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1. Acquired miR-142 deficit in leukemic stem cells suffices to drive chronic myeloid leukemia into blast crisis

Author

Zhang, Bin, Zhao, Dandan, Chen, Fang, Frankhouser, David, Wang, Huafeng, Pathak, Khyatiben V, Dong, Lei, Torres, Anakaren, Garcia-Mansfield, Krystine, Zhang, Yi, Hoang, Dinh Hoa, Chen, Min-Hsuan, Tao, Shu, Cho, Hyejin, Liang, Yong, Perrotti, Danilo, Branciamore, Sergio, Rockne, Russell, Wu, Xiwei, Ghoda, Lucy, Li, Ling, Jin, Jie, Chen, Jianjun, Yu, Jianhua, Caligiuri, Michael A, Kuo, Ya-Huei, Boldin, Mark, Su, Rui, Swiderski, Piotr, Kortylewski, Marcin, Pirrotte, Patrick, Nguyen, Le Xuan Truong, and Marcucci, Guido

Subjects
Biomedical and Clinical Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Stem Cell Research - Nonembryonic - Human, Rare Diseases, Stem Cell Research, Cancer, Prevention, Genetics, Hematology, Biotechnology, Aetiology, 2.1 Biological and endogenous factors, Animals, Humans, Mice, Blast Crisis, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Leukemia, Myeloid, Leukemia, Myeloid, Chronic-Phase, MicroRNAs, Stem Cells
Abstract

The mechanisms underlying the transformation of chronic myeloid leukemia (CML) from chronic phase (CP) to blast crisis (BC) are not fully elucidated. Here, we show lower levels of miR-142 in CD34+CD38- blasts from BC CML patients than in those from CP CML patients, suggesting that miR-142 deficit is implicated in BC evolution. Thus, we create miR-142 knockout CML (i.e., miR-142-/-BCR-ABL) mice, which develop BC and die sooner than miR-142 wt CML (i.e., miR-142+/+BCR-ABL) mice, which instead remain in CP CML. Leukemic stem cells (LSCs) from miR-142-/-BCR-ABL mice recapitulate the BC phenotype in congenic recipients, supporting LSC transformation by miR-142 deficit. State-transition and mutual information analyses of "bulk" and single cell RNA-seq data, metabolomic profiling and functional metabolic assays identify enhanced fatty acid β-oxidation, oxidative phosphorylation and mitochondrial fusion in LSCs as key steps in miR-142-driven BC evolution. A synthetic CpG-miR-142 mimic oligodeoxynucleotide rescues the BC phenotype in miR-142-/-BCR-ABL mice and patient-derived xenografts.

Published
2023

2. Treatment-induced arteriolar revascularization and miR-126 enhancement in bone marrow niche protect leukemic stem cells in AML

Author

Zhang, Bin, Nguyen, Le Xuan Truong, Zhao, Dandan, Frankhouser, David E, Wang, Huafeng, Hoang, Dinh Hoa, Qiao, Junjing, Abundis, Christina, Brehove, Matthew, Su, Yu-Lin, Feng, Yuxin, Stein, Anthony, Ghoda, Lucy, Dorrance, Adrianne, Perrotti, Danilo, Chen, Zhen, Han, Anjia, Pichiorri, Flavia, Jin, Jie, Jovanovic-Talisman, Tijana, Caligiuri, Michael A, Kuo, Calvin J, Yoshimura, Akihiko, Li, Ling, Rockne, Russell C, Kortylewski, Marcin, Zheng, Yi, Carlesso, Nadia, Kuo, Ya-Huei, and Marcucci, Guido

