tbuckley/cabot-search huggingface dataset:
76. Transgenic Expression of IL15 Improves Antiglioma Activity of IL13Rα2-CAR T Cells
Authors: Giedre Krenciute, Irina Balyasnikova, Gianpietro Dotti, Stephen Gottschalk
Journal: Molecular Therapy (2016)

BACKGROUND: Glioblastoma (GBM) is the most aggressive primary brain tumor in humans, and is virtually incurable with conventional therapies. Immunotherapy with T cells expressing chimeric antigen receptors (CARs) specific for the GBM antigen IL13Rα2 is an attractive approach to improve outcomes. We recently generated the first scFv-based CAR that is specific for IL13Rα2 and demonstrated that IL13Rα2-CARs with a CD28.ζ endodomain had potent anti-GBM activity in preclinical models. However, CAR T-cell persistence was limited, resulting in recurrence of IL13Rα2-positive GBMs. Since IL13Rα2-CARs with other endodomains (41BB, 41BB and OX40) did not improve outcomes, the goal of this project was to evaluate if transgenic expression of IL-15, a cytokine that is critical for T-cell proliferation and survival, enhances persistence and anti-tumor activity of IL13Rα2-CAR.CD28.ζ T cells. METHODS: We generated IL13Rα2-CAR.CD28.ζ T cells expressing IL-15 (IL13Rα2-CAR. IL15 T cells) by double transducing T cells with retroviruses containing expression cassettes encoding i) IL13Rα2-CAR.CD28.ζ or ii) IL-15, ΔNGFR, and iC9 separated by 2A sequences. We determined the effector function of IL13Rα2-CAR. IL15 T cells in vitro using standard assays, and in the U373 GBM xenograft model. RESULTS: Double transduction of CD3/CD28-activated T cells resulted in T-cell lines that expressed both transgenes in 45-50% of T cells. At base line IL13Rα2-CAR. IL15 T cells produced on average 69.5 pg/ml of IL15. Production was significantly increased after CD3 or antigen-specific T-cell stimulation (176.7 pg/ml; n=6; p<0.001). IL13Rα2-CAR. IL15 T cells were as efficient as IL13Rα2-CAR T cells in killing IL13Rα2-positive GBMs in vitro. After intratumoral injection into U373 glioma-bearing mice IL13Rα2-CAR. IL15 T cells persisted significantly longer than IL13Rα2-CAR T cells (p<0.05). This resulted in a significant increase in progression free (98 vs 49 days; p=0.004) and overall survival (p=0.006) of treated mice. Up to date, 4/10 IL13Rα2-CAR. IL15 T-cell treated mice remain glioma free with a follow up of at least 80 days. Recurring U373 gliomas post IL13Rα2-CAR. IL15 T-cell therapy had down regulated IL13Rα2 expression, indicating immune escape. This was specific for the targeted antigen since LL13Rα2-CAR.LL15 T-cell-treated U373 gliomas continued to express other tumor antigens such as EphA2 and HER2 at unchanged levels in comparison to controls. CONCLUSION: Here we demonstrate that transgenic expression of IL15 enhances the in vivo persistence of IL13Rα2-CAR T cells resulting in improved anti-glioma activity. However, enhanced in vivo persistence of T cells also resulted in the development of antigen-loss variants highlighting the need to target multiple antigens in tumors with heterogeneous antigen expression such as GBM.
