Search

Your search keyword '"Wu, Yuan-Qing"' showing total 26 results
Start Over Author "Wu, Yuan-Qing" Search Limiters Peer Reviewed
26 results on '"Wu, Yuan-Qing"'

5. Epistasis dominates the genetic architecture of Drosophila quantitative traits

Author

Huang, Wen, Richards, Stephen, Carbone, Mary Anna, Zhu, Dianhui, Anholt, Robert R. H., Ayroles, Julien F., Duncan, Laura, Jordan, Katherine W., Lawrence, Faye, Magwire, Michael M., Warner, Crystal B., Blankenburg, Kerstin, Han, Yi, Javaid, Mehwish, Jayaseelan, Joy, Jhangiani, Shalini N., Muzny, Donna, Ongeri, Fiona, Perales, Lora, Wu, Yuan-Qing, Zhang, Yiqing, Zou, Xiaoyan, Stone, Eric A., Gibbs, Richard A., and Mackay, Trudy F. C.

Published
2012

7. The Drosophila melanogaster Genetic Reference Panel

Author

Mackay, Trudy F.C., Richards, Stephen, Stone, Eric A., Barbadilla, Antonio, Ayroles, Julien F., Zhu, Dianhui, Casillas, Sonia, Han, Yi, Magwire, Michael M., Cridland, Julie M., Richardson, Mark F., Anholt, Robert R.H., Barron, Maite, Bess, Crystal, Blankenburg, Kerstin Petra, Carbone, Mary Anna, Castellano, David, Chaboub, Lesley, Duncan, Laura, Harris, Zeke, Javaid, Mehwish, Jayaseelan, Joy Christina, Jhangiani, Shalini N., Jordan, Katherine W., Lara, Fremiet, Lawrence, Faye, Lee, Sandra L., Librado, Pablo, Linheiro, Raquel S., Lyman, Richard F., Mackey, Aaron J., Munidasa, Mala, Muzny, Donna Marie, Nazareth, Lynne, Newsham, Irene, Perales, Lora, Pu, Ling-Ling, Qu, Carson, Ramia, Miquel, Reid, Jeffrey G., Rollmann, Stephanie M., Rozas, Julio, Saada, Nehad, Turlapati, Lavanya, Worley, Kim C., Wu, Yuan-Qing, Yamamoto, Akihiko, Zhu, Yiming, Bergman, Casey M., Thornton, Kevin R., Mittelman, David, and Gibbs, Richard A.

Subjects
Genetic variation -- Research, Drosophila -- Genetic aspects -- Research, X chromosome -- Physiological aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

A major challenge of biology is understanding the relationship between molecular genetic variation and variation in quantitative traits, including fitness. This relationship determines our ability to predict phenotypes from genotypes and to understand how evolutionary forces shape variation within and between species. Previous efforts to dissect the genotype-phenotype map were based on incomplete genotypic information. Here, we describe the Drosophila melanogaster Genetic Reference Panel (DGRP), a community resource for analysis of population genomics and quantitative traits. The DGRP consists of fully sequenced inbred lines derived from a natural population. Population genomic analyses reveal reduced polymorphism in centromeric autosomal regions and the X chromosome, evidence for positive and negative selection, and rapid evolution of the X chromosome. Many variants in novel genes, most at low frequency, are associated with quantitative traits and explain a large fraction of the phenotypic variance. The DGRP facilitates genotype-phenotype mapping using the power of Drosophila genetics., Understanding how molecular variation maps to phenotypic variation for quantitative traits is central for understanding evolution, animal and plant breeding, and personalized medicine (1,2). The principles of mapping quantitative trait [...]