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Oncology and Carcinogenesis, Pediatric, Rare Diseases, Hematology, Pediatric Cancer, Stem Cell Research, Cancer, Stem Cell Research - Nonembryonic - Non-Human, Childhood Leukemia, Aetiology, 2.1 Biological and endogenous factors, Animals, Bone Marrow, Gene Expression Regulation, Leukemic, Humans, Leukemia, Myeloid, Acute, Mice, Mice, Inbred C57BL, MicroRNAs, Neoplastic Stem Cells, Up-Regulation, fms-Like Tyrosine Kinase 3, Acute myeloid leukemia, BM vascular niche, TNF alpha, miR-126, Leukemic stem cell, Treatment resistance, TNFα, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology, Oncology and carcinogenesis
Abstract

BackgroundDuring acute myeloid leukemia (AML) growth, the bone marrow (BM) niche acquires significant vascular changes that can be offset by therapeutic blast cytoreduction. The molecular mechanisms of this vascular plasticity remain to be fully elucidated. Herein, we report on the changes that occur in the vascular compartment of the FLT3-ITD+ AML BM niche pre and post treatment and their impact on leukemic stem cells (LSCs).MethodsBM vasculature was evaluated in FLT3-ITD+ AML models (MllPTD/WT/Flt3ITD/ITD mouse and patient-derived xenograft) by 3D confocal imaging of long bones, calvarium vascular permeability assays, and flow cytometry analysis. Cytokine levels were measured by Luminex assay and miR-126 levels evaluated by Q-RT-PCR and miRNA staining. Wild-type (wt) and MllPTD/WT/Flt3ITD/ITD mice with endothelial cell (EC) miR-126 knockout or overexpression served as controls. The impact of treatment-induced BM vascular changes on LSC activity was evaluated by secondary transplantation of BM cells after administration of tyrosine kinase inhibitors (TKIs) to MllPTD/WT/Flt3ITD/ITD mice with/without either EC miR-126 KO or co-treatment with tumor necrosis factor alpha (TNFα) or anti-miR-126 miRisten.ResultsIn the normal BM niche, CD31+Sca-1high ECs lining arterioles have miR-126 levels higher than CD31+Sca-1low ECs lining sinusoids. We noted that during FLT3-ITD+ AML growth, the BM niche lost arterioles and gained sinusoids. These changes were mediated by TNFα, a cytokine produced by AML blasts, which induced EC miR-126 downregulation and caused depletion of CD31+Sca-1high ECs and gain in CD31+Sca-1low ECs. Loss of miR-126high ECs led to a decreased EC miR-126 supply to LSCs, which then entered the cell cycle and promoted leukemia growth. Accordingly, antileukemic treatment with TKI decreased the BM blast-produced TNFα and increased miR-126high ECs and the EC miR-126 supply to LSCs. High miR-126 levels safeguarded LSCs, as shown by more severe disease in secondary transplanted mice. Conversely, EC miR-126 deprivation via genetic or pharmacological EC miR-126 knock-down prevented treatment-induced BM miR-126high EC expansion and in turn LSC protection.ConclusionsTreatment-induced CD31+Sca-1high EC re-vascularization of the leukemic BM niche may represent a LSC extrinsic mechanism of treatment resistance that can be overcome with therapeutic EC miR-126 deprivation.

Published
2021

3. Cytoplasmic DROSHA and non-canonical mechanisms of MiR-155 biogenesis in FLT3-ITD acute myeloid leukemia

Author

Nguyen, Le Xuan Truong, Zhang, Bin, Hoang, Dinh Hoa, Zhao, Dandan, Wang, Huafeng, Wu, Herman, Su, Yu-Lin, Dong, Haojie, Rodriguez-Rodriguez, Sonia, Armstrong, Brian, Ghoda, Lucy Y, Perrotti, Danilo, Pichiorri, Flavia, Chen, Jianjun, Li, Ling, Kortylewski, Marcin, Rockne, Russell C, Kuo, Ya-Huei, Khaled, Samer, Carlesso, Nadia, and Marcucci, Guido