Nationwide genomic screening network for the development of targeted therapies in NSCLC (LC-SCRUM-Japan)
Authors: Shingo Matsumoto, Kiyotaka Yoh, Yukio Hosomi, Takehito Shukuya, Yoshihiro Miyata, Takashi Kohno, Koji Tsuta, Genichiro Ishii, Katsuya Tsuchihara, Koichi Goto
Journal: Annals of Oncology (2015)
Abstract 4984: EMT and breast cancer metastasis driven by plasma membrane fluidity
Authors: Jeffrey T. Chang
Journal: Cancer Research (2015)

Abstract New therapeutic targets that can inhibit cancer metastasis are desperately needed. To address this issue, we have leveraged a computational approach and performed an unbiased screen for therapies that can inhibit an epithelial-to-mesenchymal transition (EMT) gene expression profile, a phenotype that is believed to promote metastases. This yielded predictions of drugs that can both promote and inhibit an EMT transcriptional profile. Following up on these predictions, we confirmed that these drugs can induce or repress an EMT in a range of breast cancer cell lines. Furthermore, we discovered that they do so by altering the fluidity of the plasma membrane. An increase in plasma membrane fluidity is necessary and sufficient to induce and maintain an EMT state, increased motility, and increased mammosphere forming ability. Therapies that decrease fluidity can inhibit metastasis in xenograft mouse models. Finally, we found that human cancers can regulate their membrane fluidity through cholesterol homeostasis pathways. 41% of human breast cancers have alterations in cholesterol regulatory pathways, and are associated with a 9 year loss in time to distant metastasis. These data demonstrate that plasma membrane fluidity is a cellular attribute that is leveraged by human tumors to increase metastatic capacity, and that it can, in principle, be targeted by therapeutics to prevent metastasis. Citation Format: Jeffrey T. Chang. EMT and breast cancer metastasis driven by plasma membrane fluidity. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4984. doi:10.1158/1538-7445.AM2015-4984
Barth Syndrome: An Under-Recognized Cause of Chronic Neutropenia
Authors: Colin G. Steward, Sarah J. Groves, Carolyn L. Taylor, Melissa K. Maisenbacher, Birgitta Versluys, Ruth Newbury-Ecob, Hulya Ozsahin, Leo Hamilton, Michaela K. Damin, Valerie M. Bowen, Katherine R. McCurdy, Michael C. Mackey, Audrey Anna Bolyard, David C. Dale
Journal: Blood (2015)
Hepatocyte and Mesenchymal Stem Cell Co-Transplantation in Rats of Acute Liver Failure
Authors: Cheng-Maw Ho, Ya-Hui Chen, Chin-Sung Chien, Shu-Li Ho, Daniel Tzu-bi Shih, Po-Huang Lee, Hui-Ling Chen
Journal: Clinical Gastroenterology and Hepatology (2016)
Targeting Early Events of B-Cell Receptor Signaling in Chronic Lymphocytic Leukemia: Suppressed Syk and PLCγ2 Activities Predict Apoptotic Response of Leukemic Cells to Dasatinib
Authors: Y. Lynn Wang, Zibo Song, Pin Lu, John P. Leonard, Morton Coleman, Peter Martin, Chaowei Wu, Francis Y. Lee, Daniel M. Knowles, Richard Furman
Journal: Blood (2008)
Benzalkonium tolerance genes and outcome in Listeria monocytogenes meningitis
Authors: P.H.C. Kremer, J.A. Lees, M.M. Koopmans, B. Ferwerda, A.W.M. Arends, M.M. Feller, K. Schipper, M. Valls Seron, A. van der Ende, M.C. Brouwer, D. van de Beek, S.D. Bentley
Journal: Clinical Microbiology and Infection (2016)

ObjectivesListeria monocytogenes is a food-borne pathogen that can cause meningitis. The listerial genotype ST6 has been linked to increasing rates of unfavourable outcome over time. We investigated listerial genetic variation and the relation with clinical outcome in meningitis.MethodsWe sequenced 96 isolates from adults with listerial meningitis included in two prospective nationwide cohort studies by whole genome sequencing, and evaluated associations between bacterial genetic variation and clinical outcome. We validated these results by screening listerial genotypes of 445 cerebrospinal fluid and blood isolates from patients over a 30-year period from the Dutch national surveillance cohort.ResultsWe identified a bacteriophage, phiLMST6 co-occurring with a novel plasmid, pLMST6, in ST6 isolates to be associated with unfavourable outcome in patients (p 2.83e-05). The plasmid carries a benzalkonium chloride tolerance gene, emrC, conferring decreased susceptibility to disinfectants used in the food-processing industry. Isolates harbouring emrC were growth inhibited at higher levels of benzalkonium chloride (median 60 mg/L versus 15 mg/L; p <0.001), and had higher MICs for amoxicillin and gentamicin compared with isolates without emrC (both p <0.001). Transformation of pLMST6 into naive strains led to benzalkonium chloride tolerance and higher MICs for gentamicin.ConclusionsThese results show that a novel plasmid, carrying the efflux transporter emrC, is associated with increased incidence of ST6 listerial meningitis in the Netherlands. Suggesting increased disease severity, our findings warrant consideration of disinfectants used in the food-processing industry that select for resistance mechanisms and may, inadvertently, lead to increased risk of poor disease outcome.