Published
2012
Full Text
View/download PDF

10. Comprehensive molecular characterization of human colon and rectal cancer

Author

Muzny, Donna M., Bainbridge, Matthew N., Chang, Kyle, Dinh, Huyen H., Drummond, Jennifer A., Fowler, Gerald, Kovar, Christie L., Lewis, Lora R., Morgan, Margaret B., Newsham, Irene F., Reid, Jeffrey G., Santibanez, Jireh, Shinbrot, Eve, Trevino, Lisa R., Wu, Yuan-Qing, Wang, Min, Gunaratne, Preethi, Donehower, Lawrence A., Creighton, Chad J., Wheeler, David A., Gibbs, Richard A., Lawrence, Michael S., Voet, Douglas, Jing, Rui, Cibulskis, Kristian, Sivachenko, Andrey, Stojanov, Petar, McKenna, Aaron, Lander, Eric S., Gabriel, Stacey, Getz, Gad, Ding, Li, Fulton, Robert S., Koboldt, Daniel C., Wylie, Todd, Walker, Jason, Dooling, David J., Fulton, Lucinda, Delehaunty, Kim D., Fronick, Catrina C., Demeter, Ryan, Mardis, Elaine R., Wilson, Richard K., Chu, Andy, Chun, Hye-Jung E., Mungall, Andrew J., Pleasance, Erin, Robertson, Gordon A., Stoll, Dominik, Balasundaram, Miruna, Birol, Inanc, Butterfield, Yaron S. N., Chuah, Eric, Coope, Robin J. N., Dhalla, Noreen, Guin, Ranabir, Hirst, Carrie, Hirst, Martin, Holt, Robert A., Lee, Darlene, Li, Haiyan I., Mayo, Michael, Moore, Richard A., Schein, Jacqueline E., Slobodan, Jared R., Tam, Angela, Thiessen, Nina, Varhol, Richard, Zeng, Thomas, Zhao, Yongjun, Jones, Steven J. M., Marra, Marco A., Bass, Adam J., Ramos, Alex H., Saksena, Gordon, Cherniack, Andrew D., Schumacher, Stephen E., Tabak, Barbara, Carter, Scott L., Pho, Nam H., Nguyen, Huy, Onofrio, Robert C., Crenshaw, Andrew, Ardlie, Kristin, Beroukhim, Rameen, Winckler, Wendy, Meyerson, Matthew, Protopopov, Alexei, Zhang, Juinhua, Hadjipanayis, Angela, Lee, Eunjung, Xi, Ruibin, Yang, Lixing, Ren, Xiaojia, Zhang, Hailei, Sathiamoorthy, Narayanan, Shukla, Sachet, Chen, Peng-Chieh, Haseley, Psalm, Xiao, Yonghong, Lee, Semin, Seidman, Jonathan, Chin, Lynda, Park, Peter J., Kucherlapati, Raju, Auman, Todd J., Hoadley, Katherine A., Du, Ying, Wilkerson, Matthew D., Shi, Yan, Liquori, Christina, Meng, Shaowu, Li, Ling, Turman, Yidi J., Topal, Michael D., Tan, Donghui, Waring, Scot, Buda, Elizabeth, Walsh, Jesse, Jones, Corbin D., Mieczkowski, Piotr A., Singh, Darshan, Wu, Junyuan, Gulabani, Anisha, Dolina, Peter, Bodenheimer, Tom, Hoyle, Alan P., Simons, Janae V., Soloway, Matthew, Mose, Lisle E., Jefferys, Stuart R., Balu, Saianand, O’Connor, Brian D., Prins, Jan F., Chiang, Derek Y., Hayes, Neil D., Perou, Charles M., Hinoue, Toshinori, Weisenberger, Daniel J., Maglinte, Dennis T., Pan, Fei, Berman, Benjamin P., Van Den Berg, David J., Shen, Hui, Triche, Timothy, Jr, Baylin, Stephen B., Laird, Peter W., Noble, Michael, Voet, Doug, Gehlenborg, Nils, DiCara, Daniel, Wu, Chang-Jiun, Yingchun