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54. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, Keith I., Gyllenhaal, Charlotte, Lowe, Leroy, Amedei, Amedeo, Amin, A.R.M. Ruhul, Amin, Amr, Aquilano, Katia, Arbiser, Jack, Arreola, Alexandra, Arzumanyan, Alla, Ashraf, S. Salman, Azmi, Asfar S., Benencia, Fabian, Bhakta, Dipita, Bilsland, Alan, Bishayee, Anupam, Blain, Stacy W., Block, Penny B., Boosani, Chandra S., Carey, Thomas E., Carnero, Amancio, Carotenuto, Marianeve, Casey, Stephanie C., Chakrabarti, Mrinmay, Chaturvedi, Rupesh, Chen, Georgia Zhuo, Chen, Helen, Chen, Sophie, Chen, Yi Charlie, Choi, Beom K., Ciriolo, Maria Rosa, Coley, Helen M., Collins, Andrew R., Connell, Marisa, Crawford, Sarah, Curran, Colleen S., Dabrosin, Charlotta, Damia, Giovanna, Dasgupta, Santanu, DeBerardinis, Ralph J., Decker, William K., Dhawan, Punita, Diehl, Anna Mae E., Dong, Jin-Tang, Dou, Q. Ping, Drew, Janice E., Elkord, Eyad, El-Rayes, Bassel, Feitelson, Mark A., Felsher, Dean W., Ferguson, Lynnette R., Fimognari, Carmela, Firestone, Gary L., Frezza, Christian, Fujii, Hiromasa, Fuster, Mark M., Generali, Daniele, Georgakilas, Alexandros G., Gieseler, Frank, Gilbertson, Michael, Green, Michelle F., Grue, Brendan, Guha, Gunjan, Halicka, Dorota, Helferich, William G., Heneberg, Petr, Hentosh, Patricia, Hirschey, Matthew D., Hofseth, Lorne J., Holcombe, Randall F., Honoki, Kanya, Hsu, Hsue-Yin, Huang, Gloria S., Jensen, Lasse D., Jiang, Wen G., Jones, Lee W., Karpowicz, Phillip A., Keith, W. Nicol, Kerkar, Sid P., Khan, Gazala N., Khatami, Mahin, Ko, Young H., Kucuk, Omer, Kulathinal, Rob J., Kumar, Nagi B., Kwon, Byoung S., Le, Anne, Lea, Michael A., Lee, Ho-Young, Lichtor, Terry, Lin, Liang-Tzung, Locasale, Jason W., Lokeshwar, Bal L., Longo, Valter D., Lyssiotis, Costas A., MacKenzie, Karen L., Malhotra, Meenakshi, Marino, Maria, Martinez-Chantar, Maria L., Matheu, Ander, Maxwell, Christopher, McDonnell, Eoin, Meeker, Alan K., Mehrmohamadi, Mahya, Mehta, Kapil, Michelotti, Gregory A., Mohammad, Ramzi M., Mohammed, Sulma I., Morre, D. James, Muralidhar, Vinayak, Muqbil, Irfana, Murphy, Michael P., Nagaraju, Ganji Purnachandra, Nahta, Rita, Niccolai, Elena, Nowsheen, Somaira, Panis, Carolina, Pantano, Francesco, Parslow, Virginia R., Pawelec, Graham, Pedersen, Peter L., Poore, Brad, Poudyal, Deepak, Prakash, Satya, Prince, Mark, Raffaghello, Lizzia, Rathmell, Jeffrey C., Rathmell, W. Kimryn, Ray, Swapan K., Reichrath, Jörg, Rezazadeh, Sarallah, Ribatti, Domenico, Ricciardiello, Luigi, Robey, R. Brooks, Rodier, Francis, Rupasinghe, H.P. Vasantha, Russo, Gian Luigi, Ryan, Elizabeth P., Samadi, Abbas K., Sanchez-Garcia, Isidro, Sanders, Andrew J., Santini, Daniele, Sarkar, Malancha, Sasada, Tetsuro, Saxena, Neeraj K., Shackelford, Rodney E., Shantha Kumara, H.M.C., Sharma, Dipali, Shin, Dong M., Sidransky, David, Siegelin, Markus David, Signori, Emanuela, Singh, Neetu, Sivanand, Sharanya, Sliva, Daniel, Smythe, Carl, Spagnuolo, Carmela, Stafforini, Diana M., Stagg, John, Subbarayan, Pochi R., Sundin, Tabetha, Talib, Wamidh H., Thompson, Sarah K., Tran, Phuoc T., Ungefroren, Hendrik, Vander Heiden, Matthew G., Venkateswaran, Vasundara, Vinay, Dass S., Vlachostergios, Panagiotis J., Wang, Zongwei, Wellen, Kathryn E., Whelan, Richard L., Yang, Eddy S., Yang, Huanjie, Yang, Xujuan, Yaswen, Paul, Yedjou, Clement, Yin, Xin, Zhu, Jiyue, and Zollo, Massimo

