Samantha Kendrick
Associate Professor
Also affiliated: University of Arizona (2009–2018); BioEnergetics (United States) (2009); Winthrop Rockefeller Foundation (2019–2022); Arizona Oncology (2014); University of Arizona Cancer Center (2015); Arizona State University (2009)
Faculty Researcher
Biochemistry & Molecular Biology, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Samantha Kendrick's research focuses on understanding the molecular mechanisms underlying cancer, with a particular emphasis on lymphoma and other oncogenic processes. She investigates novel therapeutic targets, including specific DNA structures like G-quadruplexes and i-motifs, and their roles in gene regulation within cancer cells. Her work has explored the potential of targeting these structures with small molecules, as demonstrated by research on naptho(2,1-b)furan-1-ethanol derivatives against a novel G-quadruplex in the CARD11 oncogene promoter.
Kendrick's laboratory also examines the impact of various compounds on cancer and viral reactivation. This includes investigating the anti-COVID-19 drug remdesivir's role in promoting oncogenic herpesvirus reactivation and identifying natural compounds like tubercidin and lycorine HCl as potential treatments for small-cell lung cancer. Furthermore, her group has identified NEK2 as a therapeutic target and regulator of oncogenic pathways in lymphoma, developing bifunctional inhibitors for this purpose. Her research is supported by federal grants from the NIH/National Cancer Institute and the NSF, totaling over $1.2 million, and she collaborates extensively with colleagues at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 16
- Publications: 104
- Citations: 1,837
Selected Publications
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Human REV1 interacts with DHX36 to promote replication and tolerance of G-quadruplex DNA (2026)
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DNA secondary structures in <i>BCL2</i> and <i>MYC</i> elicit activation-induced cytidine deaminase binding and activity (2026)
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G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptor MYD88 (2025)
Federal Grants 2 $1,243,511 total
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Targeting unique DNA structures to repress oncogenic signaling in lymphoma DoD Principal Investigator
- Targeting unique DNA structures to repress oncogenic signaling in lymphoma US Department of Defense Principal Investigator
- Impact of DNA topology on facilitating mutational events in lymphoma American Cancer Society, Inc. Principal Investigator
- Seeds of Science Pilot award UAMS Internal Research Awards Principal Investigator
- Targeting oncogenic regulation through unique DNA structures in lymphoma NIH/NIGMS Principal Investigator
- ABI C. OBrien NIH COBRE FY26 Y4 State of Arkansas Principal Investigator
- Impact of HIV on lymphomagenesis NIH/NIGMS Principal Investigator
Collaboration Network
Top Collaborators
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Clinical implications of loss of bone marrow minimal residual disease negativity in multiple myeloma
- Persistent bone marrow minimal residual disease as a “high‐risk” disease feature in multiple myeloma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Targeting a Novel G-Quadruplex in the CARD11 Oncogene Promoter with Naptho(2,1-b)furan-1-ethanol,2-nitro- Requires the Nitro Group
- Development of Humanized Diffuse Large B-Cell Lymphoma Mouse Models
- The Anti-COVID-19 Drug Remdesivir Promotes Oncogenic Herpesvirus Reactivation through Regulation of Intracellular Signaling Pathways
- Identification of natural compounds tubercidin and lycorine HCl against small‐cell lung cancer and BCAT1 as a therapeutic target
- Oncolytic strategy using new bifunctional HDACs/BRD4 inhibitors against virus-associated lymphomas
- The Anti-COVID-19 Drug Remdesivir Promotes Oncogenic Herpesvirus Reactivation through Regulation of Intracellular Signaling Pathways
- Identification of natural compounds tubercidin and lycorine HCl against small‐cell lung cancer and BCAT1 as a therapeutic target
- Oncolytic strategy using new bifunctional HDACs/BRD4 inhibitors against virus-associated lymphomas
- The Anti-COVID-19 Drug Remdesivir Promotes Oncogenic Herpesvirus Reactivation through Regulation of Intracellular Signaling Pathways
- Identification of natural compounds tubercidin and lycorine HCl against small‐cell lung cancer and BCAT1 as a therapeutic target
- Oncolytic strategy using new bifunctional HDACs/BRD4 inhibitors against virus-associated lymphomas
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Targeting a Novel G-Quadruplex in the CARD11 Oncogene Promoter with Naptho(2,1-b)furan-1-ethanol,2-nitro- Requires the Nitro Group
- G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptor MYD88
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Targeting a Novel G-Quadruplex in the CARD11 Oncogene Promoter with Naptho(2,1-b)furan-1-ethanol,2-nitro- Requires the Nitro Group
- G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptor MYD88
- The i-Motif as a Molecular Target: More Than a Complementary DNA Secondary Structure
- G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptor MYD88
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