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1. An immunophenotype-coupled transcriptomic atlas of human hematopoietic progenitors

Author

Zhang, Xuan, Song, Baobao, Carlino, Maximillian J., Li, Guangyuan, Ferchen, Kyle, Chen, Mi, Thompson, Evrett N., Kain, Bailee N., Schnell, Dan, Thakkar, Kairavee, Kouril, Michal, Jin, Kang, Hay, Stuart B., Sen, Sidharth, Bernardicius, David, Ma, Siyuan, Bennett, Sierra N., Croteau, Josh, Salvatori, Ornella, Lye, Melvin H., Gillen, Austin E., Jordan, Craig T., Singh, Harinder, Krause, Diane S., Salomonis, Nathan, and Grimes, H. Leighton

Published
2024
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2. Resilient anatomy and local plasticity of naive and stress haematopoiesis

Author

Wu, Qingqing, Zhang, Jizhou, Kumar, Sumit, Shen, Siyu, Kincaid, Morgan, Johnson, Courtney B., Zhang, Yanan Sophia, Turcotte, Raphaël, Alt, Clemens, Ito, Kyoko, Homan, Shelli, Sherman, Bryan E., Shao, Tzu-Yu, Slaughter, Anastasiya, Weinhaus, Benjamin, Song, Baobao, Filippi, Marie Dominique, Grimes, H. Leighton, Lin, Charles P., Ito, Keisuke, Way, Sing Sing, Kofron, J. Matthew, and Lucas, Daniel

Published
2024
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3. Sex-associated differences in frequencies and prognostic impact of recurrent genetic alterations in adult acute myeloid leukemia (Alliance, AMLCG)

Author

Ozga, Michael, Nicolet, Deedra, Mrózek, Krzysztof, Yilmaz, Ayse S., Kohlschmidt, Jessica, Larkin, Karilyn T., Blachly, James S., Oakes, Christopher C., Buss, Jill, Walker, Christopher J., Orwick, Shelley, Jurinovic, Vindi, Rothenberg-Thurley, Maja, Dufour, Annika, Schneider, Stephanie, Sauerland, Maria Cristina, Görlich, Dennis, Krug, Utz, Berdel, Wolfgang E., Woermann, Bernhard J., Hiddemann, Wolfgang, Braess, Jan, Subklewe, Marion, Spiekermann, Karsten, Carroll, Andrew J., Blum, William G., Powell, Bayard L., Kolitz, Jonathan E., Moore, Joseph O., Mayer, Robert J., Larson, Richard A., Uy, Geoffrey L., Stock, Wendy, Metzeler, Klaus H., Grimes, H. Leighton, Byrd, John C., Salomonis, Nathan, Herold, Tobias, Mims, Alice S., and Eisfeld, Ann-Kathrin

Published
2024
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5. Gestational diabetes in mice induces hematopoietic memory that affects the long-term health of the offspring

Author

Govindarajah, Vinothini, Sakabe, Masahide, Good, Samantha, Solomon, Michael, Arasu, Ashok, Chen, Nong, Zhang, Xuan, Grimes, H. Leighton, Kendler, Ady, Xin, Mei, and Reynaud, Damien

Subjects
Immunologic memory -- Research, Immunological research, Diabetes in pregnancy -- Complications and side effects, Chronic diseases -- Risk factors, Hematopoietic system -- Health aspects, Prenatal influences -- Research, Health care industry
Abstract

Gestational diabetes is a common medical complication of pregnancy that is associated with adverse perinatal outcomes and an increased risk of metabolic diseases and atherosclerosis in adult offspring. The mechanisms responsible for this delayed pathological transmission remain unknown. In mouse models, we found that the development of atherosclerosis in adult offspring born to diabetic pregnancy can be in part linked to hematopoietic alterations. Although they do not show any gross metabolic disruptions, the adult offspring maintain hematopoietic features associated with diabetes, indicating the acquisition of a lasting diabetic hematopoietic memory. We show that the induction of this hematopoietic memory during gestation relies on the activity of the advanced glycation end product receptor (AGER) and the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, which lead to increased placental inflammation. In adult offspring, we find that this memory is associated with DNA methyltransferase 1 (DNMT1) upregulation and epigenetic changes in hematopoietic progenitors. Together, our results demonstrate that the hematopoietic system can acquire a lasting memory of gestational diabetes and that this memory constitutes a pathway connecting gestational health to adult pathologies., Introduction One in six pregnancies is affected by some form of gestational diabetes (GD), a prevalence that is steadily rising in the context of the worldwide epidemics of obesity and [...]