Published
2015
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69. Parabens and human epidermal growth factor receptor ligand cross-talk in breast cancer cells

Author

Pan, Shawn, Yuan, Chaoshen, Tagmount, Abderrahmane, Rudel, Ruthann A., Ackerman, Janet M., Yaswen, Paul, Vulpe, Chris D., and Leitman, Dale C.

Subjects
Breast cancer -- Research -- Complications and side effects, Oncogenes -- Research, Environmental issues, Health
Abstract

BACKGROUND: Xenoestrogens are synthetic compounds that mimic endogenous estrogens by binding to and activating estrogen receptors. Exposure to estrogens and to some xenoestrogens has been associated with cell proliferation and an increased risk of breast cancer. Despite evidence of estrogenicity, parabens are among the most widely used xenoestrogens in cosmetics and personalcare products and are generally considered safe. However, previous cell-based studies with parabens do not take into account the signaling cross-talk between estrogen receptor a (ERa) and the human epidermal growth factor receptor (HER) family. OBJECTIVES: We investigated the hypothesis that the potency of parabens can be increased with HER ligands, such as heregulin (HRG). METHODS: The effects of HER ligands on paraben activation of c-Myc expression and cell proliferation were determined by real-time polymerase chain reaction, Western blots, flow cytometry, and chromatin immunoprecipitation assays in ERa- and HER2-positive human BT-474 breast cancer cells. RESULTS: Butylparaben (BP) and HRG produced a synergistic increase in c-Myc mRNA and protein levels in BT-474 cells. Estrogen receptor antagonists blocked the synergistic increase in c-Myc protein levels. The combination of BP and HRG also stimulated proliferation of BT-474 cells compared with the effects of BP alone. HRG decreased the dose required for BP-mediated stimulation of c-Myc mRNA expression and cell proliferation. HRG caused the phosphorylation of serine 167 in ERa. BP and HRG produced a synergistic increase in ERa recruitment to the c-Myc gene. CONCLUSION: Our results show that HER ligands enhanced the potency of BP to stimulate oncogene expression and breast cancer cell proliferation in vitro via ERa, suggesting that parabens might be active at exposure levels not previously considered toxicologically relevant from studies testing their effects in isolation. http://dx.doi.org/10.1289/ehp.1409200, Introduction Xenoestrogens are a class of synthetic estrogens known as endocrine-disrupting chemicals that bind to estrogen receptors in cells to mimic or antagonize the action of endogenous estrogens, such as [...]

Published
2016
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86. Expression of the telomerase catalytic subunit, hTERT, induces resistance to transforming growth factor [Beta] growth inhibition in [p16.sup.INK4A](-) human mammary epithelial cells

Author

Stampfer, Martha R., Garbe, James, Levine, Gerri, Lichtsteiner, Serge, Vasserot, Alain P., and Yaswen, Paul

Subjects
Telomerase -- Research, Epithelial cells -- Abnormalities, Growth factors -- Research, Cancer -- Research, Science and technology
Abstract

