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1. Personalized Cancer Monitoring Assay for the Detection of ctDNA in Patients with Solid Tumors

Author

Zhao, Jianhua, Reuther, Jacquelyn, Scozzaro, Kaylee, Hawley, Megan, Metzger, Emily, Emery, Matthew, Chen, Ingrid, Barbosa, Michelle, Johnson, Laura, O’Connor, Alijah, Washburn, Mike, Hartje, Luke, Reckase, Erik, Johnson, Verity, Zhang, Yuhua, Westheimer, Emily, O’Callaghan, William, Malani, Nirav, Chesh, Adrian, Moreau, Michael, and Daber, Robert

Published
2023
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2. Considerations for reporting variants in novel candidate genes identified during clinical genomic testing

Author

Abouhala, Siwaar, Albert, Jessica, Almalvez, Miguel, Alvarez, Raquel, Amin, Mutaz, Anderson, Peter, Aradhya, Swaroop, Ashley, Euan, Assimes, Themistocles, Auriga, Light, Austin-Tse, Christina, Bamshad, Mike, Barseghyan, Hayk, Baxter, Samantha, Behera, Sairam, Beheshti, Shaghayegh, Bejerano, Gill, Berger, Seth, Bernstein, Jon, Best, Sabrina, Blankenmeister, Benjamin, Blue, Elizabeth, Boerwinkle, Eric, Bonkowski, Emily, Bonner, Devon, Boone, Philip, Bornhorst, Miriam, Brand, Harrison, Buckingham, Kati, Calame, Daniel, Carter, Jennefer, Casadei, Silvia, Chadwick, Lisa, Chavez, Clarisa, Chen, Ziwei, Chinn, Ivan, Chong, Jessica, Coban-Akdemir, Zeynep, Cohen, Andrea J., Conner, Sarah, Conomos, Matthew, Coveler, Karen, Cui, Ya Allen, Currin, Sara, Daber, Robert, Dardas, Zain, Davis, Colleen, Dawood, Moez, de Dios, Ivan, de Esch, Celine, Delaney, Meghan, Delot, Emmanuele, DiTroia, Stephanie, Doddapaneni, Harsha, Du, Haowei, Duan, Ruizhi, Dugan-Perez, Shannon, Duong, Nhat, Duyzend, Michael, Eichler, Evan, Emami, Sara, Fraser, Jamie, Fusaro, Vincent, Galey, Miranda, Ganesh, Vijay, Garcia, Brandon, Garimella, Kiran, Gibbs, Richard, Gifford, Casey, Ginsburg, Amy, Goddard, Page, Gogarten, Stephanie, Gogate, Nikhita, Gordon, William, Gorzynski, John E., Greenleaf, William, Grochowski, Christopher, Groopman, Emily, Sousa, Rodrigo Guarischi, Gudmundsson, Sanna, Gulati, Ashima, Hall, Stacey, Harvey, William, Hawley, Megan, Heavner, Ben, Horike-Pyne, Martha, Hu, Jianhong, Huang, Yongqing, Hwang, James, Jarvik, Gail, Jensen, Tanner, Jhangiani, Shalini, Jimenez-Morales, David, Jin, Christopher, Saad, Ahmed K., Kahn-Kirby, Amanda, Kain, Jessica, Kaur, Parneet, Keehan, Laura, Knoblach, Susan, Ko, Arthur, Kundaje, Anshul, Kundu, Soumya, Lancaster, Samuel M., Larsson, Katie, Lee, Arthur, Lemire, Gabrielle, Lewis, Richard, Li, Wei, Li, Yidan, Liu, Pengfei, LoTempio, Jonathan, Lupski, James (Jim), Ma, Jialan, MacArthur, Daniel, Mahmoud, Medhat, Malani, Nirav, Mangilog, Brian, Marafi, Dana, Marmolejos, Sofia, Marten, Daniel, Martinez, Eva, Marvin, Colby, Marwaha, Shruti, Mastrorosa, Francesco Kumara, Matalon, Dena, May, Susanne, McGee, Sean, Meador, Lauren, Mefford, Heather, Mendez, Hector Rodrigo, Miller, Alexander, Miller, Danny E., Mitani, Tadahiro, Montgomery, Stephen, Moyses, Mariana, Munderloh, Chloe, Muzny, Donna, Nelson, Sarah, Nguyen, Thuy-mi P., Nguyen, Jonathan, Nussbaum, Robert, Nykamp, Keith, O'Callaghan, William, O'Heir, Emily, O'Leary, Melanie, Olsen, Jeren, Osei-Owusu, Ikeoluwa, O'Donnell-Luria, Anne, Padhi, Evin, Pais, Lynn, Pan, Miao, Panchal, Piyush, Patterson, Karynne, Payne, Sheryl, Pehlivan, Davut, Petrowski, Paul, Pham, Alicia, Pitsava, Georgia, Podesta, Astaria`Sara, Ponce, Sarah, Porter, Elizabeth, Posey, Jennifer, Prosser, Jaime, Quertermous, Thomas, Rai, Archana, Ramani, Arun, Rehm, Heidi, Reuter, Chloe, Reuter, Jason, Richardson, Matthew, Rivera-Munoz, Andres, Rubio, Oriane, Sabo, Aniko, Salani, Monica, Samocha, Kaitlin, Sanchis-Juan, Alba, Savage, Sarah, Scott, Evette, Scott, Stuart, Sedlazeck, Fritz, Shah, Gulalai, Shojaie, Ali, Singh, Mugdha, Smith, Kevin, Smith, Josh, Snow, Hana, Snyder, Michael, Socarras, Kayla, Starita, Lea, Stark, Brigitte, Stenton, Sarah, Stergachis, Andrew, Stilp, Adrienne, Sutton, V. Reid, Tai, Jui-Cheng, Talkowski, Michael (Mike), Tise, Christina, Tong, Catherine (Cat), Tsao, Philip, Ungar, Rachel, VanNoy, Grace, Vilain, Eric, Voutos, Isabella, Walker, Kim, Wei, Chia-Lin, Weisburd, Ben, Weiss, Jeff, Wellington, Chris, Weng, Ziming, Westheimer, Emily, Wheeler, Marsha, Wheeler, Matthew, Wiel, Laurens, Wilson, Michael, Wojcik, Monica, Wong, Quenna, Xiao, Changrui, Yadav, Rachita, Yi, Qian, Yuan, Bo, Zhao, Jianhua, Zhen, Jimmy, Zhou, Harry, Chong, Jessica X., Berger, Seth I., Smith, Erica, Calame, Daniel G., Hawley, Megan H., Rivera-Munoz, E. Andres, Bamshad, Michael J., and Rehm, Heidi L.