110. Enhanced Intratumoral Accumulation of Nucleic Acid and Oncolytic Adenovirus by Complexation with Biocompatible and Bioreducible Polymer
Authors: Jung-Woo Choi, Jaesung Kim, Yan Li, Chae-Ok Yun, Sung Wan Kim
Journal: Molecular Therapy (2016)

As an effective and safe strategy to overcome the limits of therapeutic nucleic acid or adenovirus (Ad) vectors for in vivo application, various technologies to modify the surface of vectors with nonimmunogenic/biocompatible polymers have been emerging in the field of gene therapy. However, the transfection efficacy of the polymer to transfer genetic matrials is still relatively weak. To develop more advanced and effective polymer to deliver not only Ad vectors, but also nucleic acids, 6 biocompatible polymers were newly designed and synthesized to different sizes (2k, 3,4k, or 5k) of poly(ethylene) glycol (PEG) and different numbers of amine groups (2 or 5) based on methoxy poly(ethylene glycol)-b-poly{N-[N-(2-aminoethyl)-2-aminoethyl]-L-glutamate (PNLG). We characterized size distribution and surface charge of 6 PNLGs after complexation with either nucleic acid or Ad. Among all 6 PNLGs, the 5amine group PNLG showed the strongest efficacy in delivering nucleic acid as well as Ad vectors. Interestingly, cellular uptake results showed higher uptake ability in Ad complexed with 2 amine group PNLGs is more essential than the surface charge for cellular uptake in polymers with charges greater than 30 mV. Moreover, the endosome escape ability of Ad/PNLGs increased depending on the number of amine groups, but decreased by PEG size. Cancer cell killing efficacy and immune response studies of oncolytic Ad/PNLGs showed 5 amine group PNLG to be a more effective and safe carrier for delivering Ad. Overall, these studies provide new insights into the functional mechanism of polymer-based approaches to either nucleic acid or Ad/nanocomplex. Furthermore, the identified ideal biocompatible PNLG polymer formulation (5 amine/2k PEG for nucleic acid, 5 amine/5k PEG for Ad) demonstrated high transduction efficiency as well as therapeutic value (efficacy and safety) and thus has strong potential for in vivo therapeutic use in the future.
Can Allo-HSCT Improve the Poor Clinical Outcome of the “Internal Tandem Duplication” of the FLT3 Gene?
Authors: Paolo Bernasconi, Catherine Klersy, Anna Amelia Colombo, Daniela Caldera, Francesco Ripamonti, Patrizia Zappasodi, Barbara Rocca, Celeste Calvello, Matteo Giovanni Della Porta, Marianna Rossi, Manuela Santantonio, Irene Dambruoso, Rita Zappatore, Mirko Farina, Daniela Troletti, Marina Boni, Carlo Castagnola, Emilio Paolo Alessandrino
Journal: Blood (2014)
Reduction of myeloid-derived suppressor cells in peripheral blood by local hyperthermia in patients with advanced solid tumors.
