Mark R. Kelley

ORCID: 0000-0002-6120-9532
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About
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Research Areas
  • DNA Repair Mechanisms
  • RNA modifications and cancer
  • Epigenetics and DNA Methylation
  • Cancer, Hypoxia, and Metabolism
  • Cancer therapeutics and mechanisms
  • CRISPR and Genetic Engineering
  • DNA and Nucleic Acid Chemistry
  • Biochemical and Molecular Research
  • PARP inhibition in cancer therapy
  • Cancer Genomics and Diagnostics
  • Cancer Treatment and Pharmacology
  • Acute Lymphoblastic Leukemia research
  • Advanced biosensing and bioanalysis techniques
  • Adenosine and Purinergic Signaling
  • Mitochondrial Function and Pathology
  • RNA Interference and Gene Delivery
  • Growth Hormone and Insulin-like Growth Factors
  • Pancreatic function and diabetes
  • ATP Synthase and ATPases Research
  • Polyomavirus and related diseases
  • Genomics, phytochemicals, and oxidative stress
  • Pancreatic and Hepatic Oncology Research
  • Hypothalamic control of reproductive hormones
  • Carcinogens and Genotoxicity Assessment
  • Chemical Reactions and Isotopes

Indiana University School of Medicine
2015-2024

Indiana University – Purdue University Indianapolis
2015-2024

Indiana University Health
2007-2024

University of Indianapolis
2001-2024

Battelle
2019-2021

Palmetto Hematology Oncology
2001-2019

Indiana University Indianapolis
2015-2019

University of Ljubljana
2018

University of Florida
2017

Indiana University
1994-2017

To update the ASCO guideline on recommended prevention and treatment approaches in management of chemotherapy-induced peripheral neuropathy (CIPN) adult cancer survivors.An Expert Panel conducted targeted systematic literature reviews to identify new studies.The search strategy identified 257 references, which led a full-text review 87 manuscripts. A total 3 reviews, 2 with meta-analyses, 28 primary trials for CIPN addition 14 related established CIPN, are included this update.The data...

10.1200/jco.20.01399 article EN Journal of Clinical Oncology 2020-07-14

The Notch locus is essential for proper differentiation of the ectoderm in Drosophila melanogaster. corresponds to a 37-kilobase transcription unit that codes major 10.4-kilobase polyadenylated RNA. DNA sequence this presented, except portions two largest intervening sequences. sequences also were obtained from three cDNA clones, allowing 5' and 3' ends gene be mapped, structures locations nine RNA coding regions determined. transcript encodes protein 2,703 amino acids. probably associated...

10.1128/mcb.6.9.3094 article EN Molecular and Cellular Biology 1986-09-01

The cancer chemopreventive properties of selenium compounds are well documented, yet little is known the mechanism(s) by which these agents inhibit carcinogenesis. We show that in form selenomethionine (SeMet) can activate p53 tumor suppressor protein a redox mechanism requires factor Ref1. Assays to measure direct reduction/oxidation showed SeMet-dependent response was blocked dominant–negative By using peptide containing only cysteine residues 275 and 277, we demonstrate importance...

10.1073/pnas.212319799 article EN Proceedings of the National Academy of Sciences 2002-09-30

Osteosarcoma is the most common highly malignant bone tumor with primary appearance during second and third decade of life. It associated a high risk relapse, possibly resulting from developed resistance to chemotherapy agents. As means overcome osteosarcoma cell and/or sensitize cells currently used chemotherapeutic treatments, we examined role human apurinic endonuclease 1 (APE1) in prognosis. Sixty samples archived conventional (intramedullary) were analyzed. APE1 protein was elevated 72%...

10.1158/1535-7163.679.3.6 article EN Molecular Cancer Therapeutics 2004-06-01

APE1/Ref-1 (hereafter, APE1), a DNA repair enzyme and transcriptional coactivator, is vital protein in mammals. Its role controlling cell growth the molecular mechanisms that fine-tune its different cellular functions are still not known. By an unbiased proteomic approach, we have identified characterized several novel APE1 partners which, unexpectedly, include number of proteins involved ribosome biogenesis RNA processing. In particular, interaction between nucleophosmin (NPM1) was...