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Oncology and Carcinogenesis, Pediatric, Genetics, Rare Diseases, Hematology, Pediatric Cancer, Biotechnology, Cancer, Childhood Leukemia, Animals, Cytoplasm, Disease Models, Animal, Humans, Leukemia, Myeloid, Acute, Mice, MicroRNAs, Ribonuclease III, Tandem Repeat Sequences, Tumor Cells, Cultured, fms-Like Tyrosine Kinase 3, Immunology, Cardiovascular medicine and haematology, Clinical sciences, Oncology and carcinogenesis
Abstract

We report here on a novel pro-leukemogenic role of FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) that interferes with microRNAs (miRNAs) biogenesis in acute myeloid leukemia (AML) blasts. We showed that FLT3-ITD interferes with the canonical biogenesis of intron-hosted miRNAs such as miR-126, by phosphorylating SPRED1 protein and inhibiting the "gatekeeper" Exportin 5 (XPO5)/RAN-GTP complex that regulates the nucleus-to-cytoplasm transport of pre-miRNAs for completion of maturation into mature miRNAs. Of note, despite the blockage of "canonical" miRNA biogenesis, miR-155 remains upregulated in FLT3-ITD+ AML blasts, suggesting activation of alternative mechanisms of miRNA biogenesis that circumvent the XPO5/RAN-GTP blockage. MiR-155, a BIC-155 long noncoding (lnc) RNA-hosted oncogenic miRNA, has previously been implicated in FLT3-ITD+ AML blast hyperproliferation. We showed that FLT3-ITD upregulates miR-155 by inhibiting DDX3X, a protein implicated in the splicing of lncRNAs, via p-AKT. Inhibition of DDX3X increases unspliced BIC-155 that is then shuttled by NXF1 from the nucleus to the cytoplasm, where it is processed into mature miR-155 by cytoplasmic DROSHA, thereby bypassing the XPO5/RAN-GTP blockage via "non-canonical" mechanisms of miRNA biogenesis.

Published
2021

5. Precision immunotherapy, mutational landscape, and emerging tools to optimize clinical outcomes in patients with classical myeloproliferative neoplasms

Author

Mughal, Tariq I, Lion, Thomas, Abdel‐Wahab, Omar, Mesa, Ruben, Scherber, Robyn M, Perrotti, Danilo, Mauro, Michael, Verstovsek, Srdan, Saglio, Giuseppe, Van Etten, Richard A, and Kralovics, Robert

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Cancer, Rare Diseases, Good Health and Well Being, Amino Acid Substitution, Fusion Proteins, bcr-abl, Hematologic Neoplasms, Humans, Immunotherapy, Janus Kinase 2, Mutation, Missense, Myeloproliferative Disorders, Precision Medicine, Translational Research, Biomedical, Chronic myeloroliferative neoplasms, immunotherapy, genomics, treatment, Cardiorespiratory Medicine and Haematology, Immunology, Cardiovascular medicine and haematology
Abstract

Following the 47th American Society of Hematology Meeting in 2005, the late John Goldman and Tariq Mughal commenced a conference, the 1st Post-ASH Workshop, which brought together clinicians and scientists, to accelerate the adoption of new therapies for patients with myeloproliferative neoplasms (MPNs). The concept began with recognition of the CML success story following imatinib therapy, the discovery of JAK2V617F , and the demonstration that BCR-ABL1-negative MPNs are driven by abnormal JAK2 activation. This review is based on the presentations and deliberations at the XIIth Post-ASH Workshop on BCR-ABL1 positive and negative MPNs that took place on December 12 to 13, 2017, in Atlanta, Georgia, immediately following the 59th American Society of Hematology Meeting. We have selected some of the translational research and clinical topics, rather than an account of the proceedings. We discuss the role of immunotherapy in MPNs and the impact of the mutational landscape on TKI treatment in CML. We also consider how we might reduce TKI cardiovascular side effects, the potential role of nutrition as adjunctive nonpharmacologic intervention to reduce chronic inflammation in MPNs, and novel investigational therapies for MPNs.

Published
2018

6. Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop.

