Search Results - "Thatikonda, Venu"

Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma by Merk, Daniel J., Ohli, Jasmin, Merk, Natalie D., Thatikonda, Venu, Morrissy, Sorana, Schoof, Melanie, Schmid, Susanne N., Harrison, Luke, Filser, Severin, Ahlfeld, Julia, Erkek, Serap, Raithatha, Kaamini, Andreska, Thomas, Weißhaar, Marc, Launspach, Michael, Neumann, Julia E., Shakarami, Mehdi, Plenker, Dennis, Marra, Marco A., Li, Yisu, Mungall, Andrew J., Moore, Richard A., Ma, Yussanne, Jones, Steven J.M., Lutz, Beat, Ertl-Wagner, Birgit, Rossi, Andrea, Wagener, Rabea, Siebert, Reiner, Jung, Andreas, Eberhart, Charles G., Lach, Boleslaw, Sendtner, Michael, Pfister, Stefan M., Taylor, Michael D., Chavez, Lukas, Kool, Marcel, Schüller, Ulrich

“…Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB)…”
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Genetic dependencies associated with transcription factor activities in human cancer cell lines by Thatikonda, Venu, Supper, Verena, Wachter, Johannes, Kaya, Onur, Kombara, Anju, Bilgilier, Ceren, Ravichandran, Madhwesh C., Lipp, Jesse J., Sharma, Rahul, Badertscher, Lukas, Boghossian, Andrew S., Rees, Matthew G., Ronan, Melissa M., Roth, Jennifer A., Grosche, Sarah, Neumüller, Ralph A., Mair, Barbara, Mauri, Federico, Popa, Alexandra

“…Transcription factors (TFs) are important mediators of aberrant transcriptional programs in cancer cells. In this study, we focus on TF activity (TFa) as a…”
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A subtype of cancer-associated fibroblasts with lower expression of alpha-smooth muscle actin suppresses stemness through BMP4 in oral carcinoma by Patel, Ankit Kumar, Vipparthi, Kavya, Thatikonda, Venu, Arun, Indu, Bhattacharjee, Samsiddhi, Sharan, Rajeev, Arun, Pattatheyil, Singh, Sandeep

“…Cancer-associated fibroblasts (CAFs) demonstrate the characteristics of myofibroblast differentiation by often expressing the ultrastructure of alpha-smooth…”
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Aberrant ERBB4-SRC Signaling as a Hallmark of Group 4 Medulloblastoma Revealed by Integrative Phosphoproteomic Profiling by Forget, Antoine, Martignetti, Loredana, Puget, Stéphanie, Calzone, Laurence, Brabetz, Sebastian, Picard, Daniel, Montagud, Arnau, Liva, Stéphane, Sta, Alexandre, Dingli, Florent, Arras, Guillaume, Rivera, Jaime, Loew, Damarys, Besnard, Aurore, Lacombe, Joëlle, Pagès, Mélanie, Varlet, Pascale, Dufour, Christelle, Yu, Hua, Mercier, Audrey L., Indersie, Emilie, Chivet, Anaïs, Leboucher, Sophie, Sieber, Laura, Beccaria, Kevin, Gombert, Michael, Meyer, Frauke D., Qin, Nan, Bartl, Jasmin, Chavez, Lukas, Okonechnikov, Konstantin, Sharma, Tanvi, Thatikonda, Venu, Bourdeaut, Franck, Pouponnot, Celio, Ramaswamy, Vijay, Korshunov, Andrey, Borkhardt, Arndt, Reifenberger, Guido, Poullet, Patrick, Taylor, Michael D., Kool, Marcel, Pfister, Stefan M., Kawauchi, Daisuke, Barillot, Emmanuel, Remke, Marc, Ayrault, Olivier

“…The current consensus recognizes four main medulloblastoma subgroups (wingless, Sonic hedgehog, group 3 and group 4). While medulloblastoma subgroups have been…”
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Abstract 3623: Targetable cofactor landscape of transcription factors in human cancers by Thatikonda, Venu, Lipp, Jesse, Schlattl, Andreas, Gerlach, Daniel, Popa, Alexandra

“…Abstract Transcription factors (TF) are proteins that bind to DNA to regulate target gene expression and play a crucial role in maintaining tumor initiating…”
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Interrogation of cancer gene dependencies reveals paralog interactions of autosome and sex chromosome-encoded genes by Köferle, Anna, Schlattl, Andreas, Hörmann, Alexandra, Thatikonda, Venu, Popa, Alexandra, Spreitzer, Fiona, Ravichandran, Madhwesh C., Supper, Verena, Oberndorfer, Sarah, Puchner, Teresa, Wieshofer, Corinna, Corcokovic, Maja, Reiser, Christoph, Wöhrle, Simon, Popow, Johannes, Pearson, Mark, Martinez, Javier, Weitzer, Stefan, Mair, Barbara, Neumüller, Ralph A.

