Search

Your search keyword '"Esopi, David"' showing total 153 results
Start Over Author "Esopi, David"
153 results on '"Esopi, David"'

1. CD38 is methylated in prostate cancer and regulates extracellular NAD+

Author

Mottahedeh, Jack, Haffner, Michael C, Grogan, Tristan R, Hashimoto, Takao, Crowell, Preston D, Beltran, Himisha, Sboner, Andrea, Bareja, Rohan, Esopi, David, Isaacs, William B, Yegnasubramanian, Srinivasan, Rettig, Matthew B, Elashoff, David A, Platz, Elizabeth A, De Marzo, Angelo M, Teitell, Michael A, and Goldstein, Andrew S

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Genetics, Urologic Diseases, Aging, Cancer, 2.1 Biological and endogenous factors, Prostate, CD38, NAD(+), Methylation, NAD+, Medical biochemistry and metabolomics, Oncology and carcinogenesis
Abstract

BackgroundCancer cell metabolism requires sustained pools of intracellular nicotinamide adenine dinucleotide (NAD+) which is maintained by a balance of NAD+ hydrolase activity and NAD+ salvage activity. We recently reported that human prostate cancer can be initiated following oncogene expression in progenitor-like luminal cells marked by low expression of the NAD+-consuming enzyme CD38. CD38 expression is reduced in prostate cancer compared to benign prostate, suggesting that tumor cells may reduce CD38 expression in order to enhance pools of NAD+. However, little is known about how CD38 expression is repressed in advanced prostate cancer and whether CD38 plays a role in regulating NAD+ levels in prostate epithelial cells.MethodsCD38 expression, its association with recurrence after prostatectomy for clinically localized prostate cancer, and DNA methylation of the CD38 promoter were evaluated in human prostate tissues representing various stages of disease progression. CD38 was inducibly over-expressed in benign and malignant human prostate cell lines in order to determine the effects on cell proliferation and levels of NAD+ and NADH. NAD+ and NADH were also measured in urogenital tissues from wild-type and CD38 knockout mice.ResultsCD38 mRNA expression was reduced in metastatic castration-resistant prostate cancer compared to localized prostate cancer. In a large cohort of men undergoing radical prostatectomy, CD38 protein expression was inversely correlated with recurrence. We identified methylation of the CD38 promoter in primary and metastatic prostate cancer. Over-expression of wild-type CD38, but not an NAD+ hydrolase-deficient mutant, depleted extracellular NAD+ levels in benign and malignant prostate cell lines. However, expression of CD38 did not significantly alter intracellular NAD+ levels in human prostate cell lines grown in vitro and in urogenital tissues isolated from wild-type and CD38 knockout mice.ConclusionsCD38 protein expression in prostate cancer is associated with risk of recurrence. Methylation results suggest that CD38 is epigenetically regulated in localized and metastatic prostate cancer tissues. Our study provides support for CD38 as a regulator of extracellular, but not intracellular, NAD+ in epithelial cells. These findings suggest that repression of CD38 by methylation may serve to increase the availability of extracellular NAD+ in prostate cancer tissues.

Published
2018

2. Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1-mediated cell-intrinsic resistance

Author

Liu, Jianyong, primary, He, Qing-Li, additional, Zhou, Jianya, additional, Chikarmane, Roshan, additional, Hauk, Glenn, additional, Rachakonda, Archana, additional, Vaghasia, Ajay M., additional, Castagna, Nicole, additional, Steinberg, Ruchama C., additional, Pham, Minh-Tam, additional, Anders, Nicole M., additional, Wanjiku, Teresia M., additional, Nuhn, Philipp, additional, Shim, Joong Sup, additional, Giovinazzo, Hugh, additional, Esopi, David M., additional, Kim, Kunhwa, additional, Coulter, Jonathan, additional, Wang, Rulin, additional, Zhou, Jianying, additional, Rudek, Michelle A., additional, Berger, James M., additional, Liu, Jun O., additional, Nelson, William G., additional, and Yegnasubramanian, Srinivasan, additional

Published
2024
Full Text
View/download PDF

4. Comprehensive Evaluation of Programmed Death-Ligand 1 Expression in Primary and Metastatic Prostate Cancer

Author

Haffner, Michael C., Guner, Gunes, Taheri, Diana, Netto, George J., Palsgrove, Doreen N., Zheng, Qizhi, Guedes, Liana Benevides, Kim, Kunhwa, Tsai, Harrison, Esopi, David M., Lotan, Tamara L., Sharma, Rajni, Meeker, Alan K., Chinnaiyan, Arul M., Nelson, William G., Yegnasubramanian, Srinivasan, Luo, Jun, Mehra, Rohit, Antonarakis, Emmanuel S., Drake, Charles G., and De Marzo, Angelo M.

