Search Results - "Jacob Glass"

LINE-1 Activity in Facultative Heterochromatin Formation during X Chromosome Inactivation by Chow, Jennifer C., Ciaudo, Constance, Fazzari, Melissa J., Mise, Nathan, Servant, Nicolas, Glass, Jacob L., Attreed, Matthew, Avner, Philip, Wutz, Anton, Barillot, Emmanuel, Greally, John M., Voinnet, Olivier, Heard, Edith

“…During X chromosome inactivation (XCI), Xist RNA coats and silences one of the two X chromosomes in female cells. Little is known about how XCI spreads across…”
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Epigenetic Identity in AML Depends on Disruption of Nonpromoter Regulatory Elements and Is Affected by Antagonistic Effects of Mutations in Epigenetic Modifiers by Glass, Jacob L, Hassane, Duane, Wouters, Bas J, Kunimoto, Hiroyoshi, Avellino, Roberto, Garrett-Bakelman, Francine E, Guryanova, Olga A, Bowman, Robert, Redlich, Shira, Intlekofer, Andrew M, Meydan, Cem, Qin, Tingting, Fall, Mame, Alonso, Alicia, Guzman, Monica L, Valk, Peter J M, Thompson, Craig B, Levine, Ross, Elemento, Olivier, Delwel, Ruud, Melnick, Ari, Figueroa, Maria E

“…We performed cytosine methylation sequencing on genetically diverse patients with acute myeloid leukemia (AML) and found leukemic DNA methylation patterning is…”
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Multilineage involvement in KMT2A‐rearranged B acute lymphoblastic leukaemia: cell‐of‐origin, biology, and clinical implications by Aypar, Umut, Dilip, Deepika, Gadde, Ramya, Londono, Dory M, Liu, Ying, Gao, Qi, Geyer, Mark B, Derkach, Andriy, Zhang, Yanming, Glass, Jacob L, Roshal, Mikhail, Xiao, Wenbin

“…Aims B lymphoblastic leukaemia/lymphoma (B‐ALL) is thought to originate from Pro/Pre‐B cells and the genetic aberrations largely reside in lymphoid‐committed…”
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Comparative isoschizomer profiling of cytosine methylation: the HELP assay by Khulan, Batbayar, Thompson, Reid F, Ye, Kenny, Fazzari, Melissa J, Suzuki, Masako, Stasiek, Edyta, Figueroa, Maria E, Glass, Jacob L, Chen, Quan, Montagna, Cristina, Hatchwell, Eli, Selzer, Rebecca R, Richmond, Todd A, Green, Roland D, Melnick, Ari, Greally, John M

“…The distribution of cytosine methylation in 6.2 Mb of the mouse genome was tested using cohybridization of genomic representations from a methylation-sensitive…”
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PRC2-Inactivating Mutations in Cancer Enhance Cytotoxic Response to DNMT1-Targeted Therapy via Enhanced Viral Mimicry by Patel, Amish J, Warda, Sarah, Maag, Jesper L V, Misra, Rohan, Miranda-Román, Miguel A, Pachai, Mohini R, Lee, Cindy J, Li, Dan, Wang, Naitao, Bayshtok, Gabriella, Fishinevich, Eve, Meng, Yinuo, Wong, Elissa W P, Yan, Juan, Giff, Emily, Pappalardi, Melissa B, McCabe, Michael T, Fletcher, Jonathan A, Rudin, Charles M, Chandarlapaty, Sarat, Scandura, Joseph M, Koche, Richard P, Glass, Jacob L, Antonescu, Cristina R, Zheng, Deyou, Chen, Yu, Chi, Ping

