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Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-08
S
Samantha L. Kendrick
Federal Grant PI
Associate Professor
Also affiliated: University of Arizona (2009–2018); BIO5 Institute (2009); University of Arizona Cancer Center (2009–2015); Arizona State University (2009)
Biochemistry & Molecular Biology, College of Medicine
17 h-index
100 pubs
1,902 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Samantha L. Kendrick's research focuses on understanding the molecular mechanisms of cancer, particularly in relation to gene regulation and alternative DNA structures. She investigates the role of G-quadruplexes and i-motifs, non-canonical DNA secondary structures, in the promoter regions of oncogenes. Her work has explored how these structures, such as the i-motif in the BCL2 P1 promoter, can be modulated by small molecules to influence gene expression and potentially impact cancer progression. This research has led to publications on the dynamic character of these DNA structures and their function as regulatory elements.
Her federally funded research includes a PI role on a Partnership in Cancer Research (PCAR) grant from the NIH/National Cancer Institute, totaling $143,511, and a Co-PI role on a National Science Foundation grant for $1,100,000 studying the replication of G-quadruplex DNA by translesion polymerases. Kendrick has published over 100 research papers, accumulating approximately 1,860 citations and an h-index of 16. She collaborates extensively with colleagues at the University of Arkansas for Medical Sciences, including Ying-Zhi Xu, Mason McCrury, Kennith Swafford, and Syed Hassan Mehdi, with whom she shares a significant number of publications.
Metrics
- h-index: 17
- Publications: 100
- Citations: 1,902
Positions
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Associate Professor 2017–presentUniversity of Arkansas for Medical Sciences Biochemistry & Molecular Biology, College of Medicine Institutional directory
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 BCL2 and MYC 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
NIH
Contact PI
Sep 2020 - Apr 2031
NSF
Co-PI
May 2024 - Apr 2028
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
Ying-Zhi Xu
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
- Discovery of DNA G-Quadruplexes As a New Target for B-Cell Receptor Signaling Inhibition in Diffuse Large B-Cell Lymphoma
- Development of Humanized Diffuse Large B-Cell Lymphoma Mouse Models
Brendan Frett
University of Arkansas for Medical Sciences
4 shared publications
In database
- ProteoViz: a tool for the analysis and interactive visualization of phosphoproteomics data
- Intramolecular cyclization of imidazo[1,2- a ]pyridines via a silver mediated/palladium catalyzed C–H activation strategy
- 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
Jungang Chen
Winthrop Rockefeller Foundation (US)
4 shared publications
- 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
- Mechanistic Insights into Chemoresistance Mediated by Oncogenic Viruses in Lymphomas
Zhiqiang Qin
Winthrop Rockefeller Foundation
4 shared publications
In database
- 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
- Mechanistic Insights into Chemoresistance Mediated by Oncogenic Viruses in Lymphomas
Mason McCrury
University of Arkansas for Medical Sciences
4 shared publications
In database
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptor MYD88
- Targeting a Novel G-Quadruplex in the CARD11 Oncogene Promoter with Naptho(2,1-b)furan-1-ethanol,2-nitro- Requires the Nitro Group
- DNA secondary structures in BCL2 and MYC elicit activation-induced cytidine deaminase binding and activity
Debasmita Saha
University of Arkansas for Medical Sciences (US)
3 shared publications
- Intramolecular cyclization of imidazo[1,2- a ]pyridines via a silver mediated/palladium catalyzed C–H activation strategy
- 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
Hongyu Li
University of Arkansas for Medical Sciences (US)
3 shared publications
- ProteoViz: a tool for the analysis and interactive visualization of phosphoproteomics data
- Intramolecular cyclization of imidazo[1,2- a ]pyridines via a silver mediated/palladium catalyzed C–H activation strategy
- Oncolytic strategy using new bifunctional HDACs/BRD4 inhibitors against virus-associated lymphomas
Meera Mohan
Medical College of Wisconsin (US)
3 shared publications
- 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
Sharmilan Thanendrarajan
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Carolina Schinke
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Daisy Alapat
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Erming Tian
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Guido Tricot
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Frits van Rhee
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Maurizio Zangari
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
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