Published
2018
Full Text
View/download PDF

9. Data from PTEN Protein Loss by Immunostaining: Analytic Validation and Prognostic Indicator for a High Risk Surgical Cohort of Prostate Cancer Patients

Author

Lotan, Tamara L., primary, Gurel, Bora, primary, Sutcliffe, Siobhan, primary, Esopi, David, primary, Liu, Wennuan, primary, Xu, Jianfeng, primary, Hicks, Jessica L., primary, Park, Ben H., primary, Humphreys, Elizabeth, primary, Partin, Alan W., primary, Han, Misop, primary, Netto, George J., primary, Isaacs, William B., primary, and De Marzo, Angelo M., primary

Published
2023
Full Text
View/download PDF

10. Supplementary Table 1 from PTEN Protein Loss by Immunostaining: Analytic Validation and Prognostic Indicator for a High Risk Surgical Cohort of Prostate Cancer Patients

Author

Lotan, Tamara L., primary, Gurel, Bora, primary, Sutcliffe, Siobhan, primary, Esopi, David, primary, Liu, Wennuan, primary, Xu, Jianfeng, primary, Hicks, Jessica L., primary, Park, Ben H., primary, Humphreys, Elizabeth, primary, Partin, Alan W., primary, Han, Misop, primary, Netto, George J., primary, Isaacs, William B., primary, and De Marzo, Angelo M., primary

Published
2023
Full Text
View/download PDF

13. Supplementary Figure S5. SPARCL-1 coated beads do not reinforce cellular traction. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

14. Supplementary Figure S7. Responses to SPARCL1-coated beads are concentration dependent. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

15. Data from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

16. Supplementary Figure S3. The tumor microenvironment in Sparcl1-/- models. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

17. Supplementary Figure S6. SPARCL1 engages cell-ECM interactions. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

18. Supplementary Figure S2. AR directly represses SPARCL1 expression in prostate cancer. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

19. Supplementary Figure S4. SPARCL1 inhibits cytoskeletal remodeling. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

20. Supplementary Figure S1. Androgen suppresses SPARCL1 expression. from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

21. Supplementary Materials and Methods and Supplementary Figure Legends from Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., primary, Simons, Brian W., primary, Huang, Jessie, primary, Miller, Rebecca M., primary, Shinder, Brian, primary, Haffner, Michael C., primary, Esopi, David, primary, Kimura, Yasunori, primary, Jabbari, Javaneh, primary, Ross, Ashley E., primary, Erho, Nicholas, primary, Vergara, Ismael A., primary, Faraj, Sheila F., primary, Davicioni, Elai, primary, Netto, George J., primary, Yegnasubramanian, Srinivasan, primary, An, Steven S., primary, and Schaeffer, Edward M., primary

Published
2023
Full Text
View/download PDF

23. A Protein-Truncating HSD17B13 Variant and Protection from Chronic Liver Disease

Author

Abul-Husn, Noura S., Cheng, Xiping, Li, Alexander H., Xin, Yurong, Schurmann, Claudia, Stevis, Panayiotis, Liu, Yashu, Kozlitina, Julia, Stender, Stefan, Wood, Craig G., Stepanchick, Ann N., Still, Matthew D., McCarthy, Shane, OʼDushlaine, Colm, Packer, Jonathan S., Balasubramanian, Suganthi, Gosalia, Nehal, Esopi, David, Kim, Sun Y., Mukherjee, Semanti, Lopez, Alexander E., Fuller, Erin D., Penn, John, Chu, Xin, Luo, Jonathan Z., Mirshahi, Uyenlinh L., Carey, David J., Still, Christopher D., Feldman, Michael D., Small, Aeron, Damrauer, Scott M., Rader, Daniel J., Zambrowicz, Brian, Olson, William, Murphy, Andrew J., Borecki, Ingrid B., Shuldiner, Alan R., Reid, Jeffrey G., Overton, John D., Yancopoulos, George D., Hobbs, Helen H., Cohen, Jonathan C., Gottesman, Omri, Teslovich, Tanya M., Baras, Aris, Mirshahi, Tooraj, Gromada, Jesper, and Dewey, Frederick E.