“…Genetic networks are characterized by extensive buffering. During tumor evolution, disruption of functional redundancies can create de novo vulnerabilities…”
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Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified medulloblastoma by Ecker, Jonas, Thatikonda, Venu, Sigismondo, Gianluca, Selt, Florian, Valinciute, Gintvile, Oehme, Ina, Müller, Carina, Buhl, Juliane L, Ridinger, Johannes, Usta, Diren, Qin, Nan, van Tilburg, Cornelis M, Herold-Mende, Christel, Remke, Marc, Sahm, Felix, Westermann, Frank, Kool, Marcel, Wechsler-Reya, Robert J, Chavez, Lukas, Krijgsveld, Jeroen, Jäger, Natalie, Pfister, Stefan M, Witt, Olaf, Milde, Till

“…Abstract Background The sensitivity of myelocytomatosis oncogene (MYC) amplified medulloblastoma to class I histone deacetylase (HDAC) inhibition has been…”
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TBIO-04. Comprehensive analysis of mutational signatures in pediatric cancers by Thatikonda, Venu, Islam, S M Ashiqul, Autry, Robert J, Jones, Barbara C, Gröbner, Susanne, Warsow, Gregor, Hutter, Barbara, Huebschmann, Daniel, Fröhling, Stefan, Blattner-Johnson, Mirjam, Jones, David T W, Alexandrov, Ludmil B, M, Pfister, Stefan, Jäger, Natalie

“…Abstract Analysis of mutational signatures can reveal the underlying molecular processes that have caused the somatic mutations found in genomes. We performed…”
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Class I HDAC inhibitor entinostat synergizes with PLK1 inhibitors in MYC-amplified medulloblastoma cells by Valinciute, Gintvile, Ecker, Jonas, Selt, Florian, Hielscher, Thomas, Sigaud, Romain, Ridinger, Johannes, Thatikonda, Venu, Gatzweiler, Charlotte, Robinson, Sarah, Talbot, Julie, Bernardi, Flavia, Picard, Daniel, Blattner-Johnson, Mirjam, Schmid, Simone, Jones, David T., van Tilburg, Cornelis M., Capper, David, Kool, Marcel, Remke, Marc, Oehme, Ina, Pfister, Stefan M., Roussel, Martine F., Ayrault, Olivier, Witt, Olaf, Milde, Till

“…Purpose We and others have demonstrated that MYC -amplified medulloblastoma (MB) cells are susceptible to class I histone deacetylase inhibitor (HDACi)…”
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Two novel cell culture models of buccal mucosal oral cancer from patients with no risk-habits of tobacco smoking or chewing by Vipparthi, Kavya, Patel, Ankit Kumar, Ghosh, Subhashis, Das, Subrata, Das, Chitrarpita, Das, Koyeli, Sarkar, Anwesha, Thatikonda, Venu, Pal, Biswajoy, Remani, Arun Sasi kumaran Nair, Arora, Neeraj, Parihar, Mayur, Vijayakumar, Maleppillil Vavachan, Bhat, Manoj Kumar, Boppana, Ramanamurthy, Bhattacharjee, Samsiddhi, Biswas, Nidhan Kumar, Arun, Pattatheyil, Sharan, Rajeev, Singh, Sandeep

“…[Display omitted] •Two cell line models of buccal mucosal oral cancer from patients with no tobacco consumption habits.•Germ-line mutation status is considered…”
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Abstract 1926: MRAS the forgotten member of the GTPase superfamily plays a role in KRASG12Ci resistance by Thatikonda, Venu, Kostyrko, Kaja, Jurado, Sabine, Lieb, Simone, Hinkel, Melanie, Alpar, Donat, Bergner, Oliver, Jeschko, Astrid, Pearson, Mark, Hofmann, Marco H.