10.1128/mcb.01337-08 article EN Molecular and Cellular Biology 2009-02-03

The DNA base excision-repair pathway is responsible for the repair of damage caused by oxidation/alkylation and protects cells against effects endogenous exogenous agents. Removal damaged creates a baseless (AP) site. AP endonuclease1 (Ape1) acts on this site to continue BER-pathway repair. Failure sites leads strand breaks cytotoxicity. In addition role Ape1, it also functions as major redox-signaling factor reduce activate transcription factors such AP1, p53, HIF-1α, others that control...

10.1089/ars.2008.2120 article EN Antioxidants and Redox Signaling 2008-07-17

Reduction-oxidation factor 1-apurinic/apyrimidinic endonuclease (Ref-1/APE1) is a critical node in tumor cells, both as redox regulator of transcription activation and part the DNA damage response. As signaling protein, Ref-1/APE1 enhances transcriptional activity STAT3, HIF-1α, nuclear kappa B, other factors to promote growth, migration, survival cells well inflammation angiogenesis microenvironment. activated variety cancers, including prostate, colon, pancreatic, ovarian, lung leukemias,...

10.1038/s41698-017-0023-0 article EN cc-by npj Precision Oncology 2017-05-31

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related mortality in United States. Aggressive treatment regimens have not changed disease course, and median survival has just recently reached a year. Several mechanisms are proposed to play role PDAC therapeutic resistance, including hypoxia, which creates more aggressive phenotype with increased metastatic potential impaired efficacy. AP Endonuclease-1/Redox Effector Factor 1 (APE1/Ref-1) multifunctional...

10.1158/1535-7163.mct-16-0253 article EN Molecular Cancer Therapeutics 2016-08-18

Although chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of platinum drugs, the mechanisms this toxicity remain unknown. Previous work in our laboratory suggests that cisplatin-induced CIPN secondary to DNA damage which susceptible base excision repair (BER). To further examine hypothesis, we studied effects cisplatin, oxaliplatin, and carboplatin on cell survival, damage, ROS production, functional endpoints rat sensory neurons culture absence or presence...

10.1371/journal.pone.0106485 article EN cc-by PLoS ONE 2014-09-04

Purpose: Analysis of patients with late relapse (LR) germ cell tumor (GCT) reports on clinical characteristics, outcomes, and molecular cytogenetic features. Patients Methods: Eighty-three evaluated at Indiana University from 1993 through 2000 for GCT more than 2 years initial therapy were reviewed. Available specimens investigated expression the transcription regulator FoxD3 apurinic/apyrimidinic endonuclease presence chromosome 12 abnormalities. Results: Median interval presentation to LR...

10.1200/jco.2003.03.019 article EN Journal of Clinical Oncology 2002-12-28

The POU homeodomain protein Oct-4 and the Forkhead Box FoxD3 (previously Genesis) are transcriptional regulators expressed in embryonic stem cells. Down-regulation of during gastrulation is essential for proper endoderm development. After gastrulation, generally down-regulated early formation, although it specifically remains neural crest. In these studies, we have found that can bind to identical regulatory DNA sequences. addition, physically interacted with DNA-binding domain....

10.1073/pnas.062041099 article EN Proceedings of the National Academy of Sciences 2002-03-12

Oxidative damage to mitochondrial DNA (mtDNA) has been implicated as a causative factor in many disease processes and aging. We have recently discovered that different cell types vary their capacity repair this damage, variability correlates with ability withstand oxidative stress. To explore strategies enhance of lesions mtDNA, we constructed vector containing transport sequence upstream the for human 8-oxoguanine glycosylase. This enzyme is glycosylase/AP lyase participates purine lesions,...

10.1074/jbc.m000831200 article EN cc-by Journal of Biological Chemistry 2000-12-01
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