Author

Van Etten, Richard A, Mauro, Michael, Radich, Jerald P, Goldman, John M, Saglio, Giuseppe, Jamieson, Catriona, Soverini, Simona, Gambacorti-Passerini, Carlo, Hehlmann, Rüdiger, Martinelli, Giovanni, Perrotti, Danilo, Scadden, David T, Skorski, Tomasz, Tefferi, Ayalew, and Mughal, Tariq I

Subjects
Animals, Antineoplastic Agents: therapeutic use, Genomics, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive: etiology, therapy, Molecular Targeted Therapy, Neoplastic Stem Cells: metabolism, Protein Kinase Inhibitors: therapeutic use, Stem Cell Niche, Treatment Outcome
Abstract

Following the 53rd annual meeting of the American Society of Hematology (ASH) in San Diego in December 2011, a group of clinical and laboratory investigators convened for the 6th Post-ASH International Workshop on Chronic Myeloid Leukemia (CML) and Myeloproliferative Neoplasms (MPN). The Workshop took place on 13-14 December at the Estancia, La Jolla, California, USA. This report summarizes the most recent advances in the biology and therapy of CML that were presented at the ASH meeting and discussed at the Workshop. Preclinical studies focused on the CML stem cell and its niche, and on early results of deep sequencing of CML genomes. Clinical advances include updates on second- and third-generation tyrosine kinase inhibitors (TKIs), molecular monitoring, TKI discontinuation studies and new therapeutic agents. A report summarizing the pertinent advances in MPN has been published separately.

Published
2013

7. The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues

Author

Van Etten, Richard A., Koschmieder, Steffen, Delhommeau, Francois, Perrotti, Danilo, Holyoake, Tessa, Pardanani, Animesh, Mesa, Ruben, Green, Tony, Ibrahim, Amr R., Mughal, Tariq, Gale, Robert Peter, and Goldman, John

Subjects
myeloproliferative neoplasm, JAK2, Ph-negative, Ph-positive
Abstract

This review focuses on topical issues in the biology and treatment of the myeloproliferative neoplasms (MPNs). Studies in transgenic mice suggest that BCR-ABL1 reduces the fraction of self-renewing ‘leukemic’ stem cells in the bone marrow but that some of these cells survive treatment with imatinib. This also seems to operate in humans. Data from models also strongly support the notion that JAK2V617F can initiate and sustain MPNs in mice; relevance to disease in humans is less clear. These data also support the hypothesis that level of JAK2V617F expression influences the MPN phenotype: higher levels favor erythrocytosis whereas lower levels favor thrombocytosis. Although TET2-mutations were thought to precede JAK2V617F in some persons with MPNs, it now appears that TET2 mutations may occur after JAK2V617F. Further understanding of signal-transduction pathways activated in chronic myeloid leukemia suggests various possible targets for new therapies including the WNT/beta catenin, notch and hedgehog pathways. Finally, the clinical role of the new JAK2- and BCR-ABL1-inhibitors is considered. Much further progress is likely in several of these areas soon.

Published
2011

8. Src homology 2 domain–containing inositol-5-phosphatase and CCAAT enhancer-binding protein β are targeted by miR-155 in B cells of Eμ-MiR-155 transgenic mice

Author

Costinean, Stefan, Sandhu, Sukhinder K, Pedersen, Irene M, Tili, Esmerina, Trotta, Rossana, Perrotti, Danilo, Ciarlariello, David, Neviani, Paolo, Harb, Jason, Kauffman, Lauren Rachel, Shidham, Aaditya, and Croce, Carlo Maria

Subjects
Hematology, Genetics, Biotechnology, Childhood Leukemia, Pediatric Cancer, Cancer, Rare Diseases, Pediatric, Lymphoma, Aetiology, 2.1 Biological and endogenous factors, Animals, CCAAT-Enhancer-Binding Protein-beta, Cell Transformation, Neoplastic, Down-Regulation, Gene Expression Regulation, Leukemic, Inositol Polyphosphate 5-Phosphatases, Interleukin-6, Lymphoma, B-Cell, Mice, Mice, Transgenic, MicroRNAs, Phosphoric Monoester Hydrolases, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Precursor Cells, B-Lymphoid, Signal Transduction, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine, Immunology
Abstract