Published
2024
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8. Lsd1 as a therapeutic target in Gfi1-activated medulloblastoma.

Author

Lee, Catherine, Rudneva, Vasilisa A, Erkek, Serap, Zapatka, Marc, Chau, Lianne Q, Tacheva-Grigorova, Silvia K, Garancher, Alexandra, Rusert, Jessica M, Aksoy, Ozlem, Lea, Robin, Mohammad, Helai P, Wang, Jianxun, Weiss, William A, Grimes, H Leighton, Pfister, Stefan M, Northcott, Paul A, and Wechsler-Reya, Robert J

Subjects
NIH 3T3 Cells, Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Mice, Mice, SCID, Retroviridae, Oncogenic Viruses, Medulloblastoma, Cerebellar Neoplasms, Doxorubicin, DNA-Binding Proteins, Transcription Factors, Antibiotics, Antineoplastic, Neoplasm Transplantation, Cell Proliferation, Gene Expression Regulation, Neoplastic, Histone Demethylases, HEK293 Cells, Carcinogenesis, Antibiotics, Antineoplastic, Gene Expression Regulation, Neoplastic, Inbred C57BL, Knockout, SCID
Abstract

Drugs that modify the epigenome are powerful tools for treating cancer, but these drugs often have pleiotropic effects, and identifying patients who will benefit from them remains a major clinical challenge. Here we show that medulloblastomas driven by the transcription factor Gfi1 are exquisitely dependent on the enzyme lysine demethylase 1 (Kdm1a/Lsd1). We demonstrate that Lsd1 physically associates with Gfi1, and that these proteins cooperate to inhibit genes involved in neuronal commitment and differentiation. We also show that Lsd1 is essential for Gfi1-mediated transformation: Gfi1 proteins that cannot recruit Lsd1 are unable to drive tumorigenesis, and genetic ablation of Lsd1 markedly impairs tumor growth in vivo. Finally, pharmacological inhibitors of Lsd1 potently inhibit growth of Gfi1-driven tumors. These studies provide important insight into the mechanisms by which Gfi1 contributes to tumorigenesis, and identify Lsd1 inhibitors as promising therapeutic agents for Gfi1-driven medulloblastoma.

Published
2019

9. Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.

Author

Hayashi, Yoshihiro, Zhang, Yue, Yokota, Asumi, Yan, Xiaomei, Liu, Jinqin, Choi, Kwangmin, Li, Bing, Sashida, Goro, Peng, Yanyan, Xu, Zefeng, Huang, Rui, Zhang, Lulu, Freudiger, George M, Wang, Jingya, Dong, Yunzhu, Zhou, Yile, Wang, Jieyu, Wu, Lingyun, Bu, Jiachen, Chen, Aili, Zhao, Xinghui, Sun, Xiujuan, Chetal, Kashish, Olsson, Andre, Watanabe, Miki, Romick-Rosendale, Lindsey E, Harada, Hironori, Shih, Lee-Yung, Tse, William, Bridges, James P, Caligiuri, Michael A, Huang, Taosheng, Zheng, Yi, Witte, David P, Wang, Qian-Fei, Qu, Cheng-Kui, Salomonis, Nathan, Grimes, H Leighton, Nimer, Stephen D, Xiao, Zhijian, and Huang, Gang

Subjects
Animals, Mice, Knockout, Humans, Mice, Myelodysplastic Syndromes, Histone-Lysine N-Methyltransferase, Gene Expression Regulation, Neoplastic, Core Binding Factor Alpha 2 Subunit, Myeloid-Lymphoid Leukemia Protein, Hypoxia-Inducible Factor 1, alpha Subunit, Metabolome, Hypoxia, Rare Diseases, Hematology, Genetics, Cancer, Stem Cell Research, Aging, 2.1 Biological and endogenous factors, Aetiology, Oncology and Carcinogenesis
Abstract

Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic aberrations have been identified in patients with MDS, their clinical features are quite similar. Here, we show that hypoxia-independent activation of hypoxia-inducible factor 1α (HIF1A) signaling is both necessary and sufficient to induce dysplastic and cytopenic MDS phenotypes. The HIF1A transcriptional signature is generally activated in MDS patient bone marrow stem/progenitors. Major MDS-associated mutations (Dnmt3a, Tet2, Asxl1, Runx1, and Mll1) activate the HIF1A signature. Although inducible activation of HIF1A signaling in hematopoietic cells is sufficient to induce MDS phenotypes, both genetic and chemical inhibition of HIF1A signaling rescues MDS phenotypes in a mouse model of MDS. These findings reveal HIF1A as a central pathobiologic mediator of MDS and as an effective therapeutic target for a broad spectrum of patients with MDS.Significance: We showed that dysregulation of HIF1A signaling could generate the clinically relevant diversity of MDS phenotypes by functioning as a signaling funnel for MDS driver mutations. This could resolve the disconnection between genotypes and phenotypes and provide a new clue as to how a variety of driver mutations cause common MDS phenotypes. Cancer Discov; 8(11); 1438-57. ©2018 AACR. See related commentary by Chen and Steidl, p. 1355 This article is highlighted in the In This Issue feature, p. 1333.

Published
2018

10. Broad de-regulated U2AF1 splicing is prognostic and augments leukemic transformation via protein arginine methyltransferase activation

Author

Venkatasubramanian, Meenakshi, primary, Schwartz, Leya, additional, Ramachandra, Nandini, additional, Bennett, Joshua, additional, Subramanian, Krithika R., additional, Chen, Xiaoting, additional, Gordon-Mitchell, Shanisha, additional, Fromowitz, Ariel, additional, Pradhan, Kith, additional, Shechter, David, additional, Sahu, Srabani, additional, Heiser, Diane, additional, Scherle, Peggy, additional, Chetal, Kashish, additional, Kulkarni, Aishwarya, additional, Myers, Kasiani C., additional, Weirauch, Matthew T., additional, Grimes, H. Leighton, additional, Starczynowski, Daniel T., additional, Verma, Amit, additional, and Salomonis, Nathan, additional

Published
2024
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11. Splicing neoantigen discovery with SNAF reveals shared targets for cancer immunotherapy

Author

Li, Guangyuan, primary, Mahajan, Shweta, additional, Ma, Siyuan, additional, Jeffery, Erin D., additional, Zhang, Xuan, additional, Bhattacharjee, Anukana, additional, Venkatasubramanian, Meenakshi, additional, Weirauch, Matthew T., additional, Miraldi, Emily R., additional, Grimes, H. Leighton, additional, Sheynkman, Gloria M., additional, Tilburgs, Tamara, additional, and Salomonis, Nathan, additional

Published
2024
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13. In situ mapping identifies distinct vascular niches for myelopoiesis

Author

Zhang, Jizhou, Wu, Qingqing, Johnson, Courtney B., Pham, Giang, Kinder, Jeremy M., Olsson, Andre, Slaughter, Anastasiya, May, Margot, Weinhaus, Benjamin, D’Alessandro, Angelo, Engel, James Douglas, Jiang, Jean X., Kofron, J. Matthew, Huang, L. Frank, Prasath, V. B. Surya, Way, Sing Sing, Salomonis, Nathan, Grimes, H. Leighton, and Lucas, Daniel

Published
2021
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14. Combinatorial Single-Cell Analyses of Granulocyte-Monocyte Progenitor Heterogeneity Reveals an Early Uni-potent Neutrophil Progenitor

Author

Kwok, Immanuel, Becht, Etienne, Xia, Yu, Ng, Melissa, Teh, Ye Chean, Tan, Leonard, Evrard, Maximilien, Li, Jackson L.Y., Tran, Hoa T.N., Tan, Yingrou, Liu, Dehua, Mishra, Archita, Liong, Ka Hang, Leong, Keith, Zhang, Yuning, Olsson, Andre, Mantri, Chinmay Kumar, Shyamsunder, Pavithra, Liu, Zhaoyuan, Piot, Cecile, Dutertre, Charles-Antoine, Cheng, Hui, Bari, Sudipto, Ang, Nicholas, Biswas, Subhra K., Koeffler, H. Philip, Tey, Hong Liang, Larbi, Anis, Su, I-Hsin, Lee, Bernett, St. John, Ashley, Chan, Jerry K.Y., Hwang, William Y.K., Chen, Jinmiao, Salomonis, Nathan, Chong, Shu Zhen, Grimes, H. Leighton, Liu, Bing, Hidalgo, Andrés, Newell, Evan W., Cheng, Tao, Ginhoux, Florent, and Ng, Lai Guan