Published
2024
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3. Beyond the exome: What’s next in diagnostic testing for Mendelian conditions

Author

Abouhala, Siwaar, Albert, Jessica, Almalvez, Miguel, Alvarez, Raquel, Amin, Mutaz, Anderson, Peter, Aradhya, Swaroop, Ashley, Euan, Assimes, Themistocles, Auriga, Light, Austin-Tse, Christina, Bamshad, Mike, Barseghyan, Hayk, Baxter, Samantha, Behera, Sairam, Beheshti, Shaghayegh, Bejerano, Gill, Berger, Seth, Bernstein, Jon, Best, Sabrina, Blankenmeister, Benjamin, Blue, Elizabeth, Boerwinkle, Eric, Bonkowski, Emily, Bonner, Devon, Boone, Philip, Bornhorst, Miriam, Bozkurt-Yozgatli, Tugce, Brand, Harrison, Buckingham, Kati, Calame, Daniel, Casadei, Silvia, Chadwick, Lisa, Chavez, Clarisa, Chen, Ziwei, Chinn, Ivan, Chong, Jessica, Coban-Akdemir, Zeynep, Cohen, Andrea J., Conner, Sarah, Conomos, Matthew, Coveler, Karen, Cui, Ya Allen, Currin, Sara, Daber, Robert, Dardas, Zain, Davis, Colleen, Dawood, Moez, de Dios, Ivan, de Esch, Celine, Delaney, Meghan, Délot, Emmanuèle, DiTroia, Stephanie, Doddapaneni, Harsha, Du, Haowei, Duan, Ruizhi, Dugan-Perez, Shannon, Duong, Nhat, Duyzend, Michael, Eichler, Evan, Emami, Sara, Fatih, Jawid, Fraser, Jamie, Fusaro, Vincent, Galey, Miranda, Ganesh, Vijay, Garimella, Kiran, Gibbs, Richard, Gifford, Casey, Ginsburg, Amy, Goddard, Pagé, Gogarten, Stephanie, Gogate, Nikhita, Gordon, William, Gorzynski, John E., Greenleaf, William, Grochowski, Christopher, Groopman, Emily, Guarischi Sousa, Rodrigo, Gudmundsson, Sanna, Gulati, Ashima, Guo, Daniel, Hale, Walker, Hall, Stacey, Harvey, William, Hawley, Megan, Heavner, Ben, Herman, Isabella, Horike-Pyne, Martha, Hu, Jianhong, Huang, Yongqing, Hwang, James, Jarvik, Gail, Jensen, Tanner, Jhangiani, Shalini, Jimenez-Morales, David, Jin, Christopher, Saad, Ahmed K., Kahn-Kirby, Amanda, Kain, Jessica, Kaur, Parneet, Keehan, Laura, Knoblach, Susan, Ko, Arthur, Kohler, Jennefer, Kundaje, Anshul, Kundu, Soumya, Lancaster, Samuel M., Larsson, Katie, Lemire, Gabrielle, Lewis, Richard, Li, Wei, Li, Yidan, Liu, Pengfei, LoTempio, Jonathan, Lupski, James, Ma, Jialan, MacArthur, Daniel, Mahmoud, Medhat, Malani, Nirav, Mangilog, Brian, Marafi, Dana, Marmolejos, Sofia, Marten, Daniel, Martinez, Eva, Marvin, Colby, Marwaha, Shruti, Kumara Mastrorosa, Francesco, Matalon, Dena, May, Susanne, McGee, Sean, Meador, Lauren, Mefford, Heather, Rodrigo Mendez, Hector, Miller, Alexander, Miller, Danny E., Mitani, Tadahiro, Montgomery, Stephen, Moussa, Hala Mohamed, Moyses, Mariana, Munderloh, Chloe, Muzny, Donna, Nelson, Sarah, Neu, Matthew B., Nguyen, Jonathan, Nguyen, Thuy-mi P., Nussbaum, Robert, Nykamp, Keith, O'Callaghan, William, O'Heir, Emily, O'Leary, Melanie, Olsen, Jeren, Osei-Owusu, Ikeoluwa, O'Donnell-Luria, Anne, Padhi, Evin, Pais, Lynn, Pan, Miao, Panchal, Piyush, Patterson, Karynne, Payne, Sheryl, Pehlivan, Davut, Petrowski, Paul, Pham, Alicia, Pitsava, Georgia, Podesta, Astaria, Ponce, Sarah, Posey, Jennifer, Prosser, Jaime, Quertermous, Thomas, Rai, Archana, Ramani, Arun, Rehm, Heidi, Reuter, Chloe, Reuter, Jason, Richardson, Matthew, Rivera-Munoz, Andres, Rubio, Oriane, Sabo, Aniko, Salani, Monica, Samocha, Kaitlin, Sanchis-Juan, Alba, Savage, Sarah, Scott, Stuart, Scott, Evette, Sedlazeck, Fritz, Shah, Gulalai, Shojaie, Ali, Singh, Mugdha, Smith, Josh, Smith, Kevin, Snow, Hana, Snyder, Michael, Socarras, Kayla, Starita, Lea, Stark, Brigitte, Stenton, Sarah, Stergachis, Andrew, Stilp, Adrienne, Sundaram, Laksshman, Sutton, V. Reid, Tai, Jui-Cheng, Talkowski, Michael, Tise, Christina, Tong, Catherine, Tsao, Philip, Ungar, Rachel, VanNoy, Grace, Vilain, Eric, Voutos, Isabella, Walker, Kim, Weisburd, Ben, Weiss, Jeff, Wellington, Chris, Weng, Ziming, Westheimer, Emily, Wheeler, Marsha, Wheeler, Matthew, Wiel, Laurens, Wilson, Michael, Wojcik, Monica, Wong, Quenna, Wong, Issac, Xiao, Changrui, Yadav, Rachita, Yi, Qian, Yuan, Bo, Zhao, Jianhua, Zhen, Jimmy, Zhou, Harry, Wojcik, Monica H., Reuter, Chloe M., Duyzend, Michael H., Boone, Philip M., Groopman, Emily E., Délot, Emmanuèle C., Jain, Deepti, Starita, Lea M., Montgomery, Stephen B., Bamshad, Michael J., Chong, Jessica X., Wheeler, Matthew T., Berger, Seth I., and Sedlazeck, Fritz J.