Authors: P. Shen, S. Huang, M. He, L. Yu, G. Shi, J. Deng, J. Chen, L. Yang, X. Wang, N. Xu, X. Zhang
Journal: Journal of Clinical Oncology (2011)

e21058 Background: Circulating levels of myeloid-derived suppressor cells (MDSCs) correlate with clinical cancer stage, metastatic tumor burden and tumor immune evasion. The potential contribution of MDSCs to thermotherapy has not been explored. The aim of this study was to investigate the impact of treatment of local hyperthermia on the levels of MDSCs in peripheral blood. Methods: Thirty patients with advanced solid tumors treated with local hyperthermia were enrolled. Peripheral blood samples were obtained before and after treatment immediately. Circulating MDSCs (identified as HLA-Dr-/low, CD11b+, CD33+ cells) were measured by flow cytometry. Meanwhile lymphocyte subpopulations in peripheral blood samples (T-helper-/T4-cells, T-suppressor-/T8-cells, natural-killer-/NK-cells, CD19+cells) were also analyzed using the same method. The association between MDSCs and the other lymphocyte subpopulation was examined by ultivariate linear regression analysis. Results: The percentage of MDSCs and other lymphocyte subpopulations before and after treatment are shown in the Table1. MDSCs were significantly reduced after local hyperthermia, so were the T-suppressor cells and the NK cells. But the T-helper cells and the ratio of T-helper/T-suppressor cells were increased. The numbers of CD3+ cells and CD19+ cells were not significantly affected by the treatment. This reduction of MDSCs is not associated with any other lymphocyte subtype. Conclusions: It was demonstrated that local hyperthermia can reduce abnormal accumulation of circulating MDSCs. The reduction of MDSCs was not associated with the other lymphocyte subpopulation. The percentage of MDSCs and lymphocyte subpopulations before and after treatment. MDSC CD3+CD4+ CD3+CD8+ CD4+/CD8+ CD3+ NK CD19+ B# 7.71±5.92 38.84±10.72 28.26±10.05 1.56±0.71 65.65±13.49 23.77±11.37 5.69±5.13 A* 6.45±4.85 43.80±10.89 26.92±9.93 1.98±1.26 68.80±14.23 19.37±10.58 6.37±6.25 P value 0.042 0.003 0.006 0.004 0.052 0.004 0.150 B# Before Local Hyperthermia. A* After Local Hyperthermia.
Mitochondrial Apoptotic Priming Measured by BH3 Profiling Regulates Clinical Response to Chemotherapy in Myeloma and Acute Lymphoblastic Leukemia and Explains Therapeutic Index
Authors: Triona Ni Chonghaile, Kristopher Sarosiek, Jeremy Ryan, Vicki Del Gaizo Moore, Yu-Tzu Tai, Paul G. Richardson, Kenneth C. Anderson, Richard M. Stone, Daniel J DeAngelo, Constantine S. Mitsiades, Stephen E. Sallan, Michelle Hirsch, Lewis B. Silverman, Ruben Carrasco, Anthony G. Letai
Journal: Blood (2011)
116. MegaTAL Nucleases Outperform TALENs in Promoting Homology-Directed-Gene Modification in Primary Human T Cells
Authors: Gabrielle Curinga, Guillermo Romano, Blythe Sather, Karen Sommer, Malika Hale, Iram Khan, Swati Singh, Yumei Song, Kamila Gwiazda, Andy Scharenberg, David J. Rawlings
Journal: Molecular Therapy (2015)

Advances in rare cleaving nuclease technologies have dramatically increased the potential for seamless manipulation of virtually any gene (i.e. gene editing). Among these platforms, TALENs and Cas9-based nucleases have become broadly applied owing to ease in customizing their DNA recognition properties. In contrast, LAGLIDADG homing endonucleases (LHE) are more challenging to engineer, yet exhibit superior physical attributes, DNA recognition and hydrolysis properties. Recent advances have overcome hurdles in LHE engineering leading to the ability to more rapidly customize LHEs as therapeutic nucleases. In addition, LHEs can be fused to TAL effector arrays to create chimeric proteins [referred to here as megaTALs (MTAL)] that exhibit further enhancements in activity. We previously developed a CCR5-specific MTAL as a potential HIV therapeutic. In parallel, we generated high-activity TALEN pairs targeting the identical region in CCR5. In the current study, we directly compared the ability of these nuclease platforms to induce homology directed repair (HDR) in primary human T-cells. We first verified that both reagents facilitated efficient disruption of the CCR5 locus. We directly compared activity in primary CD4 T cells using mRNA nuclease delivery. Indel frequency was estimated using both the T7 endonuclease assay and a re-cleavage assay (RCA; where genomic DNA surrounding the cleavage site is amplified and digested in vitro with the original LHE used to create the MTAL). NHEJ rates were 65-82% for the TALEN vs. 44-61% (6 experiments) for the MTAL using these respective assays. Next, we coupled mRNA-mediated nuclease expression with AAV delivery of a donor template. We co-delivered mRNA with a range of doses of an AAV-CCR5-GFP donor (containing 1.3kb CCR5 homology arms and an internal MND-GFP expression cassette). Cell viability was not significantly different; and control experiments using AAV BFP (lacking homology arms) demonstrated that infection and expression rates were equivalent. Strikingly, the proportion of cells with sustained GFP expression (at day 16) was up to 5-fold higher in MTAL treated cells (across a range of AAV doses; n=6, independent donors); with the greatest differences observed when access to donor template was limiting. Molecular analysis verified HDR in both test groups. While the mechanism for these differences remains incompletely defined, preliminary comparisons of HR:NHEJ ratios using single cell analysis suggest that alternative DNA repair pathways may be preferentially utilized by the 3' vs 5' overhangs generated by LHE vs Fok1 nucleases, respectively. Taken together, our findings suggest that the MTAL platform and the co-delivery method described here may provide significant clinical utility in future editing applications in human hematopoietic cells.