Published
2020
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15. DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia

Author

Meyer, Sara E, Qin, Tingting, Muench, David E, Masuda, Kohei, Venkatasubramanian, Meenakshi, Orr, Emily, Suarez, Lauren, Gore, Steven D, Delwel, Ruud, Paietta, Elisabeth, Tallman, Martin S, Fernandez, Hugo, Melnick, Ari, Le Beau, Michelle M, Kogan, Scott, Salomonis, Nathan, Figueroa, Maria E, and Grimes, H Leighton

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Pediatric, Pediatric Research Initiative, Childhood Leukemia, Rare Diseases, Pediatric Cancer, Cancer, Hematology, Aetiology, 2.1 Biological and endogenous factors, Animals, Biopsy, Bone Marrow, Cell Transformation, Neoplastic, Cluster Analysis, DNA (Cytosine-5-)-Methyltransferases, DNA Methylation, DNA Methyltransferase 3A, Disease Models, Animal, Disease Progression, Gene Expression Profiling, Gene Expression Regulation, Genetic Loci, Genotype, Haploinsufficiency, High-Throughput Nucleotide Sequencing, Humans, Karyotype, Leukemia, Myeloid, Acute, Mice, Mice, Transgenic, Mutation, Myeloproliferative Disorders, Penetrance, Tandem Repeat Sequences, fms-Like Tyrosine Kinase 3, Oncology and Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

UnlabelledCytogenetically normal acute myeloid leukemia (CN-AML) represents nearly 50% of human AML. Co-occurring mutations in the de novo DNA methyltransferase DNMT3A and the FMS related tyrosine kinase 3 (FLT3) are common in CN-AML and confer a poorer prognosis. We demonstrate that mice with Flt3-internal tandem duplication (Flt3(ITD)) and inducible deletion of Dnmt3a spontaneously develop a rapidly lethal, completely penetrant, and transplantable AML of normal karyotype. AML cells retain a single Dnmt3a floxed allele, revealing the oncogenic potential of Dnmt3a haploinsufficiency. FLT3(ITD)/DNMT3A-mutant primary human and murine AML exhibit a similar pattern of global DNA methylation associated with changes in the expression of nearby genes. In the murine model, rescuing Dnmt3a expression was accompanied by DNA remethylation and loss of clonogenic potential, suggesting that Dnmt3a-mutant oncogenic effects are reversible. Dissection of the cellular architecture of the AML model using single-cell assays, including single-cell RNA sequencing, identified clonogenic subpopulations that express genes sensitive to the methylation of nearby genomic loci and responsive to DNMT3A levels. Thus, Dnmt3a haploinsufficiency transforms Flt3(ITD) myeloproliferative disease by modulating methylation-sensitive gene expression within a clonogenic AML subpopulation.SignificanceDNMT3A haploinsufficiency results in reversible epigenetic alterations that transform FLT3(ITD)-mutant myeloproliferative neoplasm into AML. Cancer Discov; 6(5); 501-15. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 461.

Published
2016

16. Sex-associated differences in frequencies and prognostic impact of recurrent genetic alterations in adult acute myeloid leukemia (Alliance, AMLCG)

Author

Ozga, Michael, primary, Nicolet, Deedra, additional, Mrózek, Krzysztof, additional, Yilmaz, Ayse S., additional, Kohlschmidt, Jessica, additional, Larkin, Karilyn T., additional, Blachly, James S., additional, Oakes, Christopher C., additional, Buss, Jill, additional, Walker, Christopher J., additional, Orwick, Shelley, additional, Jurinovic, Vindi, additional, Rothenberg-Thurley, Maja, additional, Dufour, Annika, additional, Schneider, Stephanie, additional, Sauerland, Maria Cristina, additional, Görlich, Dennis, additional, Krug, Utz, additional, Berdel, Wolfgang E., additional, Woermann, Bernhard J., additional, Hiddemann, Wolfgang, additional, Braess, Jan, additional, Subklewe, Marion, additional, Spiekermann, Karsten, additional, Carroll, Andrew J., additional, Blum, William G., additional, Powell, Bayard L., additional, Kolitz, Jonathan E., additional, Moore, Joseph O., additional, Mayer, Robert J., additional, Larson, Richard A., additional, Uy, Geoffrey L., additional, Stock, Wendy, additional, Metzeler, Klaus H., additional, Grimes, H. Leighton, additional, Byrd, John C., additional, Salomonis, Nathan, additional, Herold, Tobias, additional, Mims, Alice S., additional, and Eisfeld, Ann-Kathrin, additional