Liu, Spring, Zhou, Lihua, Lin, Pei, Park, Richard W., Nazaire, Marc-Danie, Robinson, Jim, Thorvaldsdottir, Helga, Mesirov, Jill, Thorsson, Vesteinn, Reynolds, Sheila M., Bernard, Brady, Kreisberg, Richard, Lin, Jake, Iype, Lisa, Bressler, Ryan, Erkkilä, Timo, Gundapuneni, Madhumati, Liu, Yuexin, Norberg, Adam, Robinson, Tom, Yang, Da, Zhang, Wei, Shmulevich, Ilya, de Ronde, Jorma J., Schultz, Nikolaus, Cerami, Ethan, Ciriello, Giovanni, Goldberg, Arthur P., Gross, Benjamin, Jacobsen, Anders, Gao, Jianjiong, Kaczkowski, Bogumil, Sinha, Rileen, Aksoy, Arman B., Antipin, Yevgeniy, Reva, Boris, Shen, Ronglai, Taylor, Barry S., Chan, Timothy A., Ladanyi, Marc, Sander, Chris, Akbani, Rehan, Zhang, Nianxiang, Broom, Bradley M., Casasent, Tod, Unruh, Anna, Wakefield, Chris, Hamilton, Stanley R., Cason, Craig R., Baggerly, Keith A., Weinstein, John N., Haussler, David, Benz, Christopher C., Stuart, Joshua M., Benz, Stephen C., Sanborn, Zachary J., Vaske, Charles J., Zhu, Jingchun, Szeto, Christopher, Scott, Gary K., Yau, Christina, Ng, Sam, Goldstein, Ted, Ellrott, Kyle, Collisson, Eric, Cozen, Aaron E., Zerbino, Daniel, Wilks, Christopher, Craft, Brian, Spellman, Paul, Penny, Robert, Shelton, Troy, Hatfield, Martha, Morris, Scott, Yena, Peggy, Shelton, Candace, Sherman, Mark, Paulauskis, Joseph, Gastier-Foster, Julie M., Bowen, Jay, Ramirez, Nilsa C., Black, Aaron, Pyatt, Robert, Wise, Lisa, White, Peter, Bertagnolli, Monica, Brown, Jen, Chu, Gerald C., Czerwinski, Christine, Denstman, Fred, Dhir, Rajiv, Dörner, Arnulf, Fuchs, Charles S., Guillem, Jose G., Iacocca, Mary, Juhl, Hartmut, Kaufman, Andrew, Kohl, Bernard, III, Van Le, Xuan, Mariano, Maria C., Medina, Elizabeth N., Meyers, Michael, Nash, Garrett M., Paty, Phillip B., Petrelli, Nicholas, Rabeno, Brenda, Richards, William G., Solit, David, Swanson, Pat, Temple, Larissa, Tepper, Joel E., Thorp, Richard, Vakiani, Efsevia, Weiser, Martin R., Willis, Joseph E., Witkin, Gary, Zeng, Zhaoshi, Zinner, Michael J., Zornig, Carsten, Jensen, Mark A., Sfeir, Robert, Kahn, Ari B., Chu, Anna L., Kothiyal, Prachi, Wang, Zhining, Snyder, Eric E., Pontius, Joan, Pihl, Todd D., Ayala, Brenda, Backus, Mark, Walton, Jessica, Whitmore, Jon, Baboud, Julien, Berton, Dominique L., Nicholls, Matthew C., Srinivasan, Deepak, Raman, Rohini, Girshik, Stanley, Kigonya, Peter A., Alonso, Shelley, Sanbhadti, Rashmi N., Barletta, Sean P., Greene, John M., Pot, David A., Mills Shaw, Kenna R., Dillon, Laura A. L., Buetow, Ken, Davidsen, Tanja, Demchok, John A., Eley, Greg, Ferguson, Martin, Fielding, Peter, Schaefer, Carl, Sheth, Margi, Yang, Liming, Guyer, Mark S., Ozenberger, Bradley A., Palchik, Jacqueline D., Peterson, Jane, Sofia, Heidi J., and Thomson, Elizabeth