Published
2023
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4. INSPIIRED: A Pipeline for Quantitative Analysis of Sites of New DNA Integration in Cellular Genomes

Author

Sherman, Eric, Nobles, Christopher, Berry, Charles C, Six, Emmanuelle, Wu, Yinghua, Dryga, Anatoly, Malani, Nirav, Male, Frances, Reddy, Shantan, Bailey, Aubrey, Bittinger, Kyle, Everett, John K, Caccavelli, Laure, Drake, Mary J, Bates, Paul, Hacein-Bey-Abina, Salima, Cavazzana, Marina, and Bushman, Frederic D

Subjects
Human Genome, Networking and Information Technology R&D (NITRD), Bioengineering, Genetics, Biotechnology, Generic health relevance, SCID-X1, gammaretrovirus, gene therapy, insertional mutagenesis, lentivirus, mutagenesis, recombination, retrovirus, vector, vector driving
Abstract

Integration of new DNA into cellular genomes mediates replication of retroviruses and transposons; integration reactions have also been adapted for use in human gene therapy. Tracking the distributions of integration sites is important to characterize populations of transduced cells and to monitor potential outgrow of pathogenic cell clones. Here, we describe a pipeline for quantitative analysis of integration site distributions named INSPIIRED (integration site pipeline for paired-end reads). We describe optimized biochemical steps for site isolation using Illumina paired-end sequencing, including new technology for suppressing recovery of unwanted contaminants, then software for alignment, quality control, and management of integration site sequences. During library preparation, DNAs are broken by sonication, so that after ligation-mediated PCR the number of ligation junction sites can be used to infer abundance of gene-modified cells. We generated integration sites of known positions in silico, and we describe optimization of sample processing parameters refined by comparison to truth. We also present a novel graph-theory-based method for quantifying integration sites in repeated sequences, and we characterize the consequences using synthetic and experimental data. In an accompanying paper, we describe an additional set of statistical tools for data analysis and visualization. Software is available at https://github.com/BushmanLab/INSPIIRED.

Published
2017

5. INSPIIRED: Quantification and Visualization Tools for Analyzing Integration Site Distributions

Author

Berry, Charles C, Nobles, Christopher, Six, Emmanuelle, Wu, Yinghua, Malani, Nirav, Sherman, Eric, Dryga, Anatoly, Everett, John K, Male, Frances, Bailey, Aubrey, Bittinger, Kyle, Drake, Mary J, Caccavelli, Laure, Bates, Paul, Hacein-Bey-Abina, Salima, Cavazzana, Marina, and Bushman, Frederic D

Subjects
Biotechnology, Networking and Information Technology R&D (NITRD), Human Genome, Genetics, Bioengineering, Cancer, SCID-X1, data visualization, gammaretrovirus, gene therapy, insertional mutagenesis, lentivirus, mutagenesis, recombination, retrovirus, vector, vector driving
Abstract

Analysis of sites of newly integrated DNA in cellular genomes is important to several fields, but methods for analyzing and visualizing these datasets are still under development. Here, we describe tools for data analysis and visualization that take as input integration site data from our INSPIIRED pipeline. Paired-end sequencing allows inference of the numbers of transduced cells as well as the distributions of integration sites in target genomes. We present interactive heatmaps that allow comparison of distributions of integration sites to genomic features and that support numerous user-defined statistical tests. To summarize integration site data from human gene therapy samples, we developed a reproducible report format that catalogs sample population structure, longitudinal dynamics, and integration frequency near cancer-associated genes. We also introduce a novel summary statistic, the UC50 (unique cell progenitors contributing the most expanded 50% of progeny cell clones), which provides a single number summarizing possible clonal expansion. Using these tools, we characterize ongoing longitudinal characterization of a patient from the first trial to treat severe combined immunodeficiency-X1 (SCID-X1), showing successful reconstitution for 15 years accompanied by persistence of a cell clone with an integration site near the cancer-associated gene CCND2. Software is available at https://github.com/BushmanLab/INSPIIRED.

Published
2017

6. Comparing DNA integration site clusters with scan statistics

Author

Berry, Charles C, Ocwieja, Karen E, Malani, Nirav, and Bushman, Frederic D

Subjects
Bioengineering, Gene Therapy, Genetics, Algorithms, Artificial Intelligence, DNA, Data Interpretation, Statistical, Genetic Vectors, Genomics, HIV, Humans, Jurkat Cells, Software, Virus Integration, Mathematical Sciences, Biological Sciences, Information and Computing Sciences, Bioinformatics
Abstract

MotivationGene therapy with retroviral vectors can induce adverse effects when those vectors integrate in sensitive genomic regions. Retroviral vectors are preferred that target sensitive regions less frequently, motivating the search for localized clusters of integration sites and comparison of the clusters formed by integration of different vectors. Scan statistics allow the discovery of spatial differences in clustering and calculation of false discovery rates providing statistical methods for comparing retroviral vectors.ResultsA scan statistic for comparing two vectors using multiple window widths is proposed with software to detect clustering differentials and compute false discovery rates. Application to several sets of experimentally determined HIV integration sites demonstrates the software. Simulated datasets of various sizes and signal strengths are used to determine the power to discover clusters and evaluate a convenient lower bound. This provides a toolkit for planning evaluations of new gene therapy vectors.Availability and implementationThe geneRxCluster R package containing a simple tutorial and usage hints is available from http://www.bioconductor.org.