Published
2018
Full Text
View/download PDF

25. AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination

Author

Haffner, Michael C., Esopi, David M., Chaux, Alcides, Gürel, Meltem, Ghosh, Susmita, Vaghasia, Ajay M., Tsai, Harrison, Kim, Kunhwa, Castagna, Nicole, Lam, Hong, Hicks, Jessica, Wyhs, Nicolas, Biswal Shinohara, Debika, Hurley, Paula J., Simons, Brian W., Schaeffer, Edward M., Lotan, Tamara L., Isaacs, William B., Netto, George J., De Marzo, Angelo M., Nelson, William G., An, Steven S., and Yegnasubramanian, Srinivasan

Published
2017
Full Text
View/download PDF

26. Molecular evidence that invasive adenocarcinoma can mimic prostatic intraepithelial neoplasia (PIN) and intraductal carcinoma through retrograde glandular colonization

Author

Haffner, Michael C, Weier, Christopher, Xu, Meng Meng, Vaghasia, Ajay, Gürel, Bora, Gümüşkaya, Berrak, Esopi, David M, Fedor, Helen, Tan, Hsueh-Li, Kulac, Ibrahim, Hicks, Jessica, Isaacs, William B, Lotan, Tamara L, Nelson, William G, Yegnasubramanian, Srinivasan, and De Marzo, Angelo M

Published
2016
Full Text
View/download PDF

27. Phenotypic characterization of two novel cell line models of castration‐resistant prostate cancer

Author

Haffner, Michael C., primary, Bhamidipati, Akshay, additional, Tsai, Harrison K., additional, Esopi, David M., additional, Vaghasia, Ajay M., additional, Low, Jin‐Yih, additional, Patel, Radhika A., additional, Guner, Gunes, additional, Pham, Minh‐Tam, additional, Castagna, Nicole, additional, Hicks, Jessica, additional, Wyhs, Nicolas, additional, Aebersold, Ruedi, additional, De Marzo, Angelo M., additional, Nelson, William G., additional, Guo, Tiannan, additional, and Yegnasubramanian, Srinivasan, additional

Published
2021
Full Text
View/download PDF

28. Tracking the clonal origin of lethal prostate cancer

Author

Haffner, Michael C., Mosbruger, Timothy, Esopi, David M., Fedor, Helen, Heaphy, Christopher M., Walker, David A., Adejola, Nkosi, Gürel, Meltem, Hicks, Jessica, Meeker, Alan K., Halushka, Marc K., Simons, Jonathan W., Isaacs, William B., De Marzo, Angelo M., Nelson, William G., and Yegnasubramanian, Srinivasan

Published
2013
Full Text
View/download PDF

32. A high-throughput screen of pharmacologically active compounds for inhibitors of UHRF1 reveals epigenetic activity of anthracycline derivative chemotherapeutic drugs

Author

Giovinazzo, Hugh, primary, Walker, David, additional, Wyhs, Nicolas, additional, Liu, Jianyong, additional, Esopi, David M., additional, Vaghasia, Ajay M., additional, Jain, Yash, additional, Bhamidipati, Akshay, additional, Zhou, Jianya, additional, Nelson, William G., additional, and Yegnasubramanian, Srinivasan, additional

Published
2019
Full Text
View/download PDF

33. Chromosome-wide mapping of DNA methylation patterns in normal and malignant prostate cells reveals pervasive methylation of gene-associated and conserved intergenic sequences

Author

De Marzo Angelo M, Zheng Qizhi, Carvalho Benilton, Morgan James D, He Tony L, Badrinath Raghav, Aryee Martin J, Esopi David, Haffner Michael C, Wu Zhijin, Yegnasubramanian Srinivasan, Irizarry Rafael A, and Nelson William G