Abstract 4108: NKX6.1 suppresses cancer invasion and epithelial-mesenchymal transition in cervical cancer
Authors: Hsin-Jung Li, Pei-Ning Yu, Yu-Lueng Shih, Ya-Wen Lin
Journal: Cancer Research (2015)

Abstract Cervical cancer is a common women malignancy worldwide. Recent reports emphasize inactivation of tumor suppressor genes are due to promoter hypermethylation in cervical cancer. Our previous study from methylation array has shown NK6 homeobox 1 (NKX6.1) is hypermethylated and downregulated in cervical cancer cell lines and clinical samples. Nkx6.1 contains a homeobox domain and functions as a transcription factor that regulates insulin-secreting β cell differentiation and neuronal fate determination. However, the biological function of NKX6.1 in cervical cancer remains elusive. Overexpression of NKX6.1 suppressed the transformation and invasive ability of HeLa and CaSki cells in vitro as well as decreased tumor formation and metastatic property in vivo. Conversely, knockdown of NKX6.1 strongly enhanced the transformation and invasiveness of SiHa cells. Epithelial-mesenchymal transition (EMT) has been shown to play a key role in the progression of uterine cervix carcinoma in situ (CIS) to invasive squamous cell carcinoma (SCC). NKX6.1 suppresses cancer invasiveness through coordinately increasing E-cadherin and decreasing Vimentin. Moreover, we demonstrated E-cadherin and vimentin were direct targets of NKX6.1 by luciferase reporter assay, electrophoretic mobility shift assay and chromatin immunoprecipitation quantitative polymerase chain reaction (Chip-qPCR) assay. Collectively, our data demonstrate NKX6.1 acts a tumor suppressor, and inhibits tumor invasion and metastasis by suppressing Epithelial-mesenchymal transition (EMT) in cervical cancer. These data imply that modulation of NKX6.1 expression may be a novel therapeutic option for treatment of cervical cancer. Citation Format: Hsin-Jung Li, Pei-Ning Yu, Yu-Lueng Shih, Ya-Wen Lin. NKX6.1 suppresses cancer invasion and epithelial-mesenchymal transition in cervical cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4108. doi:10.1158/1538-7445.AM2015-4108
Cardiac Toxicity After High-Dose Melphlan and Autologous Hematopoietic Stem Cell Transplantation for Multiple Myeloma
Authors: Zartash Gul, Qaiser Bashir, Yago Nieto, Nazeer Sherwani, Simrit Parmar, Nina Shah, Yvonne T Dinh, Chitra M. Hosing, Uday R. Popat, Partow Kebriaei, Elizabeth J Shpall, Sergio A Giralt, Richard E. Champlin, Muzaffar H. Qazilbash
Journal: Blood (2012)
Abstract 2585: Discovery of a potent covalent mutant-selective EGFR inhibitor - the journey from high throughput screening to EGF816
Authors: Gerald Lelais, Robert Epple, Pierre-Yves Michellys, Thomas H. Marsilje, Yun Long, Matthew McNeill, Bei Chen, Wenshuo Lu, Badry Bursulaya, Michael DiDonato, Yong Jia, Shailaja Kasibhatla, Chun Li, Igor Matushansky, Steven Bender
Journal: Cancer Research (2015)

Abstract Epidermal growth factor receptor (EGFR) is a validated therapeutic target for lung cancer. First and second generation EGFR inhibitors (e.g., gefitinib, erlotinib and afatinib) have revolutionized treatment paradigms of non-small cell lung cancer (NSCLC) patients with oncogenic EGFR mutations. The use of EGFR tyrosine kinase inhibitors (TKI) provides superior efficacy compared to chemotherapy in patients with EGFR L858R or exon 19 deletion tumors. However, resistance inevitably develops after 8-12 months of treatment; most commonly via a secondary T790M point mutation at the gatekeeper residue of EGFR. Furthermore, responses are hindered