Venu Thatikonda
German Cancer Research Center
14 Papers
11 Citations
Venu Thatikonda is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Biology & Cancer. The author has an hindex of 5, co-authored 8 publications. Previous affiliations of Venu Thatikonda include Boehringer Ingelheim.
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Papers
Aberrant ERBB4-SRC Signaling as a Hallmark of Group 4 Medulloblastoma Revealed by Integrative Phosphoproteomic Profiling.
Antoine Forget,Antoine Forget,Loredana Martignetti,Stéphanie Puget,Laurence Calzone,Sebastian Brabetz,Daniel Picard,Arnau Montagud,Stéphane Liva,Alexandre Sta,Florent Dingli,Guillaume Arras,Jaime Rivera,Damarys Loew,Aurore Besnard,Joelle Lacombe,Mélanie Pagès,Pascale Varlet,Christelle Dufour,Hua Yu,Hua Yu,Audrey Mercier,Audrey Mercier,Emilie Indersie,Emilie Indersie,Anaïs Chivet,Anaïs Chivet,Sophie Leboucher,Sophie Leboucher,Laura Sieber,Kevin Beccaria,Michael Gombert,Frauke Meyer,Nan Qin,Jasmin Bartl,Lukas Chavez,Konstantin Okonechnikov,Tanvi Sharma,Venu Thatikonda,Franck Bourdeaut,Celio Pouponnot,Celio Pouponnot,Vijay Ramaswamy,Andrey Korshunov,Arndt Borkhardt,Guido Reifenberger,Patrick Poullet,Michael D. Taylor,Marcel Kool,Stefan M. Pfister,Stefan M. Pfister,Daisuke Kawauchi,Emmanuel Barillot,Marc Remke,Olivier Ayrault,Olivier Ayrault +55 more
TL;DR: Proteomic and phosphoproteomic analyses identify aberrant ERBB4-SRC signaling in group 4 and unveils an oncogenic pathway and potential therapeutic vulnerability in the most common medulloblastoma subgroup.
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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
Ankit Kumar Patel,Kavya Vipparthi,Venu Thatikonda,Indu Arun,Samsiddhi Bhattacharjee,Rajeev Sharan,Pattatheyil Arun,Sandeep Singh +7 more
- 05 Oct 2018
TL;DR: An unexplored interaction between CAFs with lower-αSMA expression and SLCCs in oral tumors is discovered and the first evidence about the involvement of CAF-expressed BMP4 in regulation of self-renewal of oral-SLCCs is provided.
Comprehensive analysis of mutational signatures reveals distinct patterns and molecular processes across 27 pediatric cancers
Venu Thatikonda,S M Ashiqul Islam,Robert J Autry,Barbara C. Jones,Susanne Gröbner,Gregor Warsow,Barbara Hutter,D. Huebschmann,Stefan Fröhling,Marcel Kool,Mirjam Blattner-Johnson,David T. Jones,Ludmil B. Alexandrov,Stefan M. Pfister,Natalie Jäger +14 more
TL;DR: In this paper , the authors analyzed single base substitutions and small insertions and deletions in pediatric cancers encompassing 785 whole-genome sequenced tumors from 27 molecularly defined cancer subtypes.
Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma
Daniel Merk,Jasmin Ohli,Natalie D. Merk,Venu Thatikonda,Sorana Morrissy,Melanie Schoof,Susanne N. Schmid,Luke Harrison,Severin Filser,Julia Ahlfeld,Serap Erkek,Kaamini Raithatha,Thomas Andreska,Marc Weißhaar,Michael Launspach,Julia E. Neumann,Julia E. Neumann,Mehdi Shakarami,Dennis Plenker,Marco A. Marra,Yisu Li,Andrew J. Mungall,Richard A. Moore,Yussanne Ma,Steven J.M. Jones,Beat Lutz,Birgit Ertl-Wagner,Andrea Rossi,Rabea Wagener,Reiner Siebert,Andreas Jung,Charles G. Eberhart,Boleslaw Lach,Michael Sendtner,Stefan M. Pfister,Michael D. Taylor,Lukas Chavez,Marcel Kool,Ulrich Schüller +38 more
TL;DR: It is reported that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB, and loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf).
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Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified medulloblastoma.
Jonas Ecker,Jonas Ecker,Venu Thatikonda,Gianluca Sigismondo,Florian Selt,Gintvile Valinciute,Gintvile Valinciute,Ina Oehme,Carina Müller,Juliane L. Buhl,Juliane L. Buhl,Johannes Ridinger,Diren Usta,Nan Qin,Cornelis M. van Tilburg,Cornelis M. van Tilburg,Christel Herold-Mende,Marc Remke,Felix Sahm,Frank Westermann,Marcel Kool,Robert J. Wechsler-Reya,Lukas Chavez,Jeroen Krijgsveld,Jeroen Krijgsveld,Natalie Jäger,Stefan M. Pfister,Stefan M. Pfister,Olaf Witt,Olaf Witt,Till Milde,Till Milde +31 more
TL;DR: The data elucidates the molecular interaction of MYC and HDAC2 and support a model in which inhibition of class I HDACs directly targets MYC´s trans-activating and trans-repressing function.
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