“…Polycomb repressive complex 2 (PRC2) has oncogenic and tumor-suppressive roles in cancer. There is clinical success of targeting this complex in PRC2-dependent…”
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Rational Targeting of Cooperating Layers of the Epigenome Yields Enhanced Therapeutic Efficacy against AML by Duy, Cihangir, Teater, Matt, Garrett-Bakelman, Francine E, Lee, Tak C, Meydan, Cem, Glass, Jacob L, Li, Meng, Hellmuth, Johannes C, Mohammad, Helai P, Smitheman, Kimberly N, Shih, Alan H, Abdel-Wahab, Omar, Tallman, Martin S, Guzman, Monica L, Muench, David, Grimes, H Leighton, Roboz, Gail J, Kruger, Ryan G, Creasy, Caretha L, Paietta, Elisabeth M, Levine, Ross L, Carroll, Martin, Melnick, Ari M

“…Disruption of epigenetic regulation is a hallmark of acute myeloid leukemia (AML), but epigenetic therapy is complicated by the complexity of the epigenome…”
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Genetic and epigenetic evolution as a contributor to WT1-mutant leukemogenesis by Pronier, Elodie, Bowman, Robert L., Ahn, Jihae, Glass, Jacob, Kandoth, Cyriac, Merlinsky, Tiffany R., Whitfield, Justin T., Durham, Benjamin H., Gruet, Antoine, Hanasoge Somasundara, Amritha Varshini, Rampal, Raajit, Melnick, Ari, Koche, Richard P., Taylor, Barry S., Levine, Ross L.

“…Genetic studies have identified recurrent somatic mutations in acute myeloid leukemia (AML) patients, including in the Wilms' tumor 1 (WT1) gene. The molecular…”
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A Phase I/II Open-Label Study of Molibresib for the Treatment of Relapsed/Refractory Hematologic Malignancies by Dawson, Mark A, Borthakur, Gautam, Huntly, Brian J P, Karadimitris, Anastasios, Alegre, Adrian, Chaidos, Aristeidis, Vogl, Dan T, Pollyea, Daniel A, Davies, Faith E, Morgan, Gareth J, Glass, Jacob L, Kamdar, Manali, Mateos, Maria-Victoria, Tovar, Natalia, Yeh, Paul, Delgado, Regina García, Basheer, Faisal, Marando, Ludovica, Gallipoli, Paolo, Wyce, Anastasia, Krishnatry, Anu Shilpa, Barbash, Olena, Bakirtzi, Evi, Ferron-Brady, Geraldine, Karpinich, Natalie O, McCabe, Michael T, Foley, Shawn W, Horner, Thierry, Dhar, Arindam, Kremer, Brandon E, Dickinson, Michael

“…Molibresib is a selective, small molecule inhibitor of the bromodomain and extra-terminal (BET) protein family. This was an open-label, two-part, Phase I/II…”
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Arsenic trioxide therapy predisposes to herpes zoster reactivation despite minimally myelosuppressive therapy by Glass, Jacob L., Derkach, Andriy, Hilden, Patrick, King, Amber, Seo, Susan K., Ahr, Katya, Kishtagari, Ashwin, Levine, Ross L., Tallman, Martin S., Douer, Dan

“…•Acute promyelocytic leukemia is highly responsive to minimally myelosuppressive therapy with all-trans retinoic acid and arsenic trioxide.•Arsenic trioxide…”
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Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms by Dunbar, Andrew J, Bowman, Robert L, Park, Young C, O'Connor, Kavi, Izzo, Franco, Myers, Robert M, Karzai, Abdul, Zaroogian, Zachary, Kim, Won Jun, Fernández-Maestre, Inés, Waarts, Michael R, Nazir, Abbas, Xiao, Wenbin, Codilupi, Tamara, Brodsky, Max, Farina, Mirko, Cai, Louise, Cai, Sheng F, Wang, Benjamin, An, Wenbin, Yang, Julie L, Mowla, Shoron, Eisman, Shira E, Hanasoge Somasundara, Amritha Varshini, Glass, Jacob L, Mishra, Tanmay, Houston, Remie, Guzzardi, Emily, Martinez Benitez, Anthony R, Viny, Aaron D, Koche, Richard P, Meyer, Sara C, Landau, Dan A, Levine, Ross L