Published
2012
Full Text
View/download PDF

11. Butterfly genome reveals promiscuous exchange of mimicry adaptations among species

Author

Dasmahapatra, Kanchon K., Walters, James R., Briscoe, Adriana D., Davey, John W., Whibley, Annabel, Nadeau, Nicola J., Zimin, Aleksey V., Hughes, Daniel S. T., Ferguson, Laura C., Martin, Simon H., Salazar, Camilo, Lewis, James J., Adler, Sebastian, Ahn, Seung-Joon, Baker, Dean A., Baxter, Simon W., Chamberlain, Nicola L., Chauhan, Ritika, Counterman, Brian A., Dalmay, Tamas, Gilbert, Lawrence E., Gordon, Karl, Heckel, David G., Hines, Heather M., Hoff, Katharina J., Holland, Peter W. H., Jacquin-Joly, Emmanuelle, Jiggins, Francis M., Jones, Robert T., Kapan, Durrell D., Kersey, Paul, Lamas, Gerardo, Lawson, Daniel, Mapleson, Daniel, Maroja, Luana S., Martin, Arnaud, Moxon, Simon, Palmer, William J., Papa, Riccardo, Papanicolaou, Alexie, Pauchet, Yannick, Ray, David A., Rosser, Neil, Salzberg, Steven L., Supple, Megan A., Surridge, Alison, Tenger-Trolander, Ayse, Vogel, Heiko, Wilkinson, Paul A., Wilson, Derek, Yorke, James A., Yuan, Furong, Balmuth, Alexi L., Eland, Cathlene, Gharbi, Karim, Thomson, Marian, Gibbs, Richard A., Han, Yi, Jayaseelan, Joy C., Kovar, Christie, Mathew, Tittu, Muzny, Donna M., Ongeri, Fiona, Pu, Ling-Ling, Qu, Jiaxin, Thornton, Rebecca L., Worley, Kim C., Wu, Yuan-Qing, Linares, Mauricio, Blaxter, Mark L., ffrench-Constant, Richard H., Joron, Mathieu, Kronforst, Marcus R., Mullen, Sean P., Reed, Robert D., Scherer, Steven E., Richards, Stephen, Mallet, James, Owen McMillan, W., and Jiggins, Chris D.