Published
2014

7. HIV latency and integration site placement in five cell-based models

Author

Sherrill-Mix, Scott, Lewinski, Mary K, Famiglietti, Marylinda, Bosque, Alberto, Malani, Nirav, Ocwieja, Karen E, Berry, Charles C, Looney, David, Shan, Liang, Agosto, Luis M, Pace, Matthew J, Siliciano, Robert F, O’Doherty, Una, Guatelli, John, Planelles, Vicente, and Bushman, Frederic D

Abstract

Abstract Background HIV infection can be treated effectively with antiretroviral agents, but the persistence of a latent reservoir of integrated proviruses prevents eradication of HIV from infected individuals. The chromosomal environment of integrated proviruses has been proposed to influence HIV latency, but the determinants of transcriptional repression have not been fully clarified, and it is unclear whether the same molecular mechanisms drive latency in different cell culture models. Results Here we compare data from five different in vitro models of latency based on primary human T cells or a T cell line. Cells were infected in vitro and separated into fractions containing proviruses that were either expressed or silent/inducible, and integration site populations sequenced from each. We compared the locations of 6,252 expressed proviruses to those of 6,184 silent/inducible proviruses with respect to 140 forms of genomic annotation, many analyzed over chromosomal intervals of multiple lengths. A regularized logistic regression model linking proviral expression status to genomic features revealed no predictors of latency that performed better than chance, though several genomic features were significantly associated with proviral expression in individual models. Proviruses in the same chromosomal region did tend to share the same expressed or silent/inducible status if they were from the same cell culture model, but not if they were from different models. Conclusions The silent/inducible phenotype appears to be associated with chromosomal position, but the molecular basis is not fully clarified and may differ among in vitro models of latency.

Published
2013

8. HIV integration targeting: a pathway involving Transportin-3 and the nuclear pore protein RanBP2.

Author

Ocwieja, Karen E, Brady, Troy L, Ronen, Keshet, Huegel, Alyssa, Roth, Shoshannah L, Schaller, Torsten, James, Leo C, Towers, Greg J, Young, John AT, Chanda, Sumit K, König, Renate, Malani, Nirav, Berry, Charles C, and Bushman, Frederic D

Subjects
Humans, HIV, beta Karyopherins, Nuclear Pore Complex Proteins, Molecular Chaperones, RNA, Small Interfering, Virus Replication, Gene Expression Regulation, Viral, gag Gene Products, Human Immunodeficiency Virus, Host-Pathogen Interactions, Gene Knockdown Techniques, HEK293 Cells, Gene Expression Regulation, Viral, RNA, Small Interfering, gag Gene Products, Human Immunodeficiency Virus, Virology, Microbiology, Immunology, Medical Microbiology
Abstract

Genome-wide siRNA screens have identified host cell factors important for efficient HIV infection, among which are nuclear pore proteins such as RanBP2/Nup358 and the karyopherin Transportin-3/TNPO3. Analysis of the roles of these proteins in the HIV replication cycle suggested that correct trafficking through the pore may facilitate the subsequent integration step. Here we present data for coupling between these steps by demonstrating that depletion of Transportin-3 or RanBP2 altered the terminal step in early HIV replication, the selection of chromosomal sites for integration. We found that depletion of Transportin-3 and RanBP2 altered integration targeting for HIV. These knockdowns reduced HIV integration frequency in gene-dense regions and near gene-associated features, a pattern that differed from that reported for depletion of the HIV integrase binding cofactor Psip1/Ledgf/p75. MLV integration was not affected by the Transportin-3 knockdown. Using siRNA knockdowns and integration targeting analysis, we also implicated several additional nuclear proteins in proper target site selection. To map viral determinants of integration targeting, we analyzed a chimeric HIV derivative containing MLV gag, and found that the gag replacement phenocopied the Transportin-3 and RanBP2 knockdowns. Thus, our data support a model in which Gag-dependent engagement of the proper transport and nuclear pore machinery mediate trafficking of HIV complexes to sites of integration.

Published
2011

9. Host cell factors in HIV replication: meta-analysis of genome-wide studies.

Author

Bushman, Frederic D, Malani, Nirav, Fernandes, Jason, D'Orso, Iván, Cagney, Gerard, Diamond, Tracy L, Zhou, Honglin, Hazuda, Daria J, Espeseth, Amy S, König, Renate, Bandyopadhyay, Sourav, Ideker, Trey, Goff, Stephen P, Krogan, Nevan J, Frankel, Alan D, Young, John AT, and Chanda, Sumit K

Subjects
Humans, HIV, Cluster Analysis, Virus Replication, Protein Binding, Genome, Human, Internet, Databases, Protein, Host-Pathogen Interactions, Genome, Human, Databases, Protein, Virology, Microbiology, Immunology, Medical Microbiology
Abstract

We have analyzed host cell genes linked to HIV replication that were identified in nine genome-wide studies, including three independent siRNA screens. Overlaps among the siRNA screens were very modest (

Published
2009

10. Detection of Biallelic Loss of DNA Repair Genes in Formalin-Fixed, Paraffin-Embedded Tumor Samples Using a Novel Tumor-Only Sequencing Panel

Author

Glodzik, Dominik, primary, Selenica, Pier, additional, Rogge, Ryan A., additional, Silverman, Ian M., additional, Mandelker, Diana, additional, Harris, Sam, additional, Zhao, Jianhua, additional, Zinda, Michael, additional, Veloso, Artur, additional, Malani, Nirav, additional, Riaz, Nadeem, additional, Koehler, Maria, additional, Daber, Robert D., additional, Johnson, Verity, additional, Rimkunas, Victoria, additional, and Reis-Filho, Jorge S., additional

Published
2023
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12. piggyBac transposase tools for genome engineering

Author

Li, Xianghong, Burnight, Erin R., Cooney, Ashley L., Malani, Nirav, Brady, Troy, Sander, Jeffry D., Staber, Janice, Wheelan, Sarah J., Joung, J. Keith, McCray,, Paul B., Bushman, Frederic D., Sinn, Patrick L., and Craig, Nancy L.

Published
2013

18. Outcomes Following Gene Therapy in Patients With Severe Wiskott-Aldrich Syndrome

Author

Hacein-Bey Abina, Salima, Gaspar, H. Bobby, Blondeau, Johanna, Caccavelli, Laure, Charrier, Sabine, Buckland, Karen, Picard, Capucine, Six, Emmanuelle, Himoudi, Nourredine, Gilmour, Kimberly, McNicol, Anne-Marie, Hara, Havinder, Xu-Bayford, Jinhua, Rivat, Christine, Touzot, Fabien, Mavilio, Fulvio, Lim, Annick, Treluyer, Jean-Marc, Héritier, Sébastien, Lefrère, Francois, Magalon, Jeremy, Pengue-Koyi, Isabelle, Honnet, Géraldine, Blanche, Stéphane, Sherman, Eric A., Male, Frances, Berry, Charles, Malani, Nirav, Bushman, Frederic D., Fischer, Alain, Thrasher, Adrian J., Galy, Anne, and Cavazzana, Marina

Published
2015
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20. In vivo genome editing restores haemostasis in a mouse model of haemophilia

Author

Li, Hojun, Haurigot, Virginia, Doyon, Yannick, Li, Tianjian, Wong, Sunnie Y., Bhagwat, Anand S., Malani, Nirav, Anguela, Xavier M., Sharma, Rajiv, Ivanciu, Lacramiora, Murphy, Samuel L., Finn, Jonathan D., Khazi, Fayaz R., Zhou, Shangzhen, Paschon, David E., Rebar, Edward J., Bushman, Frederic D., Gregory, Philip D., Holmes, Michael C., and High, Katherine A.