We showed that Emicro-MiR-155 transgenic mice develop acute lymphoblastic leukemia/high-grade lymphoma. Most of these leukemias start at approximately 9 months irrespective of the mouse strain. They are preceded by a polyclonal pre-B-cell proliferation, have variable clinical presentation, are transplantable, and develop oligo/monoclonal expansion. In this study, we show that in these transgenic mice the B-cell precursors have the highest MiR-155 transgene expression and are at the origin of the leukemias. We determine that Src homology 2 domain-containing inositol-5-phosphatase (SHIP) and CCAAT enhancer-binding protein beta (C/EBPbeta), 2 important regulators of the interleukin-6 signaling pathway, are direct targets of MiR-155 and become gradually more down-regulated in the leukemic than in the preleukemic mice. We hypothesize that miR-155, by down-modulating Ship and C/EBPbeta, initiates a chain of events that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade lymphoma.

Published
2009

9. Src homology 2 domain-containing inositol-5-phosphatase and CCAAT enhancer-binding protein beta are targeted by miR-155 in B cells of Emicro-MiR-155 transgenic mice.

Author

Costinean, Stefan, Sandhu, Sukhinder K, Pedersen, Irene M, Tili, Esmerina, Trotta, Rossana, Perrotti, Danilo, Ciarlariello, David, Neviani, Paolo, Harb, Jason, Kauffman, Lauren Rachel, Shidham, Aaditya, and Croce, Carlo Maria

Subjects
Animals, Mice, Transgenic, Mice, Lymphoma, B-Cell, Cell Transformation, Neoplastic, Phosphoric Monoester Hydrolases, CCAAT-Enhancer-Binding Protein-beta, MicroRNAs, Interleukin-6, Signal Transduction, Down-Regulation, Gene Expression Regulation, Leukemic, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Precursor Cells, B-Lymphoid, Inositol Polyphosphate 5-Phosphatases, Transgenic, Lymphoma, B-Cell, Cell Transformation, Neoplastic, Gene Expression Regulation, Leukemic, Precursor Cells, B-Lymphoid, Immunology, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine
Abstract

We showed that Emicro-MiR-155 transgenic mice develop acute lymphoblastic leukemia/high-grade lymphoma. Most of these leukemias start at approximately 9 months irrespective of the mouse strain. They are preceded by a polyclonal pre-B-cell proliferation, have variable clinical presentation, are transplantable, and develop oligo/monoclonal expansion. In this study, we show that in these transgenic mice the B-cell precursors have the highest MiR-155 transgene expression and are at the origin of the leukemias. We determine that Src homology 2 domain-containing inositol-5-phosphatase (SHIP) and CCAAT enhancer-binding protein beta (C/EBPbeta), 2 important regulators of the interleukin-6 signaling pathway, are direct targets of MiR-155 and become gradually more down-regulated in the leukemic than in the preleukemic mice. We hypothesize that miR-155, by down-modulating Ship and C/EBPbeta, initiates a chain of events that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade lymphoma.

Published
2009

13. Supplementary Tables and Figures from PP2A-activating Drugs Enhance FLT3 Inhibitor Efficacy through AKT Inhibition–Dependent GSK-3β–Mediated c-Myc and Pim-1 Proteasomal Degradation

Author

Scarpa, Mario, primary, Singh, Prerna, primary, Bailey, Christopher M., primary, Lee, Jonelle K., primary, Kapoor, Shivani, primary, Lapidus, Rena G., primary, Niyongere, Sandrine, primary, Sangodkar, Jaya, primary, Wang, Yin, primary, Perrotti, Danilo, primary, Narla, Goutham, primary, and Baer, Maria R., primary