Subjects
DNA methylation, prostate cancer, tiling microarray, epigenetics, methylated DNA binding domain, MBD-chip, ADAMTS1, SCARF2, DSCR9, HLCS, Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background DNA methylation has been linked to genome regulation and dysregulation in health and disease respectively, and methods for characterizing genomic DNA methylation patterns are rapidly emerging. We have developed/refined methods for enrichment of methylated genomic fragments using the methyl-binding domain of the human MBD2 protein (MBD2-MBD) followed by analysis with high-density tiling microarrays. This MBD-chip approach was used to characterize DNA methylation patterns across all non-repetitive sequences of human chromosomes 21 and 22 at high-resolution in normal and malignant prostate cells. Results Examining this data using computational methods that were designed specifically for DNA methylation tiling array data revealed widespread methylation of both gene promoter and non-promoter regions in cancer and normal cells. In addition to identifying several novel cancer hypermethylated 5' gene upstream regions that mediated epigenetic gene silencing, we also found several hypermethylated 3' gene downstream, intragenic and intergenic regions. The hypermethylated intragenic regions were highly enriched for overlap with intron-exon boundaries, suggesting a possible role in regulation of alternative transcriptional start sites, exon usage and/or splicing. The hypermethylated intergenic regions showed significant enrichment for conservation across vertebrate species. A sampling of these newly identified promoter (ADAMTS1 and SCARF2 genes) and non-promoter (downstream or within DSCR9, C21orf57 and HLCS genes) hypermethylated regions were effective in distinguishing malignant from normal prostate tissues and/or cell lines. Conclusions Comparison of chromosome-wide DNA methylation patterns in normal and malignant prostate cells revealed significant methylation of gene-proximal and conserved intergenic sequences. Such analyses can be easily extended for genome-wide methylation analysis in health and disease.

Published
2011
Full Text
View/download PDF

34. A high-throughput screen of pharmacologically active compounds for inhibitors of UHRF1 reveals epigenetic activity of anthracycline derivative chemotherapeutic drugs

Author

Giovinazzo, Hugh Walker, David Wyhs, Nicolas Liu, Jianyong Esopi, David M. Vaghasia, Ajay M. Jain, Yash Bhamidipati, Akshay Zhou, Jianya Nelson, William G. Yegnasubramanian, Srinivasan and Giovinazzo, Hugh Walker, David Wyhs, Nicolas Liu, Jianyong Esopi, David M. Vaghasia, Ajay M. Jain, Yash Bhamidipati, Akshay Zhou, Jianya Nelson, William G. Yegnasubramanian, Srinivasan

Abstract

DNA methylation can mediate epigenetic silencing of tumor suppressor and cancer protective genes. The protein ubiquitin-like containing PHD and ring finger domains 1 (UHRF1) is an essential component in cells for DNA methylation maintenance. The SET- and RING-associated (SRA) domain of UHRF1 can bind hemimethylated DNA, and mediate recruitment of DNA methyltransferases to copy the methylation pattern to the newly synthesized daughter strand. Loss of UHRF1 function can lead to demethylation and re-expression of epigenetically silenced tumor suppressor genes and can reduce cancer cell growth and survival. We created a high-throughput time-resolved fluorescence resonance energy transfer (TR-FRET) assay to screen for inhibitors capable of disrupting the interaction between the UHRF1-SRA domain and hemimethylated DNA. Using this assay (Z' factor of 0.74 in 384-well format) we screened the Library of Pharmacologically Active Compounds (LOPAC) for UHRF1-SRA inhibitors, and validated 7 hit compounds. These compounds included the anthracycline derivatives idarubicin and mitoxantrone, which are commonly used chemotherapeutic drugs known to mediate cytotoxicity by acting as class II topoisomerase (TOP2) poisons. In a panel of additional known topoisomerase poisons, only the anthracycline derivatives showed dose responsive inhibition of UHRF1-SRA. Additionally, mitoxantrone and doxorubicin showed dose-responsive global DNA demethylation and demonstrated a synergistic growth inhibition of multiple cancer cell lines when combined with the DNA methyltransferase (DNMT) inhibitor decitabine. These data validate a novel TR-FRET assay for identification of UHRF1 inhibitors, and revealed unexpected epigenetic properties of commonly used chemotherapeutic drugs that showed synergistic cytotoxicity of cancer cells when combined with a demethylating agent.

