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Your search keyword '"Nelson, William G."' showing total 21 results
Start Over Author "Nelson, William G." Journal cancer research
21 results on '"Nelson, William G."'

2. Abstract 680: Topoisomerase 2 beta facilitates chromatin reorganization during Androgen Receptor induced transcription and contributes to chromoplexy in prostate cancer

Author

Pham, Minh-Tam N., primary, Haffner, Michael C., additional, Wick, Heather C., additional, Coulter, Jonathan B., additional, Gupta, Anuj, additional, Chikarmane, Roshan V., additional, Gupta, Harshath, additional, Wheelan, Sarah, additional, Nelson, William G., additional, and Yegnasubramanian, Srinivasan, additional

Published
2022
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4. Abstract 5881: Novel inhibitors of the epigenetic reader protein MBD2

Author

Giovinazzo, Hugh, primary, Reichert, Zachary R., additional, Bergman, Andries, additional, Lin, Xiaohui, additional, Wyhs, Nicolas, additional, Esopi, David, additional, Vaghasia, Ajay, additional, Liu, Jianyong, additional, Jain, Yash, additional, Bhamidipati, Akshay, additional, Steinberg, Ruchama, additional, Speed, Traci, additional, Vaughn, Matthew, additional, Zhang, Yonggang, additional, Brennen, Nate, additional, Deweese, Theodore, additional, Yegnasubramanian, Srinivasan, additional, and Nelson, William G., additional

Published
2018
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10. Abstract 1773: Nucleotide-resolution genomic breakpoint analysis of TMPRSS2-ERG rearrangements in prostate cancer by target-capture next-generation sequencing.

Author

Weier, Christopher, primary, Haffner, Michael, additional, Mosbruger, Timothy, additional, Esopi, David, additional, Hicks, Jessica, additional, Zheng, Qizhi, additional, Isaacs, William B., additional, De Marzo, Angelo M., additional, Nelson, William G., additional, and Yegnasubramanian, Srinivasan, additional

Published
2013
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13. Abstract 1921: Body fatness and sex steroid hormone concentrations in US men – Results from NHANES III

Author

Rohrmann, Sabine, primary, Shiels, Meredith S., additional, Lopez, David S., additional, Rifai, Nader, additional, Nelson, William G., additional, Kanarek, Norma, additional, Guallar, Eliseo, additional, Menke, Andy, additional, Joshu, Corinne E., additional, Feinlieb, Manning, additional, Sutcliffe, Siobhan, additional, and Platz, Elizabeth A., additional

Published
2011
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15. DNA Hypomethylation Arises Later in Prostate Cancer Progression than CpG Island Hypermethylation and Contributes to Metastatic Tumor Heterogeneity

Author

Yegnasubramanian, Srinivasan, primary, Haffner, Michael C., additional, Zhang, Yonggang, additional, Gurel, Bora, additional, Cornish, Toby C., additional, Wu, Zhijin, additional, Irizarry, Rafael A., additional, Morgan, James, additional, Hicks, Jessica, additional, DeWeese, Theodore L., additional, Isaacs, William B., additional, Bova, G. Steven, additional, De Marzo, Angelo M., additional, and Nelson, William G., additional

Published
2008
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19. Enhanced radiation and chemotherapy-mediated cell killing of human cancer cells by small inhibitory RNA silencing of DNA repair factors.

Author

Collis SJ, Swartz MJ, Nelson WG, and DeWeese TL

Subjects
Ataxia Telangiectasia Mutated Proteins, Cell Cycle Proteins biosynthesis, Cell Cycle Proteins genetics, DNA Damage, DNA-Activated Protein Kinase, Down-Regulation, Gene Expression Regulation, Neoplastic, Humans, Male, Nuclear Proteins, Prostatic Neoplasms drug therapy, Prostatic Neoplasms genetics, Prostatic Neoplasms radiotherapy, Protein Serine-Threonine Kinases biosynthesis, Protein Serine-Threonine Kinases genetics, RNA, Messenger genetics, Radiation-Sensitizing Agents pharmacology, Transfection, Tumor Cells, Cultured, Tumor Suppressor Proteins, DNA Repair genetics, DNA-Binding Proteins, Genetic Therapy methods, Prostatic Neoplasms therapy, RNA, Small Interfering genetics
Abstract

