Darby G. Brooke

ORCID: 0000-0003-2450-8602
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About
Contact & Profiles
Research Areas
  • Epigenetics and DNA Methylation
  • Cancer-related gene regulation
  • Aldose Reductase and Taurine
  • Hormonal Regulation and Hypertension
  • Hormonal and reproductive studies
  • Carbohydrate Chemistry and Synthesis
  • RNA modifications and cancer
  • Histone Deacetylase Inhibitors Research
  • Free Radicals and Antioxidants
  • Computational Fluid Dynamics and Aerodynamics
  • Estrogen and related hormone effects
  • Fungal Plant Pathogen Control
  • Phytochemistry and Biological Activities
  • Catalytic Cross-Coupling Reactions
  • Cancer, Hypoxia, and Metabolism
  • Marine Ecology and Invasive Species
  • Quinazolinone synthesis and applications
  • Ginseng Biological Effects and Applications
  • Cancer Treatment and Pharmacology
  • Fluid Dynamics and Turbulent Flows
  • Marine Toxins and Detection Methods
  • Genetic and Kidney Cyst Diseases
  • Cancer therapeutics and mechanisms
  • Synthesis and Catalytic Reactions
  • Natural product bioactivities and synthesis

Weatherford College
2023

Cancer Society of New Zealand
2008-2018

University of Auckland
2008-2018

Cawthron Institute
2018

University of Canterbury
2008

James S. McDonnell Foundation
1978-1980

Abstract Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2′-deoxycytidine (decitabine) has provided an alternate approach to cancer therapy. We have shown previously that these drugs selectively rapidly induce degradation the maintenance DNA methyltransferase (DNMT) 1 a proteasomal pathway. Because toxicity compounds is largely due their incorporation into DNA, it critical explore novel, nonnucleoside can effectively reactivate genes. Here, we...

10.1158/0008-5472.can-08-3669 article EN Cancer Research 2009-05-06

A high-throughput screen identified 3-(3,4-dihydroisoquinolin-2(1H)-ylsulfonyl)benzoic acid as a novel, highly potent (low nM), and isoform-selective (1500-fold) inhibitor of aldo-keto reductase AKR1C3: target interest in both breast prostate cancer. Crystal structure studies showed that the carboxylate group occupies oxyanion hole enzyme, while sulfonamide provides correct twist to allow dihydroisoquinoline bind an adjacent hydrophobic pocket. SAR around this lead positioning was critical,...

10.1021/jm3007867 article EN Journal of Medicinal Chemistry 2012-08-09

AKR1C3 is a novel therapeutic target in castration-resistant prostate cancer (CRPC) and ER-positive breast because of its ability to produce testosterone 17β-estradiol intratumorally, thus promoting nuclear receptor signaling tumor progression. A panel CRPC, high/low AKR1C3-expressing cell lines were treated with SN33638, selective inhibitor AKR1C3, the presence hormone or prostaglandin precursors, prior evaluation proliferation levels 11β-prostaglandin F2α (11β-PGF2α), testosterone,...

10.3389/fonc.2014.00159 article EN cc-by Frontiers in Oncology 2014-06-18

A range of natural products from marine invertebrates, bacteria and fungi have been assessed as leads for nature-inspired antifouling (AF) biocides, but little attention has paid to microalgal-derived compounds. This study the AF activity spirocyclic imine portimine (1), which is produced by benthic mat-forming dinoflagellate Vulcanodinium rugosum. Portimine displayed potent in a panel four macrofouling bioassays (EC50 0.06–62.5 ng ml−1), this was distinct that related compounds...

10.1080/08927014.2018.1514461 article EN Biofouling 2018-09-14

Abstract While clinically useful, microtubule‐targeting agents are limited by factors that include their susceptibility to multidrug resistance. A series of aryl sulfonamides, terminally substituted with an amide or carboxylic acid, was synthesized and assayed for biological activity in two human cancer cell lines. The resulting antiproliferative data demonstrated superior a acid the para position. most potent compound ( 3 ) had IC 50 growth inhibition low micromolar range, caused cells...

10.1002/asia.201801313 article EN Chemistry - An Asian Journal 2018-10-12

Supplementary Figures 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity and Inducing Its Degradation

10.1158/0008-5472.22377989 preprint EN cc-by 2023-03-31

Supplementary Methods and Figure Legends 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity Inducing Its Degradation

10.1158/0008-5472.22377986 preprint EN cc-by 2023-03-31

Supplementary Methods and Figure Legends 1-2 from A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity Inducing Its Degradation

10.1158/0008-5472.22377986.v1 preprint EN cc-by 2023-03-30

Supplementary Figures 1-2 from A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity and Inducing Its Degradation

10.1158/0008-5472.22377989.v1 preprint EN cc-by 2023-03-30

<div>Abstract<p>Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2′-deoxycytidine (decitabine) has provided an alternate approach to cancer therapy. We have shown previously that these drugs selectively rapidly induce degradation the maintenance DNA methyltransferase (DNMT) 1 a proteasomal pathway. Because toxicity compounds is largely due their incorporation into DNA, it critical explore novel, nonnucleoside can effectively...

10.1158/0008-5472.c.6498779 preprint EN 2023-12-15

Supplementary Methods and Figure Legends 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity Inducing Its Degradation

10.1158/0008-5472.22377986.v2 preprint EN cc-by 2023-12-15

Supplementary Figures 1-2 from RETRACTED: A New Class of Quinoline-Based DNA Hypomethylating Agents Reactivates Tumor Suppressor Genes by Blocking Methyltransferase 1 Activity and Inducing Its Degradation

10.1158/0008-5472.22377989.v2 preprint EN cc-by 2023-12-15

<div>Abstract<p>Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2′-deoxycytidine (decitabine) has provided an alternate approach to cancer therapy. We have shown previously that these drugs selectively rapidly induce degradation the maintenance DNA methyltransferase (DNMT) 1 a proteasomal pathway. Because toxicity compounds is largely due their incorporation into DNA, it critical explore novel, nonnucleoside can effectively...

10.1158/0008-5472.c.6498779.v1 preprint EN 2023-03-30

<div>Abstract<p>Reactivation of silenced tumor suppressor genes by 5-azacytidine (Vidaza) and its congener 5-aza-2′-deoxycytidine (decitabine) has provided an alternate approach to cancer therapy. We have shown previously that these drugs selectively rapidly induce degradation the maintenance DNA methyltransferase (DNMT) 1 a proteasomal pathway. Because toxicity compounds is largely due their incorporation into DNA, it critical explore novel, nonnucleoside can effectively...

10.1158/0008-5472.c.6498779.v2 preprint EN 2023-12-15
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