Subjects
Hemostasis -- Research, Genomes -- Physiological aspects -- Health aspects, Hemophilia -- Physiological aspects -- Genetic aspects -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Editing of the human genome to correct disease-causing mutations is a promising approach for the treatment of genetic disorders. Genome editing improves on simple gene-replacement strategies by effecting in situ correction of a mutant gene, thus restoring normal gene function under the control of endogenous regulatory elements and reducing risks associated with random insertion into the genome. Gene-specific targeting has historically been limited to mouse embryonic stem cells. The development of zinc finger nucleases (ZFNs) has permitted efficient genome editing in transformed and primary cells that were previously thought to be intractable to such genetic manipulation (1). In vitro, ZFNs have been shown to promote efficient genome editing via homology-directed repair by inducing a site-specific double-strand break (DSB) at a target locus (2-4), but it is unclear whether ZFNs can induce DSBs and stimulate genome editing at a clinically meaningful level in vivo. Here we show that ZFNs are able to induce DSBs efficiently when delivered directly to mouse liver and that, when co-delivered with an appropriately designed gene-targeting vector, they can stimulate gene replacement through both homology-directed and homology-independent targeted gene insertion at the ZFN-specified locus. The level of gene targeting achieved was sufficient to correct the prolonged clotting times in a mouse model of haemophilia B, and remained persistent after induced liver regeneration. Thus, ZFN-driven gene correction can be achieved invivo, raising the possibility of genome editing as a viable strategy for the treatment of genetic disease., Viral-vector-mediated transfer of the wild-type copy of a gene that is defective in disease (gene replacement therapy) has been performed successfully in a variety of animal models and in humans [...]

Published
2011
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21. A Modified γ-Retrovirus Vector for X-Linked Severe Combined Immunodeficiency

Author

Hacein-Bey-Abina, Salima, Pai, Sung-Yun, Gaspar, Bobby H., Armant, Myriam, Berry, Charles C., Blanche, Stephane, Bleesing, Jack, Blondeau, Johanna, de Boer, Helen, Buckland, Karen F., Caccavelli, Laure, Cros, Guilhem, De Oliveira, Satiro, Fernández, Karen S., Guo, Dongjing, Harris, Chad E., Hopkins, Gregory, Lehmann, Leslie E., Lim, Annick, London, Wendy B., van der Loo, Johannes C.M., Malani, Nirav, Male, Frances, Malik, Punam, Marinovic, Angélica M., McNicol, Anne-Marie, Moshous, Despina, Neven, Benedicte, Oleastro, Matías, Picard, Capucine, Ritz, Jerome, Rivat, Christine, Schambach, Axel, Shaw, Kit L., Sherman, Eric A., Silberstein, Leslie E., Six, Emmanuelle, Touzot, Fabien, Tsytsykova, Alla, Xu-Bayford, Jinhua, Baum, Christopher, Bushman, Frederic D., Fischer, Alain, Kohn, Donald B., Filipovich, Alexandra H., Notarangelo, Luigi D., Cavazzana, Marina, Williams, David A., and Thrasher, Adrian J.

Published
2014
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24. Considerations for reporting variants in novel candidate genes identified during clinical genomic testing