Published
2012
Full Text
View/download PDF

12. A framework for human microbiome research

Author

Methé, Barbara A., Nelson, Karen E., Pop, Mihai, Creasy, Heather H., Giglio, Michelle G., Huttenhower, Curtis, Gevers, Dirk, Petrosino, Joseph F., Abubucker, Sahar, Badger, Jonathan H., Chinwalla, Asif T., Earl, Ashlee M., FitzGerald, Michael G., Fulton, Robert S., Hallsworth-Pepin, Kymberlie, Lobos, Elizabeth A., Madupu, Ramana, Magrini, Vincent, Martin, John C., Mitreva, Makedonka, Muzny, Donna M., Sodergren, Erica J., Versalovic, James, Wollam, Aye M., Worley, Kim C., Wortman, Jennifer R., Young, Sarah K., Zeng, Qiandong, Aagaard, Kjersti M., Abolude, Olukemi O., Allen-Vercoe, Emma, Alm, Eric J., Alvarado, Lucia, Andersen, Gary L., Anderson, Scott, Appelbaum, Elizabeth, Arachchi, Harindra M., Armitage, Gary, Arze, Cesar A., Ayvaz, Tulin, Baker, Carl C., Begg, Lisa, Belachew, Tsegahiwot, Bhonagiri, Veena, Bihan, Monika, Blaser, Martin J., Bloom, Toby, Bonazzi, Vivien R., Brooks, Paul, Buck, Gregory A., Buhay, Christian J., Busam, Dana A., Campbell, Joseph L., Canon, Shane R., Cantarel, Brandi L., Chain, Patrick S., Chen, I-Min A., Chen, Lei, Chhibba, Shaila, Chu, Ken, Ciulla, Dawn M., Clemente, Jose C., Clifton, Sandra W., Conlan, Sean, Crabtree, Jonathan, Cutting, Mary A., Davidovics, Noam J., Davis, Catherine C., DeSantis, Todd Z., Deal, Carolyn, Delehaunty, Kimberley D., Dewhirst, Floyd E., Deych, Elena, Ding, Yan, Dooling, David J., Dugan, Shannon P., Dunne, Michael W., Jr, Durkin, Scott A., Edgar, Robert C., Erlich, Rachel L., Farmer, Candace N., Farrell, Ruth M., Faust, Karoline, Feldgarden, Michael, Felix, Victor M., Fisher, Sheila, Fodor, Anthony A., Forney, Larry, Foster, Leslie, Di Francesco, Valentina, Friedman, Jonathan, Friedrich, Dennis C., Fronick, Catrina C., Fulton, Lucinda L., Gao, Hongyu, Garcia, Nathalia, Giannoukos, Georgia, Giblin, Christina, Giovanni, Maria Y., Goldberg, Jonathan M., Goll, Johannes, Gonzalez, Antonio, Griggs, Allison, Gujja, Sharvari, Haas, Brian J., Hamilton, Holli A., Harris, Emily L., Hepburn, Theresa A., Herter, Brandi, Hoffmann, Diane E., Holder, Michael E., Howarth, Clinton, Huang, Katherine H., Huse, Susan M., Izard, Jacques, Jansson, Janet K., Jiang, Huaiyang, Jordan, Catherine, Joshi, Vandita, Katancik, James A., Keitel, Wendy A., Kelley, Scott T., Kells, Cristyn, Kinder-Haake, Susan, King, Nicholas B., Knight, Rob, Knights, Dan, Kong, Heidi H., Koren, Omry, Koren, Sergey, Kota, Karthik C., Kovar, Christie L., Kyrpides, Nikos C., La Rosa, Patricio S., Lee, Sandra L., Lemon, Katherine P., Lennon, Niall, Lewis, Cecil M., Lewis, Lora, Ley, Ruth E., Li, Kelvin, Liolios, Konstantinos, Liu, Bo, Liu, Yue, Lo, Chien-Chi, Lozupone, Catherine A., Lunsford, Dwayne R., Madden, Tessa, Mahurkar, Anup A., Mannon, Peter J., Mardis, Elaine R., Markowitz, Victor M., Mavrommatis, Konstantinos, McCorrison, Jamison M., McDonald, Daniel, McEwen, Jean, McGuire, Amy L., McInnes, Pamela, Mehta, Teena, Mihindukulasuriya, Kathie A., Miller, Jason R., Minx, Patrick J., Newsham, Irene, Nusbaum, Chad, O’Laughlin, Michelle, Orvis, Joshua, Pagani, Ioanna, Palaniappan, Krishna, Patel, Shital M., Pearson, Matthew, Peterson, Jane, Podar, Mircea, Pohl, Craig, Pollard, Katherine S., Priest, Margaret E., Proctor, Lita M., Qin, Xiang, Raes, Jeroen, Ravel, Jacques, Reid, Jeffrey G., Rho, Mina, Rhodes, Rosamond, Riehle, Kevin P., Rivera, Maria C., Rodriguez-Mueller, Beltran, Rogers, Yu-Hui, Ross, Matthew C., Russ, Carsten, Sanka, Ravi K., Sankar, Pamela, Sathirapongsasuti, Fah J., Schloss, Jeffery A., Schloss, Patrick D., Schmidt, Thomas M., Scholz, Matthew, Schriml, Lynn, Schubert, Alyxandria M., Segata, Nicola, Segre, Julia A., Shannon, William D., Sharp, Richard R., Sharpton, Thomas J., Shenoy, Narmada, Sheth, Nihar U., Simone, Gina A., Singh, Indresh, Smillie, Chris S., Sobel, Jack D., Sommer, Daniel D., Spicer, Paul, Sutton, Granger G., Sykes, Sean M., Tabbaa, Diana G., Thiagarajan, Mathangi, Tomlinson, Chad M., Torralba, Manolito, Treangen, Todd J., Truty, Rebecca M., Vishnivetskaya, Tatiana A., Walker, Jason, Wang, Lu, Wang, Zhengyuan, Ward, Doyle V., Warren, Wesley, Watson, Mark A., Wellington, Christopher, Wetterstrand, Kris A., White, James R., Wilczek-Boney, Katarzyna, Wu, Yuan Qing, Wylie, Kristine M., Wylie, Todd, Yandava, Chandri, Ye, Liang, Ye, Yuzhen, Yooseph, Shibu, Youmans, Bonnie P., Zhang, Lan, Zhou, Yanjiao, Zhu, Yiming, Zoloth, Laurie, Zucker, Jeremy D., Birren, Bruce W., Gibbs, Richard A., Highlander, Sarah K., Weinstock, George M., Wilson, Richard K., and White, Owen

Published
2012
Full Text
View/download PDF

18. Impulsive controller for wireless networked control system: Switched system approach.

Author

Wu, Yuan-Qing, Su, Hongye, and Mathiyalagan, Kalidass

Subjects
WIRELESS communications, TIME delay systems, PACKET switching
Abstract

The problem of stabilization for wireless networked control system (NCS) with packet dropout and time delay is studied in this article. The impulsive control law for the NCS is defined with time delay and impulse. Using a switching model, the network-induced imperfections can be treated as three switching subsystems. Therein, in the case of packet dropout, the control law use the previous state via the first-order hold. The impulsive control law is designed using the switched system approach and the average dwell time method. The obtained sufficient conditions which can guarantee the exponential stability of switched system are in the form of linear matrix inequalities. Finally, a numerical example is used to demonstrate the merits and applicabilities of the proposed method. © 2015 Wiley Periodicals, Inc. Complexity 21: 291-299, 2016 [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

20. H ∞ filtering for impulsive networked control systems with random packet dropouts and randomly occurring nonlinearities.