Published
2023
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14. Supplementary figure legends from Concurrent Inhibition of Pim and FLT3 Kinases Enhances Apoptosis of FLT3-ITD Acute Myeloid Leukemia Cells through Increased Mcl-1 Proteasomal Degradation

Author

Kapoor, Shivani, primary, Natarajan, Karthika, primary, Baldwin, Patrick R., primary, Doshi, Kshama A., primary, Lapidus, Rena G., primary, Mathias, Trevor J., primary, Scarpa, Mario, primary, Trotta, Rossana, primary, Davila, Eduardo, primary, Kraus, Manfred, primary, Huszar, Dennis, primary, Tron, Adriana E., primary, Perrotti, Danilo, primary, and Baer, Maria R., primary

Published
2023
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15. Figure S5 from Concurrent Inhibition of Pim and FLT3 Kinases Enhances Apoptosis of FLT3-ITD Acute Myeloid Leukemia Cells through Increased Mcl-1 Proteasomal Degradation

Author

Kapoor, Shivani, primary, Natarajan, Karthika, primary, Baldwin, Patrick R., primary, Doshi, Kshama A., primary, Lapidus, Rena G., primary, Mathias, Trevor J., primary, Scarpa, Mario, primary, Trotta, Rossana, primary, Davila, Eduardo, primary, Kraus, Manfred, primary, Huszar, Dennis, primary, Tron, Adriana E., primary, Perrotti, Danilo, primary, and Baer, Maria R., primary

Published
2023
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16. Supplementary Table 1, Figures 1 - 5 from Targeted Delivery of microRNA-29b by Transferrin-Conjugated Anionic Lipopolyplex Nanoparticles: A Novel Therapeutic Strategy in Acute Myeloid Leukemia

Author

Huang, Xiaomeng, primary, Schwind, Sebastian, primary, Yu, Bo, primary, Santhanam, Ramasamy, primary, Wang, Hongyan, primary, Hoellerbauer, Pia, primary, Mims, Alice, primary, Klisovic, Rebecca, primary, Walker, Alison R., primary, Chan, Kenneth K., primary, Blum, William, primary, Perrotti, Danilo, primary, Byrd, John C., primary, Bloomfield, Clara D., primary, Caligiuri, Michael A., primary, Lee, Robert J., primary, Garzon, Ramiro, primary, Muthusamy, Natarajan, primary, Lee, Ly James, primary, and Marcucci, Guido, primary

Published
2023
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17. Supplementary Figure 3 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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18. Supplementary Figure 6 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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19. Supplementary Figure 2 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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20. Supplementary Figure 7 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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21. Supplementary Figure 9 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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22. Data from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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23. Supplementary Figure 5 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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24. Supplementary Figure 6 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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25. Supplementary Figure 2 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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26. Supplementary Figure 5 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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27. Supplementary Figure 10 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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28. Supplementary Figure 8 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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29. Supplementary Figure 3 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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30. Table S1 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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31. Supplementary Table 1 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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32. Supplementary Figure Legends 1-10 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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33. Supplementary Methods for Figure 1 and Table 1 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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34. Supplementary Figure 4 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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35. Data from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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36. Supplementary Figure 1 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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37. Supplementary Figure 7 from Essential Requirement for PP2A Inhibition by the Oncogenic Receptor c-KIT Suggests PP2A Reactivation as a Strategy to Treat c-KIT+ Cancers

Author

Roberts, Kathryn G., primary, Smith, Amanda M., primary, McDougall, Fiona, primary, Carpenter, Helen, primary, Horan, Martin, primary, Neviani, Paolo, primary, Powell, Jason A., primary, Thomas, Daniel, primary, Guthridge, Mark A., primary, Perrotti, Danilo, primary, Sim, Alistair T.R., primary, Ashman, Leonie K., primary, and Verrills, Nicole M., primary

Published
2023
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38. Supplementary Figure 4 from Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions

Author

Silvestri, Giovannino, primary, Trotta, Rossana, primary, Stramucci, Lorenzo, primary, Ellis, Justin J., primary, Harb, Jason G., primary, Neviani, Paolo, primary, Wang, Shuzhen, primary, Eisfeld, Ann-Kathrin, primary, Walker, Christopher J., primary, Zhang, Bin, primary, Srutova, Klara, primary, Gambacorti-Passerini, Carlo, primary, Pineda, Gabriel, primary, Jamieson, Catriona H. M., primary, Stagno, Fabio, primary, Vigneri, Paolo, primary, Nteliopoulos, Georgios, primary, May, Philippa C., primary, Reid, Alistair G., primary, Garzon, Ramiro, primary, Roy, Denis-Claude, primary, Moutuou, Moutuaata M., primary, Guimond, Martin, primary, Hokland, Peter, primary, Deininger, Michael W., primary, Fitzgerald, Garrett, primary, Harman, Christopher, primary, Dazzi, Francesco, primary, Milojkovic, Dragana, primary, Apperley, Jane F., primary, Marcucci, Guido, primary, Qi, Jianfei, primary, Polakova, Katerina Machova, primary, Zou, Ying, primary, Fan, Xiaoxuan, primary, Baer, Maria R., primary, Calabretta, Bruno, primary, and Perrotti, Danilo, primary

Published
2023
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40. Bone marrow niche trafficking of miR-126 controls the self-renewal of leukemia stem cells in chronic myelogenous leukemia

Author

Zhang, Bin, Nguyen, Le Xuan Truong, Li, Ling, Zhao, Dandan, Kumar, Bijender, Wu, Herman, Lin, Allen, Pellicano, Francesca, Hopcroft, Lisa, Su, Yu-Lin, Copland, Mhairi, Holyoake, Tessa L, Kuo, Calvin J, Bhatia, Ravi, Snyder, David S, Ali, Haris, Stein, Anthony S, Brewer, Casey, Wang, Huafeng, McDonald, Tinisha, Swiderski, Piotr, Troadec, Estelle, Chen, Ching-Cheng, Dorrance, Adrienne, Pullarkat, Vinod, Yuan, Yate-Ching, Perrotti, Danilo, Carlesso, Nadia, Forman, Stephen J, Kortylewski, Marcin, Kuo, Ya-Huei, and Marcucci, Guido

Subjects
Bone marrow -- Genetic aspects -- Health aspects, MicroRNA -- Health aspects, Stem cells -- Genetic aspects -- Health aspects, Chronic myeloid leukemia -- Genetic aspects -- Development and progression -- Care and treatment, Gene expression -- Health aspects, Biological sciences, Health
Abstract

Leukemia stem cells (LSCs) in individuals with chronic myelogenous leukemia (CML) (hereafter referred to as CML LSCs) are responsible for initiating and maintaining clonal hematopoiesis. These cells persist in the bone marrow (BM) despite effective inhibition of BCR-ABL kinase activity by tyrosine kinase inhibitors (TKIs). Here we show that although the microRNA (miRNA) miR-126 supported the quiescence, self-renewal and engraftment capacity of CML LSCs, miR-126 levels were lower in CML LSCs than in long-term hematopoietic stem cells (LT-HSCs) from healthy individuals. Downregulation of miR-126 levels in CML LSCs was due to phosphorylation of Sprouty-related EVH1-domain-containing 1 (SPRED1) by BCR-ABL, which led to inhibition of the RAN-exportin-5-RCC1 complex that mediates miRNA maturation. Endothelial cells (ECs) in the BM supply miR-126 to CML LSCs to support quiescence and leukemia growth, as shown using mouse models of CML in which Mir126a (encoding miR-126) was conditionally knocked out in ECs and/or LSCs. Inhibition of BCR-ABL by TKI treatment caused an undesired increase in endogenous miR-126 levels, which enhanced LSC quiescence and persistence. Mir126a knockout in LSCs and/or ECs, or treatment with a miR-126 inhibitor that targets miR-126 expression in both LSCs and ECs, enhanced the in vivo anti-leukemic effects of TKI treatment and strongly diminished LSC leukemia-initiating capacity, providing a new strategy for the elimination of LSCs in individuals with CML., Author(s): Bin Zhang (corresponding author) [1]; Le Xuan Truong Nguyen [1, 2]; Ling Li [1]; Dandan Zhao [1]; Bijender Kumar [1]; Herman Wu [1]; Allen Lin [1]; Francesca Pellicano [3]; [...]