“…Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly JAK2V617F…”
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Molecular predictors of immunophenotypic measurable residual disease clearance in acute myeloid leukemia by Stahl, Maximilian, Derkach, Andriy, Farnoud, Noushin, Bewersdorf, Jan Philipp, Robinson, Troy, Famulare, Christopher, Cho, Christina, Devlin, Sean, Menghrajani, Kamal, Patel, Minal A., Cai, Sheng F., Miles, Linde A., Bowman, Robert L., Geyer, Mark B., Dunbar, Andrew, Epstein‐Peterson, Zachary D., McGovern, Erin, Schulman, Jessica, Glass, Jacob L., Taylor, Justin, Viny, Aaron D., Stein, Eytan M., Getta, Bartlomiej, Arcila, Maria E., Gao, Qi, Barker, Juliet, Shaffer, Brian C., Papadopoulos, Esperanza B., Gyurkocza, Boglarka, Perales, Miguel‐Angel, Abdel‐Wahab, Omar, Levine, Ross L., Giralt, Sergio A., Zhang, Yanming, Xiao, Wenbin, Pai, Nidhi, Papaemmanuil, Elli, Tallman, Martin S., Roshal, Mikhail, Goldberg, Aaron D.

“…Measurable residual disease (MRD) is a powerful prognostic factor in acute myeloid leukemia (AML). However, pre‐treatment molecular predictors of…”
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High-resolution genome-wide cytosine methylation profiling with simultaneous copy number analysis and optimization for limited cell numbers by Oda, Mayumi, Glass, Jacob L, Thompson, Reid F, Mo, Yongkai, Olivier, Emmanuel N, Figueroa, Maria E, Selzer, Rebecca R, Richmond, Todd A, Zhang, Xinmin, Dannenberg, Luke, Green, Roland D, Melnick, Ari, Hatchwell, Eli, Bouhassira, Eric E, Verma, Amit, Suzuki, Masako, Greally, John M

“…Many genome-wide assays involve the generation of a subset (or representation) of the genome following restriction enzyme digestion. The use of enzymes…”
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Loss of plasmacytoid dendritic cell differentiation is highly predictive for post-induction measurable residual disease and inferior outcomes in acute myeloid leukemia by Xiao, Wenbin, Goldberg, Aaron D, Famulare, Christopher A, Devlin, Sean M, Nguyen, Nghia T, Sim, Sinnifer, Kabel, Charlene C, Patel, Minal A, McGovern, Erin M, Patel, Akshar, Schulman, Jessica, Dunbar, Andrew J, Epstein-Peterson, Zachary D, Menghrajani, Kamal N, Getta, Bartlomiej M, Cai, Sheng F, Geyer, Mark B, Glass, Jacob L, Taylor, Justin, Viny, Aaron D, Levine, Ross L, Zhang, Yanming, Giralt, Sergio A, Klimek, Virginia, Tallman, Martin S, Roshal, Mikhail

“…Measurable residual disease is associated with inferior outcomes in patients with acute myeloid leukemia (AML). Measurable residual disease monitoring enhances…”
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RAS Mutations Are Independently Associated with Decreased Overall Survival and Event-Free Survival in Patients with AML Receiving Induction Chemotherapy by Ball, Brian J, Hsu, Meier, Devlin, Sean M., Famulare, Christopher, Cai, Sheng F, Dunbar, Andrew, Epstein-Peterson, Zachary D., Menghrajani, Kamal, Glass, Jacob L, Taylor, Justin, Viny, Aaron D, Goldberg, Aaron D, Tallman, Martin S., Stein, Eytan M.

