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Start Over Author "Minita Shah" Journal nature genetics
3 results on '"Minita Shah"'

1. Author Correction: PGBD5 promotes site-specific oncogenic mutations in human tumors

Author

Anne-Katrin Emde, Elisa de Stanchina, Hanno Steen, David Torrents, Ian C. MacArthur, Richard Koche, Montserrat Puiggròs, Casie Reed, Charles W. M. Roberts, Catherine Reeves, Elizabeth J. Perlman, Christopher E. Mason, Stephen P. Jackson, Eric Still, Elias Rodriguez-Fos, Nicholas D. Socci, Jiali Zhuang, Cristina R. Antonescu, Santiago Gonzalez, Eileen Jiang, Elizabeth Mullen, Minita Shah, Alex Kentsis, Mithat Gonen, Zhiping Weng, Amy Eisenberg, Anton G. Henssen, Scott A. Armstrong, Andrew N. Blackford, and Kanika Arora

Subjects
Published Erratum, Genetics, MEDLINE, Cancer research, Biology
Published
2020

2. Erratum: PGBD5 promotes site-specific oncogenic mutations in human tumors

Author

Catherine Reeves, Elizabeth Mullen, Hanno Steen, Ian C. MacArthur, Santiago Gonzalez, Cristina R. Antonescu, Elizabeth Perlman, David Torrents, Christopher E. Mason, Eileen Jiang, Elias Rodriguez-Fos, Montserrat Puiggròs, Casie Reed, Eric Still, Stephen P. Jackson, Scott A. Armstrong, Jiali Zhuang, Nicholas D. Socci, Andrew N. Blackford, Kanika Arora, Anne-Katrin Emde, Elisa de Stanchina, Charles W. M. Roberts, Alex Kentsis, Mithat Gonen, Zhiping Weng, Anton G. Henssen, Richard Koche, Minita Shah, and Amy Eisenberg

Subjects
Published Erratum, Genetics, MEDLINE, Computational biology, Biology, Article
Abstract

Genomic rearrangements are a hallmark of human cancers. Here, we identify the piggyBac transposable element derived 5 (PGBD5) gene as an active DNA transposase expressed in the majority of childhood solid tumors, including lethal rhabdoid tumors. Using assembly-based whole-genome DNA sequencing, we found previously undefined genomic rearrangements in human rhabdoid tumors. These rearrangements involved PGBD5-specific signal (PSS) sequences at their breakpoints, recurrently inactivating tumor suppressor genes. PGBD5 was physically associated with genomic PSS sequences that were also sufficient to mediate PGBD5-induced DNA rearrangements in rhabdoid tumor cells. Ectopic expression of PGBD5 in primary immortalized human cells was sufficient to promote cell transformation in vivo. This activity required specific catalytic residues in the PGBD5 transposase domain, as well as end-joining DNA repair, and induced structural rearrangements with PSS breakpoints. This defines PGBD5 as an oncogenic mutator and provides a plausible mechanism for site-specific DNA rearrangements in childhood and adult solid tumors.

Published
2017

3. PGBD5 promotes site-specific oncogenic mutations in human tumors

Author

Minita Shah, Scott A. Armstrong, Ian C. MacArthur, Amy Eisenberg, Elizabeth Mullen, Elias Rodriguez-Fos, Andrew N. Blackford, David Torrents, Nicholas D. Socci, Hanno Steen, Kanika Arora, Casie Reed, Elizabeth J. Perlman, Santiago Gonzalez, Montserrat Puiggròs, Christopher E. Mason, Stephen P. Jackson, Eileen Jiang, Richard Koche, Anton G. Henssen, Cristina R. Antonescu, Eric Still, Catherine Reeves, Mithat Gönen, Anne-Katrin Emde, Elisa de Stanchina, Charles W. M. Roberts, Jiali Zhuang, Alex Kentsis, Zhiping Weng, Jackson, Stephen [0000-0001-9317-7937], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Transposable element, Adult, DNA End-Joining Repair, DNA repair, Chromosome Breakpoints, Mice, Nude, Transposases, embryonal neoplasms, Biology, Regulatory Sequences, Nucleic Acid, DNA sequencing, Cell Line, 03 medical and health sciences, chemistry.chemical_compound, Mice, Catalytic Domain, Genetics, Animals, Humans, Genes, Tumor Suppressor, Child, Gene, Transposase, Rhabdoid Tumor, Chromosome Aberrations, Gene Rearrangement, Terminal Repeat Sequences, Infant, Gene rearrangement, DNA, Neoplasm, Recombinant Proteins, 3. Good health, 030104 developmental biology, Cell Transformation, Neoplastic, chemistry, Child, Preschool, Cancer research, Mutagenesis, Site-Directed, RNA Interference, mutagenesis, DNA
Abstract

Genomic rearrangements are a hallmark of human cancers. Here, we identify the piggyBac transposable element derived 5 (PGBD5) gene as encoding an active DNA transposase expressed in the majority of childhood solid tumors, including lethal rhabdoid tumors. Using assembly-based whole-genome DNA sequencing, we found previously undefined genomic rearrangements in human rhabdoid tumors. These rearrangements involved PGBD5-specific signal (PSS) sequences at their breakpoints and recurrently inactivated tumor-suppressor genes. PGBD5 was physically associated with genomic PSS sequences that were also sufficient to mediate PGBD5-induced DNA rearrangements in rhabdoid tumor cells. Ectopic expression of PGBD5 in primary immortalized human cells was sufficient to promote cell transformation in vivo. This activity required specific catalytic residues in the PGBD5 transposase domain as well as end-joining DNA repair and induced structural rearrangements with PSS breakpoints. These results define PGBD5 as an oncogenic mutator and provide a plausible mechanism for site-specific DNA rearrangements in childhood and adult solid tumors.

Published
2016

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