-PCR, PCR and RACE-based discovery of novel toxin genes from marine snails

  • Chemical preparation of synthetic peptide toxins

  • Xenopus oocyte two electrode voltage clamp to characterize receptor-subtype-specificity of peptide toxins

  • Characterization of receptor-toxin interactions by mutagenesis.

  • Writing and submitting manuscripts and addressing reviewer comments

  • Supervision and training of junior laboratory personnel

• University of Utah - Graduate student

  • Dates Employed 1998 – 2001 (3 years )

  • Location Greater Salt Lake City Area

  • Graduate Student: University of Utah Biology Department, Salt Lake City

    • Thesis Project: Natural and combinatorial peptide toxins

    • Discovery of a novel, non-competitive peptide antagonist of the alpha7 nAChR

    • Cloning toxin genes from marine snails

    • Use of multiple techniques in molecular biology, cell biology and biochemistry including PCR, mutagenesis, subcloning, mammalian cell culture, transient transfections, cDNA preparation, RACE, reverse phase HPLC (analytical and preparative) and radio-ligand binding assays

• Teaching assistant, undergraduate Biochemistry

Education

• University of Utah - Degree Name Doctor of Philosophy - PhD - Field Of Study Biochemistry and Molecular Biology - Dates attended or expected graduation 1996 – 2001

• University of Bath - Degree Name Bachelor of Science - BS - Field Of Study Biochemistry - Dates attended or expected graduation 1991 – 1995

Arrest Report Overview: Michael Ellison

First Name: MICHAEL

Last Name: ELLISON

Gender: Male

Arrest Date: 2018-11-01 03:57:52

Age: 46

State: Colorado

County: Adams

Dob: 1972-07-25 00:00:00

Booking Date: 2018-11-01 15:57:52

Birth Year: 1972