Published
2023
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18. Slow cycling and durable Flt3+ progenitors contribute to hematopoiesis under native conditions

Author

Solomon, Michael, primary, Song, Baobao, additional, Govindarajah, Vinothini, additional, Good, Samantha, additional, Arasu, Ashok, additional, Hinton, E. Broderick, additional, Thakkar, Kairavee, additional, Bartram, James, additional, Filippi, Marie-Dominique, additional, Cancelas, Jose A., additional, Salomonis, Nathan, additional, Grimes, H. Leighton, additional, and Reynaud, Damien, additional

Published
2023
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19. Mouse models of neutropenia reveal progenitor-stage-specific defects

Author

Muench, David E., Olsson, Andre, Ferchen, Kyle, Pham, Giang, Serafin, Rachel A., Chutipongtanate, Somchai, Dwivedi, Pankaj, Song, Baobao, Hay, Stuart, Chetal, Kashish, Trump-Durbin, Lisa R., Mookerjee-Basu, Jayati, Zhang, Kejian, Yu, Jennifer C., Lutzko, Carolyn, Myers, Kasiani C., Nazor, Kristopher L., Greis, Kenneth D., Kappes, Dietmar J., Way, Sing Sing, Salomonis, Nathan, and Grimes, H. Leighton

Published
2020
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22. Myeloid Malignancies with Chromosome 5q Deletions Acquire a Dependency on an Intrachromosomal NF-κB Gene Network

Author

Fang, Jing, Barker, Brenden, Bolanos, Lyndsey, Liu, Xiaona, Jerez, Andres, Makishima, Hideki, Christie, Susanne, Chen, Xiaoting, Rao, Dinesh S, Grimes, H Leighton, Komurov, Kakajan, Weirauch, Matthew T, Cancelas, Jose A, Maciejewski, Jaroslaw P, and Starczynowski, Daniel T

Subjects
Hematology, Pediatric Research Initiative, Pediatric Cancer, Childhood Leukemia, Genetics, Stem Cell Research, Pediatric, Cancer, Rare Diseases, Stem Cell Research - Nonembryonic - Non-Human, Adaptor Proteins, Signal Transducing, Animals, Apoptosis, Case-Control Studies, Cell Cycle, Cell Proliferation, Cells, Cultured, Chromosome Deletion, Chromosomes, Human, Pair 5, Gene Regulatory Networks, Humans, Leukemia, Myeloid, Acute, Mice, MicroRNAs, Myelodysplastic Syndromes, Myeloid Progenitor Cells, NF-kappa B, Sequestosome-1 Protein, Signal Transduction, TNF Receptor-Associated Factor 6, Biochemistry and Cell Biology, Medical Physiology
Abstract

Chromosome 5q deletions (del[5q]) are common in high-risk (HR) myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML); however, the gene regulatory networks that sustain these aggressive diseases are unknown. Reduced miR-146a expression in del(5q) HR MDS/AML and miR-146a(-/-) hematopoietic stem/progenitor cells (HSPCs) results in TRAF6/NF-κB activation. Increased survival and proliferation of HSPCs from miR-146a(low) HR MDS/AML is sustained by a neighboring haploid gene, SQSTM1 (p62), expressed from the intact 5q allele. Overexpression of p62 from the intact allele occurs through NF-κB-dependent feedforward signaling mediated by miR-146a deficiency. p62 is necessary for TRAF6-mediated NF-κB signaling, as disrupting the p62-TRAF6 signaling complex results in cell-cycle arrest and apoptosis of MDS/AML cells. Thus, del(5q) HR MDS/AML employs an intrachromosomal gene network involving loss of miR-146a and haploid overexpression of p62 via NF-κB to sustain TRAF6/NF-κB signaling for cell survival and proliferation. Interfering with the p62-TRAF6 signaling complex represents a therapeutic option in miR-146a-deficient and aggressive del(5q) MDS/AML.