Recent developments in the use of small inhibitory RNA molecules (siRNAs) to inhibit specific protein expression have highlighted the potential use of siRNA as a therapeutic agent. The double-strand break signaling/repair proteins ATM, ATR, and DNA-dependent protein kinase catalytic subunit (DNA-PK(cs)) are attractive targets to confer enhanced radio and chemosensitivity to tumor cells. We have designed and exogenously delivered plasmids encoding siRNAs targeting these critical kinases to human cancer cells to assess the feasibility of this concept as a clinically translatable experimental therapeutic. siRNA led to a approximately 90% reduction in target protein expression. siRNAs targeting ATM and DNA-PK(cs) gave rise to a dose-reduction factor of approximately 1.4 compared with untransfected and control vector-transfected cells at the clinically relevant radiation doses. This was greater than the radiosensitivity achieved using the phosphatidylinositol 3'-kinase inhibitor Wortmannin or DNA-PK(cs) competitive inhibitor LY294002. A similar increased sensitivity to the alkylating agent methyl methanesulfonate (MMS) was also observed for siRNA-mediated ATR silencing. Together, these data provide strong evidence for the potential use of siRNA as a novel radiation/chemotherapy-sensitizing agent.

Published
2003

20. Methyl-CpG-binding domain protein-2 mediates transcriptional repression associated with hypermethylated GSTP1 CpG islands in MCF-7 breast cancer cells.

Author

Lin X and Nelson WG

Subjects
Alleles, Blotting, Northern, Breast Neoplasms metabolism, CpG Islands, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Gene Silencing, Glutathione S-Transferase pi, Humans, Methyl-CpG-Binding Protein 2, Promoter Regions, Genetic, Tumor Cells, Cultured, Breast Neoplasms genetics, Chromosomal Proteins, Non-Histone, DNA Methylation, DNA-Binding Proteins physiology, Glutathione Transferase genetics, Isoenzymes genetics, Repressor Proteins physiology
Abstract

GSTP1, encoding the pi-class glutathione S-transferase, is commonly inactivated by somatic CpGisland hypermethylation in cancers of the prostate, liver, and breast. We report here thathypermethylation of CpG dinucleotides at the 5' transcriptional regulatory region was sufficient to inhibit GSTP1 transcription in MCF-7 breast cancer cells and that repression of GSTP1 transcription was mediated in part by the methyl-CpG-binding domain (MBD) protein MBD2. MCF-7 breast cancer cells contained only hypermethylated GSTP1 CpG island alleles and failed to express GSTP1 mRNA or GSTP1 polypeptides. In contrast, MCF-7/ADR cells contained only unmethylated GSTP1 CpG island alleles and exhibited abundant GSTP1 expression. Chromatin immunoprecipitation analysis detected the presence of MBD2 and DNMT1 at the GSTP1 promoter in MCF-7 breast cancer cells but not in MCF-7/ADR breast cancer cells. In a test of the contribution of MBD2 to GSTP1 repression in MCF-7 breast cancer cells, transfection of small interference RNA complementary to MBD2 mRNA into MCF-7 cells both reduced MBD2 polypeptide levels and stimulated GSTP1 mRNA expression. These findings implicate MBD2 in GSTP1 silencing associated with somatic GSTP1 CpG island hypermethylation in breast cancer cells.

Published
2003

21. 8-Hydroxyguanosine repair is defective in some microsatellite stable colorectal cancer cells.

Author

Parker AR, O'Meally RN, Oliver DH, Hua L, Nelson WG, DeWeese TL, and Eshleman JR

Subjects
Adaptor Proteins, Signal Transducing, Base Pair Mismatch, Colorectal Neoplasms metabolism, DNA, Complementary genetics, DNA, Neoplasm genetics, DNA, Neoplasm metabolism, Fungal Proteins biosynthesis, Fungal Proteins genetics, Humans, Mutation, N-Glycosyl Hydrolases biosynthesis, N-Glycosyl Hydrolases genetics, RNA, Messenger genetics, RNA, Messenger metabolism, Tumor Cells, Cultured, Colorectal Neoplasms genetics, DNA Glycosylases, DNA Repair, Guanine analogs & derivatives, Guanine metabolism, Membrane Proteins, Microsatellite Repeats genetics, Saccharomyces cerevisiae Proteins
Abstract

Mutator phenotypes are involved in the carcinogenesis of some cancers, e.g., defects in mismatch repair produce a mutator phenotype that drives carcinogenesis and causes microsatellite instability in hereditary nonpolyposis colon cancers and some sporadic colorectal cancers (CRC). Less understood, however, is the potential role of mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis. A novel transversion mutator phenotype was reported recently in an MSS CRC cell line. We hypothesized that 8-hydroxyguanosine could be involved and found elevations in 5 of 15 (33%) MSS CRC cell lines analyzed. Repair of an adenine*8-hydroxyguanosine mispair was functionally defective in the same five cell lines. The human MutY homologue transcript and MutY homologue protein levels were also decreased. These findings may reflect a MSS mutator phenotype contributing to the development of CRC.

Published
2002

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