Author

Kalidass, Mathiyalagan, Su, Hongye, Wu, Yuan‐Qing, and Rathinasamy, Sakthivel

Subjects
BINOMIAL distribution, LINEAR matrix inequalities, MATHEMATICAL optimization, DETECTORS, ACTUATORS
Abstract

In this paper, the problem of H ∞ filtering for impulsive networked control systems with random packet dropouts and randomly occurring nonlinearities is investigated. By utilizing an impulsive model, the network-induced imperfections including packet dropout and delay are described by the Bernoulli distributed sequence. The delay in the model is assumed to be time varying. Moreover, nonlinearity in the model is assumed to satisfy sector-like nonlinearities. The H ∞ filter is designed by using the linear matrix inequality (LMI) approach and convex optimization technique. The filter gain matrices for the nonlinear networked control systems can be achieved by solving LMIs, which can be easily facilitated by using some standard numerical packages. Finally, a numerical example is presented to demonstrate the effectiveness and applicability of the proposed results. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

21. Synchronisation control of dynamical networks subject to variable sampling and actuators saturation.

Author

Wu, Yuan‐Qing, Su, Hongye, and Wu, Zheng‐Guang

Abstract

This study investigates aperiodic sampled‐data synchronisation of complex dynamical network (CDN) incorporate dynamics of actuators saturation. The sampling intervals considered here are time‐varying which allowed to be variable within the lower and upper bounds. In order to fully captures the sawtooth structure characteristic of the sampled‐data systems, a novel time‐dependent continuous Lyapunov functional is employed to obtain less conservative criteria. Furthermore, the generalised sector bound condition is utilised for the estimate about the basin of the attraction. Based on the local stability condition, the sampled‐data controller is constructed to guarantee the synchronisation of CDN in the presence of actuators saturation. The obtained sufficient conditions can be cast in two optimisation cases to maximise the admissible upper bound of sampling instants or enlarge estimate about the domain of attraction for the closed‐loop systems. Subsequently, the validity and applicability of the criteria are verified through numerical examples. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

22. Whole-exome sequencing identifies compound heterozygous mutations in WDR62 in siblings with recurrent polymicrogyria.

Author

Murdock, David R., Clark, Gary D., Bainbridge, Matthew N., Newsham, Irene, Wu, Yuan-Qing, Muzny, Donna M., Cheung, Sau Wai, Gibbs, Richard A., and Ramocki, Melissa B.

Abstract

Polymicrogyria is a disorder of neuronal development resulting in structurally abnormal cerebral hemispheres characterized by over-folding and abnormal lamination of the cerebral cortex. Polymicrogyria is frequently associated with severe neurologic deficits including intellectual disability, motor problems, and epilepsy. There are acquired and genetic causes of polymicrogyria, but most patients with a presumed genetic etiology lack a specific diagnosis. Here we report using whole-exome sequencing to identify compound heterozygous mutations in the WD repeat domain 62 ( WDR62) gene as the cause of recurrent polymicrogyria in a sibling pair. Sanger sequencing confirmed that the siblings both inherited 1-bp (maternal allele) and 2-bp (paternal allele) frameshift deletions, which predict premature truncation of WDR62, a protein that has a role in early cortical development. The probands are from a non-consanguineous family of Northern European descent, suggesting that autosomal recessive PMG due to compound heterozygous mutation of WDR62 might be a relatively common cause of PMG in the population. Further studies to identify mutation frequency in the population are needed. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2011
Full Text
View/download PDF

24. Molecular refinement of the 1p36 deletion syndrome reveals size diversity and a preponderance of maternally derived deletions.

Author

Wu, Yuan-Qing, Heilstedt, Heidi A., Bedell, Joseph A., May, Kristin M., Starkey, David E., McPherson, John D., Shapira, Stuart K., and Shaffer, Lisa G.