Author

Chong, Jessica X., Berger, Seth I., Baxter, Samantha, Smith, Erica, Xiao, Changrui, Calame, Daniel G., Hawley, Megan H., Rivera-Munoz, E. Andres, DiTroia, Stephanie, Abouhala, Siwaar, Albert, Jessica, Almalvez, Miguel, Alvarez, Raquel, Amin, Mutaz, Anderson, Peter, Aradhya, Swaroop, Ashley, Euan, Assimes, Themistocles, Auriga, Light, Austin-Tse, Christina, Bamshad, Mike, Barseghyan, Hayk, Baxter, Samantha, Behera, Sairam, Beheshti, Shaghayegh, Bejerano, Gill, Berger, Seth, Bernstein, Jon, Best, Sabrina, Blankenmeister, Benjamin, Blue, Elizabeth, Boerwinkle, Eric, Bonkowski, Emily, Bonner, Devon, Boone, Philip, Bornhorst, Miriam, Brand, Harrison, Buckingham, Kati, Calame, Daniel, Carter, Jennefer, Casadei, Silvia, Chadwick, Lisa, Chavez, Clarisa, Chen, Ziwei, Chinn, Ivan, Chong, Jessica, Coban-Akdemir, Zeynep, Cohen, Andrea J., Conner, Sarah, Conomos, Matthew, Coveler, Karen, Cui, Ya Allen, Currin, Sara, Daber, Robert, Dardas, Zain, Davis, Colleen, Dawood, Moez, de Dios, Ivan, de Esch, Celine, Delaney, Meghan, Delot, Emmanuele, DiTroia, Stephanie, Doddapaneni, Harsha, Du, Haowei, Duan, Ruizhi, Dugan-Perez, Shannon, Duong, Nhat, Duyzend, Michael, Eichler, Evan, Emami, Sara, Fraser, Jamie, Fusaro, Vincent, Galey, Miranda, Ganesh, Vijay, Garcia, Brandon, Garimella, Kiran, Gibbs, Richard, Gifford, Casey, Ginsburg, Amy, Goddard, Page, Gogarten, Stephanie, Gogate, Nikhita, Gordon, William, Gorzynski, John E., Greenleaf, William, Grochowski, Christopher, Groopman, Emily, Sousa, Rodrigo Guarischi, Gudmundsson, Sanna, Gulati, Ashima, Hall, Stacey, Harvey, William, Hawley, Megan, Heavner, Ben, Horike-Pyne, Martha, Hu, Jianhong, Huang, Yongqing, Hwang, James, Jarvik, Gail, Jensen, Tanner, Jhangiani, Shalini, Jimenez-Morales, David, Jin, Christopher, Saad, Ahmed K., Kahn-Kirby, Amanda, Kain, Jessica, Kaur, Parneet, Keehan, Laura, Knoblach, Susan, Ko, Arthur, Kundaje, Anshul, Kundu, Soumya, Lancaster, Samuel M., Larsson, Katie, Lee, Arthur, Lemire, Gabrielle, Lewis, Richard, Li, Wei, Li, Yidan, Liu, Pengfei, LoTempio, Jonathan, Lupski, James (Jim), Ma, Jialan, MacArthur, Daniel, Mahmoud, Medhat, Malani, Nirav, Mangilog, Brian, Marafi, Dana, Marmolejos, Sofia, Marten, Daniel, Martinez, Eva, Marvin, Colby, Marwaha, Shruti, Mastrorosa, Francesco Kumara, Matalon, Dena, May, Susanne, McGee, Sean, Meador, Lauren, Mefford, Heather, Mendez, Hector Rodrigo, Miller, Alexander, Miller, Danny E., Mitani, Tadahiro, Montgomery, Stephen, Moyses, Mariana, Munderloh, Chloe, Muzny, Donna, Nelson, Sarah, Nguyen, Thuy-mi P., Nguyen, Jonathan, Nussbaum, Robert, Nykamp, Keith, O'Callaghan, William, O'Heir, Emily, O'Leary, Melanie, Olsen, Jeren, Osei-Owusu, Ikeoluwa, O'Donnell-Luria, Anne, Padhi, Evin, Pais, Lynn, Pan, Miao, Panchal, Piyush, Patterson, Karynne, Payne, Sheryl, Pehlivan, Davut, Petrowski, Paul, Pham, Alicia, Pitsava, Georgia, Podesta, Astaria`Sara, Ponce, Sarah, Porter, Elizabeth, Posey, Jennifer, Prosser, Jaime, Quertermous, Thomas, Rai, Archana, Ramani, Arun, Rehm, Heidi, Reuter, Chloe, Reuter, Jason, Richardson, Matthew, Rivera-Munoz, Andres, Rubio, Oriane, Sabo, Aniko, Salani, Monica, Samocha, Kaitlin, Sanchis-Juan, Alba, Savage, Sarah, Scott, Evette, Scott, Stuart, Sedlazeck, Fritz, Shah, Gulalai, Shojaie, Ali, Singh, Mugdha, Smith, Kevin, Smith, Josh, Snow, Hana, Snyder, Michael, Socarras, Kayla, Starita, Lea, Stark, Brigitte, Stenton, Sarah, Stergachis, Andrew, Stilp, Adrienne, Sutton, V. Reid, Tai, Jui-Cheng, Talkowski, Michael (Mike), Tise, Christina, Tong, Catherine (Cat), Tsao, Philip, Ungar, Rachel, VanNoy, Grace, Vilain, Eric, Voutos, Isabella, Walker, Kim, Wei, Chia-Lin, Weisburd, Ben, Weiss, Jeff, Wellington, Chris, Weng, Ziming, Westheimer, Emily, Wheeler, Marsha, Wheeler, Matthew, Wiel, Laurens, Wilson, Michael, Wojcik, Monica, Wong, Quenna, Xiao, Changrui, Yadav, Rachita, Yi, Qian, Yuan, Bo, Zhao, Jianhua, Zhen, Jimmy, Zhou, Harry, Bamshad, Michael J., and Rehm, Heidi L.

Abstract

Since the first novel gene discovery for a Mendelian condition was made via exome sequencing, the rapid increase in the number of genes known to underlie Mendelian conditions coupled with the adoption of exome (and more recently, genome) sequencing by diagnostic testing labs has changed the landscape of genomic testing for rare diseases. Specifically, many individuals suspected to have a Mendelian condition are now routinely offered clinical ES. This commonly results in a precise genetic diagnosis but frequently overlooks the identification of novel candidate genes. Such candidates are also less likely to be identified in the absence of large-scale gene discovery research programs. Accordingly, clinical laboratories have both the opportunity, and some might argue a responsibility, to contribute to novel gene discovery, which should, in turn, increase the diagnostic yield for many conditions. However, clinical diagnostic laboratories must necessarily balance priorities for throughput, turnaround time, cost efficiency, clinician preferences, and regulatory constraints and often do not have the infrastructure or resources to effectively participate in either clinical translational or basic genome science research efforts. For these and other reasons, many laboratories have historically refrained from broadly sharing potentially pathogenic variants in novel genes via networks such as Matchmaker Exchange, much less reporting such results to ordering providers. Efforts to report such results are further complicated by a lack of guidelines for clinical reporting and interpretation of variants in novel candidate genes. Nevertheless, there are myriad benefits for many stakeholders, including patients/families, clinicians, and researchers, if clinical laboratories systematically and routinely identify, share, and report novel candidate genes. To facilitate this change in practice, we developed criteria for triaging, sharing, and reporting novel candidate genes that are most likely to be promptly validated as underlying a Mendelian condition and translated to use in clinical settings.

Published
2024
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30. Feasibility of blood testing combined with PET-CT to screen for cancer and guide intervention

Author

Lennon, Anne Marie, primary, Buchanan, Adam H., additional, Kinde, Isaac, additional, Warren, Andrew, additional, Honushefsky, Ashley, additional, Cohain, Ariella T., additional, Ledbetter, David H., additional, Sanfilippo, Fred, additional, Sheridan, Kathleen, additional, Rosica, Dillenia, additional, Adonizio, Christian S., additional, Hwang, Hee Jung, additional, Lahouel, Kamel, additional, Cohen, Joshua D., additional, Douville, Christopher, additional, Patel, Aalpen A., additional, Hagmann, Leonardo N., additional, Rolston, David D., additional, Malani, Nirav, additional, Zhou, Shibin, additional, Bettegowda, Chetan, additional, Diehl, David L., additional, Urban, Bobbi, additional, Still, Christopher D., additional, Kann, Lisa, additional, Woods, Julie I., additional, Salvati, Zachary M., additional, Vadakara, Joseph, additional, Leeming, Rosemary, additional, Bhattacharya, Prianka, additional, Walter, Carroll, additional, Parker, Alex, additional, Lengauer, Christoph, additional, Klein, Alison, additional, Tomasetti, Cristian, additional, Fishman, Elliot K., additional, Hruban, Ralph H., additional, Kinzler, Kenneth W., additional, Vogelstein, Bert, additional, and Papadopoulos, Nickolas, additional