Published
2014

25. ThPOK is a critical multifaceted regulator of myeloid lineage development

Author

Basu, Jayati, primary, Olsson, Andre, additional, Ferchen, Kyle, additional, Titerina, Elizaveta K., additional, Chetal, Kashish, additional, Nicolas, Emmanuelle, additional, Czyzewicz, Philip, additional, Levchenko, Dmitry, additional, Ge, Lu, additional, Hua, Xiang, additional, Grimes, H. Leighton, additional, Salomonis, Nathan, additional, and Kappes, Dietmar J., additional

Published
2023
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31. Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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32. Supplementary Table S6 from DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia

Author

Meyer, Sara E., primary, Qin, Tingting, primary, Muench, David E., primary, Masuda, Kohei, primary, Venkatasubramanian, Meenakshi, primary, Orr, Emily, primary, Suarez, Lauren, primary, Gore, Steven D., primary, Delwel, Ruud, primary, Paietta, Elisabeth, primary, Tallman, Martin S., primary, Fernandez, Hugo, primary, Melnick, Ari, primary, Le Beau, Michelle M., primary, Kogan, Scott, primary, Salomonis, Nathan, primary, Figueroa, Maria E., primary, and Grimes, H. Leighton, primary

Published
2023
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33. Table S7 from Aging Human Hematopoietic Stem Cells Manifest Profound Epigenetic Reprogramming of Enhancers That May Predispose to Leukemia

Author

Adelman, Emmalee R., primary, Huang, Hsuan-Ting, primary, Roisman, Alejandro, primary, Olsson, André, primary, Colaprico, Antonio, primary, Qin, Tingting, primary, Lindsley, R. Coleman, primary, Bejar, Rafael, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, and Figueroa, Maria E., primary

Published
2023
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34. Supplementary Table S4 from Rational Targeting of Cooperating Layers of the Epigenome Yields Enhanced Therapeutic Efficacy against AML

Author

Duy, Cihangir, primary, Teater, Matt, primary, Garrett-Bakelman, Francine E., primary, Lee, Tak C., primary, Meydan, Cem, primary, Glass, Jacob L., primary, Li, Meng, primary, Hellmuth, Johannes C., primary, Mohammad, Helai P., primary, Smitheman, Kimberly N., primary, Shih, Alan H., primary, Abdel-Wahab, Omar, primary, Tallman, Martin S., primary, Guzman, Monica L., primary, Muench, David, primary, Grimes, H. Leighton, primary, Roboz, Gail J., primary, Kruger, Ryan G., primary, Creasy, Caretha L., primary, Paietta, Elisabeth M., primary, Levine, Ross L., primary, Carroll, Martin, primary, and Melnick, Ari M., primary

Published
2023
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35. Data from The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

Author

Ye, Haobin, primary, Minhajuddin, Mohammad, primary, Krug, Anna, primary, Pei, Shanshan, primary, Chou, Chih-Hsing, primary, Culp-Hill, Rachel, primary, Ponder, Jessica, primary, De Bloois, Erik, primary, Schniedewind, Björn, primary, Amaya, Maria L., primary, Inguva, Anagha, primary, Stevens, Brett M., primary, Pollyea, Daniel A., primary, Christians, Uwe, primary, Grimes, H. Leighton, primary, D'Alessandro, Angelo, primary, and Jordan, Craig T., primary

Published
2023
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36. Supplementary Figures S1-S6 from Rational Targeting of Cooperating Layers of the Epigenome Yields Enhanced Therapeutic Efficacy against AML

Author

Duy, Cihangir, primary, Teater, Matt, primary, Garrett-Bakelman, Francine E., primary, Lee, Tak C., primary, Meydan, Cem, primary, Glass, Jacob L., primary, Li, Meng, primary, Hellmuth, Johannes C., primary, Mohammad, Helai P., primary, Smitheman, Kimberly N., primary, Shih, Alan H., primary, Abdel-Wahab, Omar, primary, Tallman, Martin S., primary, Guzman, Monica L., primary, Muench, David, primary, Grimes, H. Leighton, primary, Roboz, Gail J., primary, Kruger, Ryan G., primary, Creasy, Caretha L., primary, Paietta, Elisabeth M., primary, Levine, Ross L., primary, Carroll, Martin, primary, and Melnick, Ari M., primary

Published
2023
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38. Data from DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia

Author

Meyer, Sara E., primary, Qin, Tingting, primary, Muench, David E., primary, Masuda, Kohei, primary, Venkatasubramanian, Meenakshi, primary, Orr, Emily, primary, Suarez, Lauren, primary, Gore, Steven D., primary, Delwel, Ruud, primary, Paietta, Elisabeth, primary, Tallman, Martin S., primary, Fernandez, Hugo, primary, Melnick, Ari, primary, Le Beau, Michelle M., primary, Kogan, Scott, primary, Salomonis, Nathan, primary, Figueroa, Maria E., primary, and Grimes, H. Leighton, primary

Published
2023
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39. Supplementary Data from Aging Human Hematopoietic Stem Cells Manifest Profound Epigenetic Reprogramming of Enhancers That May Predispose to Leukemia

Author

Adelman, Emmalee R., primary, Huang, Hsuan-Ting, primary, Roisman, Alejandro, primary, Olsson, André, primary, Colaprico, Antonio, primary, Qin, Tingting, primary, Lindsley, R. Coleman, primary, Bejar, Rafael, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, and Figueroa, Maria E., primary

Published
2023
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40. Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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41. Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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42. Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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43. Data from Rational Targeting of Cooperating Layers of the Epigenome Yields Enhanced Therapeutic Efficacy against AML

Author

Duy, Cihangir, primary, Teater, Matt, primary, Garrett-Bakelman, Francine E., primary, Lee, Tak C., primary, Meydan, Cem, primary, Glass, Jacob L., primary, Li, Meng, primary, Hellmuth, Johannes C., primary, Mohammad, Helai P., primary, Smitheman, Kimberly N., primary, Shih, Alan H., primary, Abdel-Wahab, Omar, primary, Tallman, Martin S., primary, Guzman, Monica L., primary, Muench, David, primary, Grimes, H. Leighton, primary, Roboz, Gail J., primary, Kruger, Ryan G., primary, Creasy, Caretha L., primary, Paietta, Elisabeth M., primary, Levine, Ross L., primary, Carroll, Martin, primary, and Melnick, Ari M., primary

Published
2023
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44. Supplementary Data from The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

Author

Ye, Haobin, primary, Minhajuddin, Mohammad, primary, Krug, Anna, primary, Pei, Shanshan, primary, Chou, Chih-Hsing, primary, Culp-Hill, Rachel, primary, Ponder, Jessica, primary, De Bloois, Erik, primary, Schniedewind, Björn, primary, Amaya, Maria L., primary, Inguva, Anagha, primary, Stevens, Brett M., primary, Pollyea, Daniel A., primary, Christians, Uwe, primary, Grimes, H. Leighton, primary, D'Alessandro, Angelo, primary, and Jordan, Craig T., primary

Published
2023
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45. Supplementary Figure Legends, Table Legends, Figures S1 - S4 from DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia

Author

Meyer, Sara E., primary, Qin, Tingting, primary, Muench, David E., primary, Masuda, Kohei, primary, Venkatasubramanian, Meenakshi, primary, Orr, Emily, primary, Suarez, Lauren, primary, Gore, Steven D., primary, Delwel, Ruud, primary, Paietta, Elisabeth, primary, Tallman, Martin S., primary, Fernandez, Hugo, primary, Melnick, Ari, primary, Le Beau, Michelle M., primary, Kogan, Scott, primary, Salomonis, Nathan, primary, Figueroa, Maria E., primary, and Grimes, H. Leighton, primary

Published
2023
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46. Supplementary Figure 1 from Growth Factor Independence-1 Is Expressed in Primary Human Neuroendocrine Lung Carcinomas and Mediates the Differentiation of Murine Pulmonary Neuroendocrine Cells

Author

Kazanjian, Avedis, primary, Wallis, Deeann, primary, Au, Nicholas, primary, Nigam, Rupesh, primary, Venken, Koen J. T., primary, Cagle, Philip T., primary, Dickey, Burton F., primary, Bellen, Hugo J., primary, Gilks, C. Blake, primary, and Grimes, H. Leighton, primary

Published
2023
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47. Supplementary Figure 2 from Growth Factor Independence-1 Is Expressed in Primary Human Neuroendocrine Lung Carcinomas and Mediates the Differentiation of Murine Pulmonary Neuroendocrine Cells

Author

Kazanjian, Avedis, primary, Wallis, Deeann, primary, Au, Nicholas, primary, Nigam, Rupesh, primary, Venken, Koen J. T., primary, Cagle, Philip T., primary, Dickey, Burton F., primary, Bellen, Hugo J., primary, Gilks, C. Blake, primary, and Grimes, H. Leighton, primary

Published
2023
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