Failures to arrest growth in response to senescence or transforming growth factor [Beta] (TGF-[Beta]) are key derangements associated with carcinoma progression. We report that activation of telomerase activity may overcome both inhibitory pathways. Ectopic expression of the human telomerase catalytic subunit, hTERT, in cultured human mammary epithelial cells (HMEC) lacking both telomerase activity and [p16.sup.INK4A] resulted in gaining the ability to maintain indefinite growth in the absence and presence of TGF-[Beta]. The ability to maintain growth in TGF-[Beta] was independent of telomere length and required catalytically active telomerase capable of telomere maintenance in vivo. The capacity of ectopic hTERT to induce TGF-[Beta] resistance may explain our previously described gain of TGF-[Beta] resistance after reactivation of endogenous telomerase activity in rare carcinogen-treated HMEC. In those HMEC that overcame senescence, both telomerase activity and TGF-[Beta] resistance were acquired gradually during a process we have termed conversion. This effect of hTERT may model a key change occurring during in vivo human breast carcinogenesis.

Published
2001

87. Abstract B34: PIM kinase as a novel therapeutic target for triple-negative breast cancer

Author

Horiuchi, Dai, primary, Zhou, Alicia Y., additional, Corella, Alexandra N., additional, Yau, Christina, additional, Balakrishnan, Sanjeev, additional, Kessenbrock, Kai, additional, Lawson, Devon A., additional, Camarda, Roman, additional, Anderton, Brittany N., additional, Bazarov, Alexey V., additional, Eyob, Henok, additional, Rohrberg, Julia, additional, Yaswen, Paul, additional, McManus, Michael T., additional, Rugo, Hope S., additional, Werb, Zena, additional, and Goga, Andrei, additional

Published
2016
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90. Functional Analysis of BORIS, a Novel DNA Binding Protein

Author

CALIFORNIA UNIV BERKELEY, Yaswen, Paul, CALIFORNIA UNIV BERKELEY, and Yaswen, Paul

Abstract

BORIS (cT6FL) is a paralog of tbe gene encoding CTCF, a multifunctional DNA binding protein that utilizes different sets of zinc fingers to mediate distinct gene regulatory functions, including those involved in cell growth regulation. Unlike CTCF the expression of BORIS is normally restricted to specific cells in testes (the only cells where CTCF is not expressed) where it may play a role in reprogramming the methylation pattern of male germ line DNA. To define the possible consequences of aberrant BORIS expression in human breast cancers we have used a well-characterized human mammary epithelial cell (HMEC) culture model. Our results indicate that in most breast cancer cells endogenous BORIS is unlikely to be expressed at sufficient levels to interfere with CTCF functions, and that BORIS expression alone is not an efficient immortalizing factor. However, under certain conditions BORIS may cooperate with other changes (e.g. p53 inactivation) to destabilize the genomes of the cells in which it is aberrantly expressed. BORIS expression may cause genomic instability through aberrant affects on centrosome duplication during the cell cycle, and through effects on the regulation of several key early growth response genes.

Published
2008

91. Abstract B232: PIM1 kinase is essential for the growth of MYC-overexpressing triple-negative breast tumors and is an efficacious therapeutic target.

Author

Horiuchi, Dai, primary, Zhou, Alicia Y., additional, Corella, Alexandra N., additional, Yau, Christina, additional, Lawson, Devon A., additional, Bazarov, Alexey V., additional, Yaswen, Paul, additional, McManus, Michael T., additional, Welm, Alana L., additional, Werb, Zena, additional, and Goga, Andrei, additional

Published
2013
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93. Functional Analysis of BORIS, a Novel DNA Binding Protein

Author

CALIFORNIA UNIV BERKELEY, Yaswen, Paul, CALIFORNIA UNIV BERKELEY, and Yaswen, Paul

