Richard Gaynor

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Richard B. Gaynor is an American physician specializing in hematology-oncology, educator, drug developer, and business executive. He served as an Associate Professor of Medicine at UCLA School of Medicine (Los Angeles, CA) for nearly a decade, and subsequently as an endowed Professor of Medicine and Microbiology at the University of Texas Southwestern Medical School prior to joining the pharmaceutical industry in 2002. [1] [2] His research on NF-κB, IκB kinase, and other mechanisms regulating viral and cellular gene expression has been covered in leading subject reviews. [3] [4] [5] [6] He has been a top executive at several pharmaceutical companies, [7] with respect to the development and clinical testing of novel anticancer drugs and cell therapies. [8] [9] For over a decade and a half, he worked at Eli Lilly and Company, where he became the Senior Vice President of Oncology Clinical Development and Medical Affairs in 2013. [10] Gaynor was President of R&D at Neon Therapeutics from 2016 to 2020, when he became the President of BioNTech US, both pharmaceutical companies headquartered in Cambridge, MA. [11] [12] His honors include being elected a member of the American Society for Clinical Investigation, [13] and the Association of American Physicians. [14]

Contents

Education

In 1971 Gaynor graduated with a BS in Biology from Texas Tech University (Lubbock, TX). In 1975, he graduated with an MD from the University of Texas Southwestern Medical School (Dallas, TX). [1] [2] This was followed by internship (1975-1976) and residency (1976-1978) in internal medicine at Parkland Memorial Hospital (Dallas, TX). [1] [2] From 1978 to 1981 he was a Fellow at the Division of Hematology-Oncology, Department of Medicine, UCLA School of Medicine (Los Angeles, CA). TX). [1] [2] [15]

Career

In 1982 Gaynor became an Assistant Professor of Medicine at the Division of Hematology-Oncology, Department of Medicine, UCLA School of Medicine (Los Angeles, CA), where he further became an Associate Professor of Medicine in 1988 to 1991. [1] [2] [15] In 1991 he moved to the UT Southwestern Medical School (Dallas, TX), where he became Associate Professor of Medicine and Microbiology, Andrea L. Simmons Distinguished Chair in Cancer Virology, and Chief of the Division of Molecular Virology. At UT he further became a Full Professor and Chief of the Division of Hematology-Oncology in 1993, then interim Director (1997-1999), and Director of the Harold C. Simmons Comprehensive Cancer Center from 1999 to 2002. [16] During his time in Dallas, he was also a staff physician at the Dallas Veterans Affairs Medical Center, and an attending physician at Zale Lipshy University Hospital. [1] [2] [15]

In 2002, moved from UT and joined Eli Lilly and Company (Indianapolis, IN), where he remained until 2016, in positions as Vice President of Cancer Research and Clinical Investigation, and Senior Vice President of Global Oncology, Clinical and Product Development and Medical Affairs. [17] During his tenure at Lilly, the firm was involved in FDA approval of Gemcitabine for the treatment of ovarian cancer, [18] and directed clinical trials of Ramucirumab, Pemetrexed, Cetuximab, and Abemaciclib for a number of cancer treatment indications. [2]

He is the author of 140 publications indexed on Scopus (February 2022). [19] His research partly focused on the dysregulation of the nuclear factor NF-κB pathway in inflammation, autoimmunity, immunodeficiency, and neoplasia, and the options for its therapeutic targeting. [20] [21] His discoveries include the identification of IκB kinase as a second site of the anti-inflammatory action of aspirin. [22] His laboratory made noted insights into the regulation of retroviral gene expresión, [6] [23] some of which are referred on current entries on TAF1, MNAT1, and TARBP1. In 2014, he co-authored the AACR Cancer Progress Report. [24]

As a business executive, Gaynor was President of Research and Development at Neon Therapeutics, (Cambridge, MA) from 2016 to 2020. [11] Then, he became the President and Chief of Research and Development at BioNTech US (Cambridge, MA), his current position. [25] He is a member of the Board of Directors at Damon Runyon Cancer Research Foundation, [26] Alkermes PLC, [27] Infinity Pharmaceuticals, [28] and Zai Labs. [29] He is also a member of the Scientific Advisory Board at Leap Therapeutics. [30] He was also a member of technical boards of NPOs such as Damon Runyon Cancer Foundation, Walther Cancer Foundation the American Association for Cancer Research, and Stand Up to Cancer. [31]

Works

Research papers

Some of Gaynor's most cited research papers are: [32]

Related Research Articles

<span class="mw-page-title-main">NF-κB</span> Nuclear transcriptional activator that binds to enhancer elements in many different cell types

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a protein complex that controls transcription of DNA, cytokine production and cell survival. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.