“…Abstract KRASG12C inhibitors have achieved impressive results in the clinic. However, intrinsic or acquired resistance to therapy invariably develops leading…”
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Functional relevance of genes predicted to be affected by epigenetic alterations in atypical teratoid/rhabdoid tumors by Tegeder, Isabel, Thiel, Katharina, Erkek, Serap, Johann, Pascal D., Berlandi, Johannes, Thatikonda, Venu, Frühwald, Michael C., Kool, Marcel, Jeibmann, Astrid, Hasselblatt, Martin

“…Purpose Atypical teratoid/rhabdoid tumor (ATRT) is a highly malignant brain tumor predominantly arising in infants. Mutations of SWI/SNF chromatin remodeling…”
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Comprehensive analysis of mutational signatures reveals distinct patterns and molecular processes across 27 pediatric cancers by Thatikonda, Venu, Islam, S M Ashiqul, Autry, Robert J, Jones, Barbara C, Gröbner, Susanne N, Warsow, Gregor, Hutter, Barbara, Huebschmann, Daniel, Fröhling, Stefan, Kool, Marcel, Blattner-Johnson, Mirjam, Jones, David T W, Alexandrov, Ludmil B, Pfister, Stefan M, Jäger, Natalie

“…Analysis of mutational signatures can reveal underlying molecular mechanisms of the processes that have imprinted the somatic mutations found in cancer…”
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MBRS-12. INTERFERENCE WITH THE FUNCTION OF MYC IN GROUP 3 MEDULLOBLASTOMA by Ecker, Jonas, Thatikonda, Venu, Oehme, Ina, Valinciute, Gintvile, Selt, Florian, Buhl, Juliane L, Usta, Diren, Tilburg, Cornelis M van, Herold-Mende, Christel, Schnölzer, Martina, Warnken, Uwe, Kool, Marcel, Jäger, Natalie, Pfister, Stefan M, Witt, Olaf, Milde, Till

“…Abstract High-risk medulloblastoma (MB) is a deadly disease with poor overall survival. Survivors suffer from severe treatment-associated morbidity. Patients…”
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Abstract 4004: Interrogation of cancer gene dependencies reveals novel paralog interactions of autosome and sex chromosome encoded genes by Köferle, Anna, Schlattl, Andreas, Hörmann, Alexandra, Spreitzer, Fiona, Popa, Alexandra, Thatikonda, Venu, Puchner, Teresa, Supper, Verena, Ravichandran, Madhwesh C., Oberndorfer, Sarah, Wieshofer, Corinna, Corcokovic, Maja, Reiser, Christoph, Wöhrle, Simon, Popow, Johannes, Pearson, Mark, Mair, Barbara, Neumüller, Ralph A.

“…Abstract Genetic networks are characterized by extensive buffering. During tumor evolution, disruption of these functional redundancies can create de novo…”
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Co-targeting SOS1 enhances the antitumor effects of KRAS G12C inhibitors by addressing intrinsic and acquired resistance by Thatikonda, Venu, Lyu, Hengyu, Jurado, Sabine, Kostyrko, Kaja, Bristow, Christopher A, Albrecht, Christoph, Alpar, Donat, Arnhof, Heribert, Bergner, Oliver, Bosch, Karin, Feng, Ningping, Gao, Sisi, Gerlach, Daniel, Gmachl, Michael, Hinkel, Melanie, Lieb, Simone, Jeschko, Astrid, Machado, Annette A, Madensky, Thomas, Marszalek, Ethan D, Mahendra, Mikhila, Melo-Zainzinger, Gabriella, Molkentine, Jessica M, Jaeger, Philipp A, Peng, David H, Schenk, Robyn L, Sorokin, Alexey, Strauss, Sandra, Trapani, Francesca, Kopetz, Scott, Vellano, Christopher P, Petronczki, Mark, Kraut, Norbert, Heffernan, Timothy P, Marszalek, Joseph R, Pearson, Mark, Waizenegger, Irene C, Hofmann, Marco H

“…Combination approaches are needed to strengthen and extend the clinical response to KRAS inhibitors (KRAS i). Here, we assessed the antitumor responses of KRAS…”
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Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance by Thatikonda, Venu, Lyu, Hengyu, Jurado, Sabine, Kostyrko, Kaja, Bristow, Christopher A., Albrecht, Christoph, Alpar, Donat, Arnhof, Heribert, Bergner, Oliver, Bosch, Karin, Feng, Ningping, Gao, Sisi, Gerlach, Daniel, Gmachl, Michael, Hinkel, Melanie, Lieb, Simone, Jeschko, Astrid, Machado, Annette A., Madensky, Thomas, Marszalek, Ethan D., Mahendra, Mikhila, Melo-Zainzinger, Gabriella, Molkentine, Jessica M., Jaeger, Philipp A., Peng, David H., Schenk, Robyn L., Sorokin, Alexey, Strauss, Sandra, Trapani, Francesca, Kopetz, Scott, Vellano, Christopher P., Petronczki, Mark, Kraut, Norbert, Heffernan, Timothy P., Marszalek, Joseph R., Pearson, Mark, Waizenegger, Irene C., Hofmann, Marco H.

“…Abstract Combination approaches are needed to strengthen and extend the clinical response to KRAS G12C inhibitors (KRAS G12C i). Here, we assessed the…”
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