Published
2019

35. ATRX loss induces multiple hallmarks of the alternative lengthening of telomeres (ALT) phenotype in human glioma cell lines in a cell line-specific manner

Author

Brosnan-Cashman, Jacqueline A., primary, Yuan, Ming, additional, Graham, Mindy K., additional, Rizzo, Anthony J., additional, Myers, Kaylar M., additional, Davis, Christine, additional, Zhang, Rebecca, additional, Esopi, David M., additional, Raabe, Eric H., additional, Eberhart, Charles G., additional, Heaphy, Christopher M., additional, and Meeker, Alan K., additional

Published
2018
Full Text
View/download PDF

36. 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
Full Text
View/download PDF

38. A Protein-TruncatingHSD17B13Variant and Protection from Chronic Liver Disease

Author

Abul-Husn, Noura S., primary, Cheng, Xiping, additional, Li, Alexander H., additional, Xin, Yurong, additional, Schurmann, Claudia, additional, Stevis, Panayiotis, additional, Liu, Yashu, additional, Kozlitina, Julia, additional, Stender, Stefan, additional, Wood, G. Craig, additional, Stepanchick, Ann N., additional, Still, Matthew D., additional, McCarthy, Shane, additional, O’Dushlaine, Colm, additional, Packer, Jonathan S., additional, Balasubramanian, Suganthi, additional, Gosalia, Nehal, additional, Esopi, David, additional, Kim, Sun Y., additional, Mukherjee, Semanti, additional, Lopez, Alexander E., additional, Fuller, Erin D., additional, Penn, John, additional, Chu, Xin, additional, Luo, Jonathan Z., additional, Mirshahi, Uyenlinh L., additional, Carey, David J., additional, Still, Christopher D., additional, Feldman, Michael D., additional, Small, Aeron, additional, Damrauer, Scott M., additional, Rader, Daniel J., additional, Zambrowicz, Brian, additional, Olson, William, additional, Murphy, Andrew J., additional, Borecki, Ingrid B., additional, Shuldiner, Alan R., additional, Reid, Jeffrey G., additional, Overton, John D., additional, Yancopoulos, George D., additional, Hobbs, Helen H., additional, Cohen, Jonathan C., additional, Gottesman, Omri, additional, Teslovich, Tanya M., additional, Baras, Aris, additional, Mirshahi, Tooraj, additional, Gromada, Jesper, additional, and Dewey, Frederick E., additional

Published
2018
Full Text
View/download PDF

39. MYC drives overexpression of telomerase RNA ( hTR / TERC ) in prostate cancer

Author

Baena‐Del Valle, Javier A, primary, Zheng, Qizhi, additional, Esopi, David M, additional, Rubenstein, Michael, additional, Hubbard, Gretchen K, additional, Moncaliano, Maria C, additional, Hruszkewycz, Andrew, additional, Vaghasia, Ajay, additional, Yegnasubramanian, Srinivasan, additional, Wheelan, Sarah J, additional, Meeker, Alan K, additional, Heaphy, Christopher M, additional, Graham, Mindy K, additional, and De Marzo, Angelo M, additional

Published
2017
Full Text
View/download PDF

41. Abstract 3465: Context-dependent effects of ATRX loss on telomere biology in glioma cells

Author

Brosnan-Cashman, Jacqueline A., primary, Yuan, Ming, additional, Rizzo, Anthony J., additional, Myers, Kaylar M., additional, Barry, Walter T., additional, Davis, Christine, additional, Esopi, David M., additional, Rakheja, Dinesh, additional, Raabe, Eric H., additional, Eberhart, Charles G., additional, Heaphy, Christopher M., additional, and Meeker, Alan K., additional

Published
2017
Full Text
View/download PDF

44. Abstract LB-160: Human telomerase RNA component (hTR/TERC) is consistently overexpressed in prostate cancer, required for cell proliferation and is positively regulated by MYC

Author

Baena Del Valle, Javier A., primary, Zheng, Qizhi, additional, Rubenstein, Michael, additional, Meeker, Alan K., additional, Heaphy, Christopher M., additional, Hubbard, Gretchen, additional, Bieberich, Charles J., additional, Yegnasubramanian, Srinivasan, additional, Esopi, David, additional, Wheelan, Sarah J., additional, and De Marzo, Angelo M., additional