<span class="mw-page-title-main">Richard Pestell</span> Australian oncologist and endocrinologist

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<span class="mw-page-title-main">IKBKG</span> Protein-coding gene in the species Homo sapiens

NF-kappa-B essential modulator (NEMO) also known as inhibitor of nuclear factor kappa-B kinase subunit gamma (IKK-γ) is a protein that in humans is encoded by the IKBKG gene. NEMO is a subunit of the IκB kinase complex that activates NF-κB. The human gene for IKBKG is located on the chromosome band Xq28. Multiple transcript variants encoding different isoforms have been found for this gene.

<span class="mw-page-title-main">CD27</span> Member of the tumor necrosis factor receptor superfamily.

CD27 is a member of the tumor necrosis factor receptor superfamily. It is currently of interest to immunologists as a co-stimulatory immune checkpoint molecule, and is the target of an anti-cancer drug in clinical trials.

<span class="mw-page-title-main">IKK2</span> Protein-coding gene in the species Homo sapiens

IKK-β also known as inhibitor of nuclear factor kappa-B kinase subunit beta is a protein that in humans is encoded by the IKBKB gene.

The IκB kinase is an enzyme complex that is involved in propagating the cellular response to inflammation, specifically the regulation of lymphocytes.

<span class="mw-page-title-main">IκBα</span> Protein-coding gene in the species Homo sapiens

IκBα is one member of a family of cellular proteins that function to inhibit the NF-κB transcription factor. IκBα inhibits NF-κB by masking the nuclear localization signals (NLS) of NF-κB proteins and keeping them sequestered in an inactive state in the cytoplasm. In addition, IκBα blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-κB's proper functioning.

<span class="mw-page-title-main">RELA</span> Protein-coding gene in the species Homo sapiens

Transcription factor p65 also known as nuclear factor NF-kappa-B p65 subunit is a protein that in humans is encoded by the RELA gene.

<span class="mw-page-title-main">CHUK</span> Protein-coding gene in the species Homo sapiens

Inhibitor of nuclear factor kappa-B kinase subunit alpha (IKK-α) also known as IKK1 or conserved helix-loop-helix ubiquitous kinase (CHUK) is a protein kinase that in humans is encoded by the CHUK gene. IKK-α is part of the IκB kinase complex that plays an important role in regulating the NF-κB transcription factor. However, IKK-α has many additional cellular targets, and is thought to function independently of the NF-κB pathway to regulate epidermal differentiation.

<span class="mw-page-title-main">MAP3K14</span> Protein-coding gene in the species Homo sapiens

Mitogen-activated protein kinase kinase kinase 14 also known as NF-kappa-B-inducing kinase (NIK) is an enzyme that in humans is encoded by the MAP3K14 gene.

<span class="mw-page-title-main">TANK-binding kinase 1</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">Oncology</span> Branch of medicine dealing with, or specializing in, cancer

Oncology is a branch of medicine that deals with the study, treatment, diagnosis and prevention of tumors. A medical professional who practices oncology is an oncologist. The name's etymological origin is the Greek word ὄγκος (ónkos), meaning "tumor", "volume" or "mass". Oncology is concerned with:

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<span class="mw-page-title-main">NFKBID</span> Protein-coding gene in the species Homo sapiens

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, delta also known as IκBNS is a protein in humans that is encoded by the NFKBID gene.

The interleukin-1 receptor (IL-1R) associated kinase (IRAK) family plays a crucial role in the protective response to pathogens introduced into the human body by inducing acute inflammation followed by additional adaptive immune responses. IRAKs are essential components of the Interleukin-1 receptor signaling pathway and some Toll-like receptor signaling pathways. Toll-like receptors (TLRs) detect microorganisms by recognizing specific pathogen-associated molecular patterns (PAMPs) and IL-1R family members respond the interleukin-1 (IL-1) family cytokines. These receptors initiate an intracellular signaling cascade through adaptor proteins, primarily, MyD88. This is followed by the activation of IRAKs. TLRs and IL-1R members have a highly conserved amino acid sequence in their cytoplasmic domain called the Toll/Interleukin-1 (TIR) domain. The elicitation of different TLRs/IL-1Rs results in similar signaling cascades due to their homologous TIR motif leading to the activation of mitogen-activated protein kinases (MAPKs) and the IκB kinase (IKK) complex, which initiates a nuclear factor-κB (NF-κB) and AP-1-dependent transcriptional response of pro-inflammatory genes. Understanding the key players and their roles in the TLR/IL-1R pathway is important because the presence of mutations causing the abnormal regulation of Toll/IL-1R signaling leading to a variety of acute inflammatory and autoimmune diseases.

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References

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