Published
2018
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43. Retraction Notice to: Downregulation of p53-inducible microRNAs 192, 194, and 215 Impairs the p53/MDM2 Autoregulatory Loop in Multiple Myeloma Development

Author

Pichiorri, Flavia, primary, Suh, Sung-Suk, additional, Rocci, Alberto, additional, De Luca, Luciana, additional, Taccioli, Cristian, additional, Santhanam, Ramasamy, additional, Zhou, Wenchao, additional, Benson, Don M., additional, Hofmainster, Craig, additional, Alder, Hansjuerg, additional, Garofalo, Michela, additional, Di Leva, Gianpiero, additional, Volinia, Stefano, additional, Lin, Huey-Jen, additional, Perrotti, Danilo, additional, Kuehl, Michael, additional, Aqeilan, Rami I., additional, Palumbo, Antonio, additional, and Croce, Carlo M., additional

Published
2022
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46. Preclinical and clinical efficacy of XPO1/CRM1 inhibition by the karyopherin inhibitor KPT-330 in Ph+ leukemias

Author

Walker, Christopher J., Oaks, Joshua J., Santhanam, Ramasamy, Neviani, Paolo, Harb, Jason G., Ferenchak, Gregory, Ellis, Justin J., Landesman, Yosef, Eisfeld, Ann-Kathrin, Gabrail, Nash Y., Smith, Carrie L., Caligiuri, Michael A., Hokland, Peter, Roy, Denis Claude, Reid, Alistair, Milojkovic, Dragana, Goldman, John M., Apperley, Jane, Garzon, Ramiro, Marcucci, Guido, Shacham, Sharon, Kauffman, Michael G., and Perrotti, Danilo

Published
2013
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48. Lenalidomide-mediated enhanced translation of C/EBPα-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia

Author

Hickey, Christopher J., Schwind, Sebastian, Radomska, Hanna S., Dorrance, Adrienne M., Santhanam, Ramasamy, Mishra, Anjali, Wu, Yue-Zhong, Alachkar, Houda, Maharry, Kati, Nicolet, Deedra, Mrózek, Krzysztof, Walker, Alison, Eiring, Anna M., Whitman, Susan P., Becker, Heiko, Perrotti, Danilo, Wu, Lai-Chu, Zhao, Xi, Fehniger, Todd A., Vij, Ravi, Byrd, John C., Blum, William, Lee, L. James, Caligiuri, Michael A., Bloomfield, Clara D., Garzon, Ramiro, and Marcucci, Guido

Published
2013
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50. Aberrant Overexpression of IL-15 Initiates Large Granular Lymphocyte Leukemia through Chromosomal Instability and DNA Hypermethylation

Author

Mishra, Anjali, Liu, Shujun, Sams, Gregory H., Curphey, Douglas P., Santhanam, Ramasamy, Rush, Laura J., Schaefer, Deanna, Falkenberg, Lauren G., Sullivan, Laura, Jaroncyk, Laura, Yang, Xiaojuan, Fisk, Harold, Wu, Lai-Chu, Hickey, Christopher, Chandler, Jason C., Wu, Yue-Zhong, Heerema, Nyla A., Chan, Kenneth K., Perrotti, Danilo, Zhang, Jianying, Porcu, Pierluigi, Racke, Frederick K., Garzon, Ramiro, Lee, Robert J., Marcucci, Guido, and Caligiuri, Michael A.

Published
2012
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