Published
2020
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34. Bacteriophage Mu integration in yeast and mammalian genomes

Author

Paatero, Anja O., Turakainen, Hilkka, Happonen, Lotta J., Olsson, Cia, Palomäki, Tiina, Pajunen, Maria I., Meng, Xiaojuan, Otonkoski, Timo, Tuuri, Timo, Berry, Charles, Malani, Nirav, Frilander, Mikko J., Bushman, Frederic D., and Savilahti, Harri

Published
2008

36. HRP-2 determines HIV-1 integration site selection in LEDGF/p75 depleted cells

Author

Schrijvers Rik, Vets Sofie, De Rijck Jan, Malani Nirav, Bushman Frederic D, Debyser Zeger, and Gijsbers Rik

Subjects
LEDGF/p75, HRP-2, HIV-1, Targeting, Integration site analysis, Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Lens epithelium–derived growth factor (LEDGF/p75) is a cellular co-factor of HIV-1 integrase (IN) that tethers the viral pre-integration complex to the host cell chromatin and determines the genome wide integration site distribution pattern of HIV-1. Recently, we demonstrated that HIV-1 replication was reduced in LEDGF/p75 knockout (KO) cells. LEDGF/p75 KO significantly altered the integration site preference of HIV-1, but the pattern remained distinct from a computationally generated matched random control set (MRC), suggesting the presence of an alternative tethering factor. We previously identified Hepatoma-derived growth factor related protein 2 (HRP-2) as a factor mediating LEDGF/p75-independent HIV-1 replication. However, the role of HRP-2 in HIV-1 integration site selection was not addressed. Findings We studied the HIV-1 integration site distribution in the presence and absence of LEDGF/p75 and/or HRP-2, and in LEDGF/p75-depleted cells that overexpress HRP-2. We show that HRP-2 functions as a co-factor of HIV-1 IN in LEDGF/p75-depleted cells. Endogenous HRP-2 only weakly supported HIV-1 replication in LEDGF/p75 depleted cells. However, HRP-2 overexpression rescued HIV-1 replication and restored integration in RefSeq genes to wild-type levels. Additional HRP-2 KD in LEDGF/p75-depleted cells reduces integration frequency in transcription units and shifts the integration distribution towards random. Conclusions We demonstrate that HRP-2 overexpression can compensate for the absence of LEDGF/p75 and indicate that the residual bias in integration targeting observed in the absence of LEDGF/p75 can be ascribed to HRP-2. Knockdown of HRP-2 upon LEDGF/p75 depletion results in a more random HIV-1 integration pattern. These data therefore reinforce the understanding that LEDGF/p75 is the dominant HIV-1 IN co-factor.

Published
2012
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37. A gene-rich, transcriptionally active environment and the pre-deposition of repressive marks are predictive of susceptibility to KRAB/KAP1-mediated silencing

Author

Zangger Nadine, Quenneville Simon, Malani Nirav, Ambrosini Giovanna, Groner Anna C, Meylan Sylvain, Kapopoulou Adamandia, Kauzlaric Annamaria, Rougemont Jacques, Ciuffi Angela, Bushman Frederic D, Bucher Philipp, and Trono Didier

Subjects
KAP1, KRAB-zinc finger proteins, transcriptional repression, chromatin, heterochromatin, histone modifications, Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background KRAB-ZFPs (Krüppel-associated box domain-zinc finger proteins) are vertebrate-restricted transcriptional repressors encoded in the hundreds by the mouse and human genomes. They act via an essential cofactor, KAP1, which recruits effectors responsible for the formation of facultative heterochromatin. We have recently shown that KRAB/KAP1 can mediate long-range transcriptional repression through heterochromatin spreading, but also demonstrated that this process is at times countered by endogenous influences. Method To investigate this issue further we used an ectopic KRAB-based repressor. This system allowed us to tether KRAB/KAP1 to hundreds of euchromatic sites within genes, and to record its impact on gene expression. We then correlated this KRAB/KAP1-mediated transcriptional effect to pre-existing genomic and chromatin structures to identify specific characteristics making a gene susceptible to repression. Results We found that genes that were susceptible to KRAB/KAP1-mediated silencing carried higher levels of repressive histone marks both at the promoter and over the transcribed region than genes that were insensitive. In parallel, we found a high enrichment in euchromatic marks within both the close and more distant environment of these genes. Conclusion Together, these data indicate that high levels of gene activity in the genomic environment and the pre-deposition of repressive histone marks within a gene increase its susceptibility to KRAB/KAP1-mediated repression.

Published
2011
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39. Integration target site selection by a resurrected human endogenous retrovirus

Author

Brady, Troy, Young Nam Lee, Ronen, Keshet, Malani, Nirav, Berry, Charles C., Bieniasz, Paul D., and Bushman, Frederic D.

Subjects
Retroviruses -- Genetic aspects, Human genome -- Research, Genetic regulation -- Research, Genetic transcription -- Research, Nucleotide sequence -- Analysis, Biological sciences
Published
2009

40. INSPIIRED: A Pipeline for Quantitative Analysis of Sites of New DNA Integration in Cellular Genomes

Author

Sherman, Eric, primary, Nobles, Christopher, additional, Berry, Charles C., additional, Six, Emmanuelle, additional, Wu, Yinghua, additional, Dryga, Anatoly, additional, Malani, Nirav, additional, Male, Frances, additional, Reddy, Shantan, additional, Bailey, Aubrey, additional, Bittinger, Kyle, additional, Everett, John K., additional, Caccavelli, Laure, additional, Drake, Mary J., additional, Bates, Paul, additional, Hacein-Bey-Abina, Salima, additional, Cavazzana, Marina, additional, and Bushman, Frederic D., additional

Published
2017
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41. INSPIIRED: Quantification and Visualization Tools for Analyzing Integration Site Distributions

Author

Berry, Charles C., primary, Nobles, Christopher, additional, Six, Emmanuelle, additional, Wu, Yinghua, additional, Malani, Nirav, additional, Sherman, Eric, additional, Dryga, Anatoly, additional, Everett, John K., additional, Male, Frances, additional, Bailey, Aubrey, additional, Bittinger, Kyle, additional, Drake, Mary J., additional, Caccavelli, Laure, additional, Bates, Paul, additional, Hacein-Bey-Abina, Salima, additional, Cavazzana, Marina, additional, and Bushman, Frederic D., additional

Published
2017
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42. Allosteric Inhibition of Human Immunodeficiency Virus Integrase: LATE BLOCK DURING VIRAL REPLICATION AND ABNORMAL MULTIMERIZATION INVOLVING SPECIFIC PROTEIN DOMAINS*

Author

Gupta, Kushol, Brady, Troy, Dyer, Benjamin M., Malani, Nirav, Hwang, Young, Male, Frances, Nolte, Robert T., Wang, Liping, Velthuisen, Emile, Jeffrey, Jerry, Van Duyne, Gregory D., and Bushman, Frederic D.