Abstract

The deletion of chromosome 1p36 is a newly recognized, relatively common contiguous gene deletion syndrome with a variable phenotype. The clinical features have recently been delineated and molecular analysis indicates that the prevalence of certain phenotypic features appears to correlate with deletion size. Phenotype/genotype comparisons have allowed the assignment of certain clinical features to specific deletion intervals, significantly narrowing the regions within which to search for candidate genes. We have extensively characterized the deletion regions in 30 cases using microsatellite markers and fluorescence in situ hybridization analyses. The map order of 28 microsatellite markers spanning the deletion region was obtained by a combination of genotypic analysis and physical mapping. The deletion region was divided into six intervals and breakpoints were found to cluster in mainly two regions. Molecular analysis of the deletions showed that two patients had complex re-arrangements; these cases shared their distal and proximal breakpoints in the two common breakpoint regions. Of the de novo deletions (n= 28) in whichparental samples were available and the analysis was informative (n = 27), there were significantly morematernally derived deletions (n = 21) than paternally derived deletions (n = 6) (χ[sub 1][sup 2]= 8.35, P < 0.0001). Phenotype/genotype correlations and refinements of critical regions in our naturally occurring deletion panel have delineated specific areas in which to focus the search for the causative genes for the features of this syndrome. [ABSTRACT FROM AUTHOR]

Published
1999

26. Somatostatin receptor gene transfer inhibits established pancreatic cancer xenografts1 <FN ID="FN1"><NO>1</NO>This paper was presented at the annual meeting of the Association for Academic Surgery, Boston, MA, November 7–9, 2002.</FN>

Author

Celinski, Scott A., Fisher, William E., Amaya, Felipe, Wu, Yuan Qing, Yao, Q., Youker, Keith A., and Li, Min

Subjects
*PANCREAS, *ADENOCARCINOMA, *SOMATOSTATIN, *CANCER
Abstract

Background.Most human pancreatic adenocarcinoma cells do not express somatostatin receptors, and somatostatin does not inhibit the growth of these cancers. We have demonstrated previously that somatostatin inhibits the growth of pancreatic cancers expressing somatostatin receptor subtype-2 (SSTR2), but not receptor-negative cancers. SSTR2 expression may be an important tumor-suppressor pathway that is lost in human pancreatic cancer. We hypothesized that SSTR2 gene transfer would restore the growth-inhibitory response of human pancreatic cancer to somatostatin.Materials and methods.Palpable human pancreatic adenocarcinoma tumors were established on the backs of nude mice by subcutaneous injection of cultured cells (Panc-1). The animals were divided into 5 groups (n = 10/group). Group I served as an untreated control. Group II received an intramuscular injection of the long-acting somatostatin analogue Sandostatin LAR. Group III received Lac-Z expressing adenovirus via intraperitoneal injection. Group IV received SSTR2 expressing adenovirus via intraperitoneal injection. Group V received SSTR2 expressing adenovirus via intraperitoneal injection and an intramuscular injection of Sandostatin LAR. The rate of tumor growth was assessed with calipers. After 28 days, the animals were anesthetized and exsanguanated, and the tumors were excised and weighed. Plasma somatostatin and octreotide levels were measured by radioimmunoassay. Expression of cell-surface somatostatin-receptor protein and known tumor-suppressor proteins was determined by reverse transcriptase-polymerase chain reaction, Western blot, and immunohistochemistry.Results.Systemic delivery of SSTR2-expressing adenovirus by intraperitoneal injection resulted in expression of SSTR2 protein in the subcutaneous human pancreatic cancers. Final tumor weight was significantly decreased in the groups expressing SSTR2 receptors compared to the other 3 groups. Treatment with Sandostatin LAR increased plasma octreotide levels as determined by radioimmunoassay, but had no significant effect on tumor growth. Western blot analysis revealed an up-regulation of the cyclin-dependent kinase inhibitors p27 and p16 in the SSTR2 transfected tumors.Conclusions.Expression of SSTR2 by human pancreatic cancer causes significant slowing of tumor growth by a mechanism independent of exogenous somatostatin. The mechanism may involve up-regulation of known tumor-suppressor proteins. Restoration of SSTR2 gene expression deserves further study as a potential gene-therapy strategy in human pancreatic cancer. [Copyright &y& Elsevier]

Published
2003
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results