What is he best known for?
The fields of study he is best known for:
Mark R. Kelley mainly focuses on DNA repair, DNA- lyase, Molecular biology, AP site and Base excision repair.
The study incorporates disciplines such as DNA damage and Phosphorylation, Cell biology in addition to DNA repair.
Mark R. Kelley has researched DNA- lyase in several fields, including AP endonuclease, Cancer research, Transcription factor and Sarcoma.
His work deals with themes such as Cancer and Pathology, which intersect with Cancer research.
The Transcription factor study combines topics in areas such as DNA and Transfection.
The various areas that Mark R. Kelley examines in his Base excision repair study include Nuclear DNA, Mitochondrial DNA and DNA mismatch repair.
His most cited work include:
- Going APE over ref-1. (487 citations)
- The many functions of APE1/Ref-1: Not only a DNA repair enzyme (350 citations)
- The intracellular localization of APE1/Ref-1: more than a passive phenomenon? (305 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of study are DNA repair, Cancer research, Molecular biology, AP site and Base excision repair.
His biological study spans a wide range of topics, including Oxidative stress, DNA damage and Cell biology.
His Cancer research study combines topics from a wide range of disciplines, such as Cancer, Metastasis, Pancreatic cancer, Transcription factor and STAT3.
His Molecular biology research includes elements of 8-Oxoguanine, DNA glycosylase, Apoptosis and Gene, Transfection.
His AP site study focuses mostly on DNA- lyase and AP endonuclease.
His Base excision repair study combines topics from a wide range of disciplines, such as Cancer cell and Methyl methanesulfonate.
He most often published in these fields:
- DNA repair (39.33%)
- Cancer research (33.89%)
- Molecular biology (30.13%)
What were the highlights of his more recent work (between 2017-2021)?
- Cancer research (33.89%)
- Endonuclease (13.39%)
- Cancer (17.15%)
In recent papers he was focusing on the following fields of study:
Mark R. Kelley mostly deals with Cancer research, Endonuclease, Cancer, AP site and Transcription factor.
His Endonuclease research is multidisciplinary, relying on both Base excision repair and Retinal.
His study looks at the relationship between Base excision repair and topics such as Enzyme, which overlap with DNA repair.
His AP site research is under the purview of DNA damage.
His DNA damage study introduces a deeper knowledge of Biochemistry.
His biological study spans a wide range of topics, including Cell biology, Regulation of gene expression, Downregulation and upregulation and Stroma.
Between 2017 and 2021, his most popular works were:
- Inhibition of Inflammatory Signaling in Tet2 Mutant Preleukemic Cells Mitigates Stress-Induced Abnormalities and Clonal Hematopoiesis (81 citations)
- Prevention and management of chemotherapy-induced peripheral neuropathy in survivors of adult cancers: ASCO guideline update (34 citations)
- Blocking HIF signaling via novel inhibitors of CA9 and APE1/Ref-1 dramatically affects pancreatic cancer cell survival (13 citations)
In his most recent research, the most cited papers focused on:
Mark R. Kelley spends much of his time researching Cancer research, Endonuclease, Cancer, Transcription factor and STAT3.
His study in Cancer research is interdisciplinary in nature, drawing from both Bladder cancer, Inflammation, Immunotherapy, Ape1 ref 1 and Effector.
His research integrates issues of Base excision repair and Retinal in his study of Endonuclease.
His work carried out in the field of Cancer brings together such families of science as Oncology, MEDLINE, Chemotherapy, Guideline and Chemotherapy-induced peripheral neuropathy.
The study incorporates disciplines such as Cell culture, Stroma, Reactive oxygen species, Downregulation and upregulation and Regulation of gene expression in addition to Transcription factor.
His research in AP site intersects with topics in Coactivator, Signal transduction, Cell biology and DNA Repair Pathway.
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