Subjects
musculoskeletal diseases, Molecular Bases of Disease, HIV Integrase, Crystallography, X-Ray, Virus Replication, biological factors, Cell Line, Protein Structure, Tertiary, nervous system, Allosteric Regulation, HIV-1, Humans, sense organs, HIV Integrase Inhibitors, Protein Multimerization, Adaptor Proteins, Signal Transducing, Transcription Factors
Abstract

HIV-1 replication in the presence of antiviral agents results in evolution of drug-resistant variants, motivating the search for additional drug classes. Here we report studies of GSK1264, which was identified as a compound that disrupts the interaction between HIV-1 integrase (IN) and the cellular factor lens epithelium-derived growth factor (LEDGF)/p75. GSK1264 displayed potent antiviral activity and was found to bind at the site occupied by LEDGF/p75 on IN by x-ray crystallography. Assays of HIV replication in the presence of GSK1264 showed only modest inhibition of the early infection steps and little effect on integration targeting, which is guided by the LEDGF/p75-IN interaction. In contrast, inhibition of late replication steps was more potent. Particle production was normal, but particles showed reduced infectivity. GSK1264 promoted aggregation of IN and preformed LEDGF/p75-IN complexes, suggesting a mechanism of inhibition. LEDGF/p75 was not displaced from IN during aggregation, indicating trapping of LEDGF/p75 in aggregates. Aggregation assays with truncated IN variants revealed that a construct with catalytic and C-terminal domains of IN only formed an open polymer associated with efficient drug-induced aggregation. These data suggest that the allosteric inhibitors of IN are promising antiviral agents and provide new information on their mechanism of action.

Published
2014

44. Defining the lentiviral integrome in human hematopoietic cells

Author

Recchia, Alessandra, Cattoglio, Claudia, Pellin, Danilo, Rizzi, Ermanno, Corti, Giorgio, Di Serio, Clelia, Malani, Nirav, Bushman, Frederick, De Bellis, Gianluca, and Mavilio, Fulvio

Subjects
lentiviral vector , integration, lentiviral vector, integration
Published
2011

45. Coherence analysis discriminates between retroviral integration patterns in CD34+ cells transduced under differing clinical trial conditions

Author

Hallwirth, Claus V, primary, Garg, Gagan, additional, Peters, Timothy J, additional, Kramer, Belinda A, additional, Malani, Nirav V, additional, Hyman, Jessica, additional, Ruan, Xiaoan, additional, Ginn, Samantha L, additional, Hetherington, Nicola A, additional, Veeravalli, Lavanya, additional, Shahab, Atif, additional, Ranganathan, Shoba, additional, Wei, Chia-Lin, additional, Liddle, Christopher, additional, Thrasher, Adrian J, additional, Bushman, Frederic D, additional, Buckley, Michael J, additional, and Alexander, Ian E, additional

Published
2015
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46. Allosteric Inhibition of Human Immunodeficiency Virus Integrase

Author

Gupta, Kushol, primary, Brady, Troy, additional, Dyer, Benjamin M., additional, Malani, Nirav, additional, Hwang, Young, additional, Male, Frances, additional, Nolte, Robert T., additional, Wang, Liping, additional, Velthuisen, Emile, additional, Jeffrey, Jerry, additional, Van Duyne, Gregory D., additional, and Bushman, Frederic D., additional

Published
2014
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47. A New Class of Multimerization Selective Inhibitors of HIV-1 Integrase

Author

Sharma, Amit, primary, Slaughter, Alison, additional, Jena, Nivedita, additional, Feng, Lei, additional, Kessl, Jacques J., additional, Fadel, Hind J., additional, Malani, Nirav, additional, Male, Frances, additional, Wu, Li, additional, Poeschla, Eric, additional, Bushman, Frederic D., additional, Fuchs, James R., additional, and Kvaratskhelia, Mamuka, additional

Published
2014
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48. The Major Cellular Sterol Regulatory Pathway Is Required for Andes Virus Infection

Author

Petersen, Josiah, primary, Drake, Mary Jane, additional, Bruce, Emily A., additional, Riblett, Amber M., additional, Didigu, Chukwuka A., additional, Wilen, Craig B., additional, Malani, Nirav, additional, Male, Frances, additional, Lee, Fang-Hua, additional, Bushman, Frederic D., additional, Cherry, Sara, additional, Doms, Robert W., additional, Bates, Paul, additional, and Briley, Kenneth, additional

Published
2014
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49. The BET Family of Proteins Targets Moloney Murine Leukemia Virus Integration near Transcription Start Sites

Author

De Rijck, Jan, primary, de Kogel, Christine, additional, Demeulemeester, Jonas, additional, Vets, Sofie, additional, El Ashkar, Sara, additional, Malani, Nirav, additional, Bushman, Frederic D., additional, Landuyt, Bart, additional, Husson, Steven J., additional, Busschots, Katrien, additional, Gijsbers, Rik, additional, and Debyser, Zeger, additional

Published
2013
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50. BET proteins target murine leukemia virus integration to transcription start sites

Author

Sharma, Amit, primary, Larue, Ross, additional, Plumb, Matthew, additional, Malani, Nirav, additional, Male, Frances, additional, Slaughter, Alison, additional, Kessl, Jacques, additional, Shkriabai, Nikoloz, additional, Coward, Elizabeth, additional, Aiyer, Sriram, additional, Green, Patrick, additional, Wu, Li, additional, Roth, Monica, additional, Bushman, Frederic, additional, and Kvaratskhelia, Mamuka, additional

Published
2013
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