“…Background: Activating mutations of NRAS and KRAS genes are common in newly diagnosed acute myeloid leukemia (AML), occurring in 11-16% and 4-5% of patients,…”
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The prognosis and durable clearance of RAS mutations in patients with acute myeloid leukemia receiving induction chemotherapy by Ball, Brian J., Hsu, Meier, Devlin, Sean M., Arcila, Maria, Roshal, Mikhail, Zhang, Yanming, Famulare, Chris A., Goldberg, Aaron D., Cai, Sheng F., Dunbar, Andrew, Epstein‐Peterson, Zachary, Menghrajani, Kamal N., Glass, Jacob L., Taylor, Justin, Viny, Aaron D., Giralt, Sergio S., Gyurkocza, Boglarka, Shaffer, Brian C., Tamari, Roni, Levine, Ross L., Tallman, Martin S., Stein, Eytan M.

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Lenalidomide-associated B-cell ALL: clinical and pathologic correlates and sensitivity to lenalidomide withdrawal by Geyer, Mark B., Shaffer, Brian C., Bhatnagar, Bhavana, Mims, Alice S., Klein, Victoria, Dilip, Deepika, Glass, Jacob L., Lozanski, Gerard, Hassoun, Hani, Landau, Heather, Zhang, Yanming, Xiao, Wenbin, Roshal, Mikhail, Park, Jae H.

“…•Lenalidomide-associated B-ALL has high rates of TP53 mutation and hypodiploidy.•Combination chemotherapy, antigen-targeted therapies, and allogeneic…”
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LINE-1 Activity in Facultative Heterochromatin Formation during X Chromosome Inactivation by Chow, Jennifer C., Ciaudo, Constance, Fazzari, Melissa J., Mise, Nathan, Servant, Nicolas, Glass, Jacob L., Attreed, Matthew, Avner, Philip, Wutz, Anton, Barillot, Emmanuel, Greally, John M., Voinnet, Olivier, Heard, Edith

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Interaction between myelodysplasia-related gene mutations and ontogeny in acute myeloid leukemia by McCarter, Joseph GW, Nemirovsky, David, Famulare, Christopher A., Farnoud, Noushin, Mohanty, Abhinita S., Stone-Molloy, Zoe S., Chervin, Jordan, Ball, Brian J., Epstein-Peterson, Zachary D., Arcila, Maria E., Stonestrom, Aaron J., Dunbar, Andrew, Cai, Sheng F., Glass, Jacob L., Geyer, Mark B., Rampal, Raajit K., Berman, Ellin, Abdel-Wahab, Omar I., Stein, Eytan M., Tallman, Martin S., Levine, Ross L., Goldberg, Aaron D., Papaemmanuil, Elli, Zhang, Yanming, Roshal, Mikhail, Derkach, Andriy, Xiao, Wenbin

“…●Ontogeny assignment from the database registry lacks sensitivity and specificity.●Ontogeny stratifies the outcome of AML with myelodysplasia-related gene…”
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Late-replicating heterochromatin is characterized by decreased cytosine methylation in the human genome by Suzuki, Masako, Oda, Mayumi, Ramos, María-Paz, Pascual, Marién, Lau, Kevin, Stasiek, Edyta, Agyiri, Frederick, Thompson, Reid F, Glass, Jacob L, Jing, Qiang, Sandstrom, Richard, Fazzari, Melissa J, Hansen, R Scott, Stamatoyannopoulos, John A, McLellan, Andrew S, Greally, John M

“…Heterochromatin is believed to be associated with increased levels of cytosine methylation. With the recent availability of genome-wide, high-resolution…”
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CG dinucleotide clustering is a species-specific property of the genome by Glass, Jacob L, Thompson, Reid F, Khulan, Batbayar, Figueroa, Maria E, Olivier, Emmanuel N, Oakley, Erin J, Van Zant, Gary, Bouhassira, Eric E, Melnick, Ari, Golden, Aaron, Fazzari, Melissa J, Greally, John M

“…Cytosines at cytosine-guanine (CG) dinucleotides are the near-exclusive target of DNA methyltransferases in mammalian genomes. Spontaneous deamination of…”
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