Abstract

BORIS (CTCFL) is a paralogue of the gene encoding CTCF, a multifunctional DNA binding protein that utilizes different sets of zinc fingers to mediate distinct gene regulatory functions, including those involved in cell growth regulation. Unlike CTCF, the expression of BORIS is normally restricted to specific cells in testes (the only cells where CTCF is not expressed), where it may play a role in reprogramming the methylation pattern of male germ line DNA. To define the possible consequences of aberrant BORIS expression in human breast cancers, we have used a well-characterized human mammary epithelial cell (HMEC) culture model. Our results indicate that in most breast cancer cells, endogenous BORIS is unlikely to be expressed at sufficient levels to interfere with CTCF functions, and that BORIS expression alone is not an efficient immortalizing factor. However, under certain conditions BORIS may cooperate with other changes (e.g. p53 inactivation) to destabilize the genomes of the cells in which it is aberrantly expressed. BORIS expression may cause genomic instability through aberrant affects on centrosome duplication during the cell cycle, and through effects on the regulation of several key early growth response genes.

Published
2007

94. Parabens and Human Epidermal Growth Factor Receptor Ligand Cross-Talk in Breast Cancer Cells.

Author

Shawn Pan, Chaoshen Yuan, Tagmount, Abderrahmane, Rudel, Ruthann A., Ackerman, Janet M., Yaswen, Paul, Vulpe, Chris D., and Leitman, Dale C.

Subjects
BREAST tumor risk factors, ANALYSIS of variance, CELL culture, DRUG toxicity, EPIDERMAL growth factor, FLOW cytometry, ONCOGENES, POLYMERASE chain reaction, RESEARCH funding, STATISTICS, WESTERN immunoblotting, HYDROXY acids, DATA analysis, REVERSE transcriptase polymerase chain reaction, DATA analysis software, SIGNAL peptides, DESCRIPTIVE statistics, IN vitro studies
Abstract

BACKGROUND: Xenoestrogens are synthetic compounds that mimic endogenous estrogens by binding to and activating estrogen receptors. Exposure to estrogens and to some xenoestrogens has been associated with cell proliferation and an increased risk of breast cancer. Despite evidence of estrogenicity, parabens are among the most widely used xenoestrogens in cosmetics and personal-care products and are generally considered safe. However, previous cell-based studies with parabens do not take into account the signaling cross-talk between estrogen receptor α (ERα) and the human epidermal growth factor receptor (HER) family. OBJECTIVES: We investigated the hypothesis that the potency of parabens can be increased with HER ligands, such as heregulin (HRG). METHODS: The effects of HER ligands on paraben activation of c-Myc expression and cell proliferation were determined by real-time polymerase chain reaction, Western blots, flow cytometry, and chromatin immunoprecipitation assays in ERα- and HER2-positive human BT-474 breast cancer cells. RESULTS: Butylparaben (BP) and HRG produced a synergistic increase in c-Myc mRNA and protein levels in BT-474 cells. Estrogen receptor antagonists blocked the synergistic increase in c-Myc protein levels. The combination of BP and HRG also stimulated proliferation of BT-474 cells compared with the effects of BP alone. HRG decreased the dose required for BP-mediated stimulation of c-Myc mRNA expression and cell proliferation. HRG caused the phosphorylation of serine 167 in ERα. BP and HRG produced a synergistic increase in ERα recruitment to the c-Myc gene. CONCLUSION: Our results show that HER ligands enhanced the potency of BP to stimulate oncogene expression and breast cancer cell proliferation in vitro via ERα, suggesting that parabens might be active at exposure levels not previously considered toxicologically relevant from studies testing their effects in isolation. [ABSTRACT FROM AUTHOR]

Published
2016
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95. MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition

Author

Horiuchi, Dai, primary, Kusdra, Leonard, additional, Huskey, Noelle E., additional, Chandriani, Sanjay, additional, Lenburg, Marc E., additional, Gonzalez-Angulo, Ana Maria, additional, Creasman, Katelyn J., additional, Bazarov, Alexey V., additional, Smyth, James W., additional, Davis, Sarah E., additional, Yaswen, Paul, additional, Mills, Gordon B., additional, Esserman, Laura J., additional, and Goga, Andrei, additional

Published
2012
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96. Abstract 1680: Age-associated gene expression in normal breast tissue provide insights regarding associations between aging and aggressive tumor characteristics