Published
2016
Full Text
View/download PDF

46. Molecular evidence that invasive adenocarcinoma can mimic prostatic intraepithelial neoplasia ( PIN ) and intraductal carcinoma through retrograde glandular colonization

Author

Haffner, Michael C, primary, Weier, Christopher, additional, Xu, Meng Meng, additional, Vaghasia, Ajay, additional, Gürel, Bora, additional, Gümüşkaya, Berrak, additional, Esopi, David M, additional, Fedor, Helen, additional, Tan, Hsueh‐Li, additional, Kulac, Ibrahim, additional, Hicks, Jessica, additional, Isaacs, William B, additional, Lotan, Tamara L, additional, Nelson, William G, additional, Yegnasubramanian, Srinivasan, additional, and De Marzo, Angelo M, additional

Published
2015
Full Text
View/download PDF

47. Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Author

Hurley, Paula J., primary, Hughes, Robert M., additional, Simons, Brian W., additional, Huang, Jessie, additional, Miller, Rebecca M., additional, Shinder, Brian, additional, Haffner, Michael C., additional, Esopi, David, additional, Kimura, Yasunori, additional, Jabbari, Javaneh, additional, Ross, Ashley E., additional, Erho, Nicholas, additional, Vergara, Ismael A., additional, Faraj, Sheila F., additional, Davicioni, Elai, additional, Netto, George J., additional, Yegnasubramanian, Srinivasan, additional, An, Steven S., additional, and Schaeffer, Edward M., additional

Published
2015
Full Text
View/download PDF

50. Loss of Keap1 Function in Prostate Cancer Cells Causes Chemo- and Radio-resistance and Promotes Tumor Growth

Author

Zhang, Ping, Singh, Anju, Yegnasubramanian, Srinivasan, Esopi, David, Kombairaju, Ponvijay, Bodas, Manish, Wu, Hailong, Bova, G. Steven, and Biswal, Shyam

Subjects
Male, Kelch-Like ECH-Associated Protein 1, NF-E2-Related Factor 2, Intracellular Signaling Peptides and Proteins, Mice, Nude, Prostatic Neoplasms, respiratory system, DNA Methylation, Article, Gene Expression Regulation, Neoplastic, Cytoskeletal Proteins, Mice, Drug Resistance, Neoplasm, Neoplasms, Mutation, Animals, Humans, Reactive Oxygen Species, Adaptor Proteins, Signal Transducing
Abstract

Loss-of-function mutations in the nuclear factor erythroid-2-related factor 2 (Nrf2) inhibitor Kelch-like ECH-associated protein 1 (Keap1) result in increased Nrf2 activity in non-small cell lung cancer and confer therapeutic resistance. We detected point mutations in Keap1 gene, leading to nonconservative amino acid substitutions in prostate cancer cells. We found novel transcriptional and posttranscriptional mechanisms of Keap1 inactivation, such as promoter CpG island hypermethylation and aberrant splicing of Keap1, in DU-145 cells. Very low levels of Keap1 mRNA were detected in DU-145 cells, which significantly increased by treatment with DNA methyltransferase inhibitor 5-aza-deoxycytidine. The loss of Keap1 function led to an enhanced activity of Nrf2 and its downstream electrophile/drug detoxification pathway. Inhibition of Nrf2 expression in DU-145 cells by RNA interference attenuated the expression of glutathione, thioredoxin, and the drug efflux pathways involved in counteracting electrophiles, oxidative stress, and detoxification of a broad spectrum of drugs. DU-145 cells constitutively expressing Nrf2 short hairpin RNA had lower levels of total glutathione and higher levels of intracellular reactive oxygen species. Attenuation of Nrf2 function in DU-145 cells enhanced sensitivity to chemotherapeutic drugs and radiation-induced cell death. In addition, inhibition of Nrf2 greatly suppressed in vitro and in vivo tumor growth of DU-145 prostate cancer cells. Thus, targeting the Nrf2 pathway in prostate cancer cells may provide a novel strategy to enhance chemotherapy and radiotherapy responsiveness and ameliorate the growth and tumorigenicity, leading to improved clinical outcomes.

Published
2010

Catalog

Books, media, physical & digital resources
See catalog results