due to treatment intolerance in the form of rash and diarrhea that are mediated by simultaneous inhibition of wild-type (WT) EGFR at doses required for mutant EGFR suppression. To overcome these limitations, we initiated a project to identify mutant-selective EGFR inhibitors that potently inhibit both activating and T790M resistance EGFR mutations while sparing WT EGFR. In this presentation, we report our medicinal chemistry approach and optimization that led to the discovery of EGF816, a selective and potent covalent mutant-selective EGFR inhibitor with single digit nanomolar cellular target modulation on both activating and T790M resistance mutations. In addition, we will also report validated clinical efficacy data from the first patient treated with EGF816. Citation Format: Gerald Lelais, Robert Epple, Pierre-Yves Michellys, Thomas H. Marsilje, Yun Long, Matthew McNeill, Bei Chen, Wenshuo Lu, Badry Bursulaya, Michael DiDonato, Yong Jia, Shailaja Kasibhatla, Chun Li, Igor Matushansky, Steven Bender. Discovery of a potent covalent mutant-selective EGFR inhibitor - the journey from high throughput screening to EGF816. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2585. doi:10.1158/1538-7445.AM2015-2585
A New Strategy Based On qPCR to Optimize Detection and Quantification of Eight Herpesviruses in Patients Undergoing Allogeneic Hematopoietic Stem Cell Transplantation.
Authors: Miriam Ueda, Juliana Monte Real, Paulo Guilherme A G Oliveira, Eloisa de Sa Moreira, Luiz Fernando Lima Reis, Celso FH Granato, Celso Arrais Rodrigues
Journal: Blood (2012)
A Polycythemia Vera<i>JAK2</i>Mutation Masquerading as a Duodenal Cancer Mutation
Authors: Justin Lee, Jennifer Axilbund, W. Brian Dalton, Daniel Laheru, Stanley Watkins, David Chu, Karen Cravero, Berry Button, Kelly Kyker-Snowman, Ian Waters, Christopher D. Gocke, Josh Lauring, Ben Ho Park
Journal: Journal of the National Comprehensive Cancer Network (2016)

Next-generation sequencing (NGS) is increasingly being used in cancer care to identify both somatic tumor driver mutations that can be targeted for therapy, and heritable mutations in the germline associated with increased cancer risk. This report presents a case of a JAK2 V617F mutation falsely identified as a duodenal cancer mutation via NGS. The patient was found to have a history of polycythemia vera, a disorder with a high incidence of JAK2 somatic mutations. Buccal cell DNA showed heterozygosity for the mutation, suggesting that it was potentially germline. However, subsequent resequencing of tumor, adjacent normal tissue, and fingernail DNA confirmed the mutation was somatic, and its presence in tumor and buccal cells resulted from contaminating blood cells. This report highlights important nuances of NGS that can lead to misinterpretation of results with potential clinical implications.
Specific Identification of High Risk Disease Using Molecular Profiling By Mymap (Myeloma MLPA and translocation PCR) of 1,036 Cases
Authors: Martin F Kaiser, Eileen Mary Boyle, Brian A Walker, Dil B Begum, Paula Proszek, David C Johnson, Charlotte Pawlyn, John R Jones, Suvi Savola, Roger G Owen, Mark T Drayson, David A Cairns, Gordon Cook, Walter M Gregory, Richard S Houlston, Faith E Davies, Graham H Jackson, Gareth J Morgan
Journal: Blood (2015)
MicroRNA Profiling Reveals Aberrant MicroRNA Expression in Adult ETP-ALL and Functional Studies Demonstrate a Role of Mir-222 in Acute Leukemia,
Authors: Ebru Coskun, Martin Neumann, Cornelia Schlee, Nicola Goekbuget, Dieter Hoelzer, Eckhard Thiel, Claudia D Baldus
Journal: Blood (2011)