Author

D'Arcy, Monica, primary, Pirone, Jason R., additional, Stewart, Delisha A., additional, Casbas-Hernandez, Patricia, additional, Gould, Michael N., additional, Jerry, Joseph Jerry, additional, Yaswen, Paul, additional, Schneider, Sallie Smith, additional, and Troester, Melissa A., additional

Published
2012
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97. Cooperative Interactions During Human Mammary Epithelial Cell Immortalization

Author

CALIFORNIA UNIV BERKELEY, Yaswen, Paul, CALIFORNIA UNIV BERKELEY, and Yaswen, Paul

Abstract

Our laboratories have developed and utilized cultured human mammary epithelial cells (HMEC) to gain information on the defects in growth control processes that allow finite lifespan HMEC to overcome all senescence barriers, reactivate telomerase, and gain immortal potential. We hypothesize that, due to the stringency of telomerase repression in humans, attaining these defects may be rate-limiting in human carcinogenesis. Our goal is to define the minimum number of genetic and epigenetic changes that permit telomerase reactivation and immortal transformation of finite lifespan HMEC, in a manner that models changes observed in breast cancers in vivo. Thus far, we have been able to obtain immortalized HMEC using a combination of two oncogenes (c-myc and ZNF217) with pathological relevance to human breast cancer. Although CGH analyses of some of these immortal lines did not show any detectable large-scale changes in gene copy numbers, these lines have all undergone clonal selection, suggesting that unknown stochastic changes, in addition to over-expression of c-myc and ZNF217, might be necessary for immortalization. We are currently working to identify these stochastic changes. Better understanding of the underlying molecular changes involved in telomerase reactivation may provide novel prevention strategies and/or targets for therapeutic intervention in breast cancer pathogenesis., The original document contains color images.

Published
2004

98. Cooperative Interactions During Human Mammary Epithelial Cell Immortalization

Author

CALIFORNIA UNIV BERKELEY LAWRENCE BERKELEY LAB, Yaswen, Paul, CALIFORNIA UNIV BERKELEY LAWRENCE BERKELEY LAB, and Yaswen, Paul

Abstract

Our laboratory has pioneered the development and use of cultured human mammary epithelial cells (HMEC) to gain information on the defects in growth control processes that allow finite lifespan HMEC to overcome all senescence barriers, reactivate telomerase, and gain immortal potential. We hypothesize that, due to the stringency of telomerase repression in humans, attaining these defects may be a key rate-limiting step in human carcinogenesis. The goal of this project has been to define the minimum number of genetic and epigenetic changes that permit telomerase reactivation and immortal transformation of finite lifespan HMEC, in a manner that models changes observed in breast cancers in vivo. During the past year, we were able to obtain immortalized HMEC using a combination of two oncogenes (c-myc and ZNF2l7) with pathological relevance to human breast cancer. Comparative genomic hybridization (CGH) analyses of two immortal populations obtained using c-myc and ZNF2l7 did not show any detectable additional changes in gene copy numbers, suggesting that along with unknown epigenetic changes, over-expression of these 2 genes together might be sufficient for immortalization. Better understanding of the underlying molecular changes involved in telomerase reactivation may provide novel prevention strategies and/or targets for therapeutic intervention in breast cancer pathogenesis., The original document contains color images. All DTIC reproductions will be in black and white.

Published
2003

99. Synthetic and Mechanistic Pathways of Cis and Trans-Hydroxytamoxifen Drug Derivatives Reacting with Cp*Rh Complexes that involve η1-N, η2-N,O, η1-O, and η6 Bonding Modes, via a Novel N-π Rearrangement; Relative Binding Affinities and Computer Docking Studies of Cis and Trans-η6-Cp*Rh-Hydroxytamoxifen Complexes at the Estrogen, ERα and ERβ Receptors, and Growth Inhibition to Breast Cancer Cells

Author

Top, Siden, primary, Efremenko, Irena, additional, Rager, Marie Noelle, additional, Vessières, Anne, additional, Yaswen, Paul, additional, Jaouen, Gérard, additional, and Fish, Richard H., additional

Published
2010
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