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Journal articles on the topic 'Nalm6 cells'

Author: Grafiati

Published: 6 September 2023

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1

Ramírez Saldaña, Maricela, Miguel Aguilar Santelises, Martha Moreno Lafont, Leopoldo Santos Argumedo, Vladimir Paredes Cervantes, and Rubén López Santiago. "Human B cells are targets for Brucella abortus infection. (P3130)." Journal of Immunology 190, no. 1_Supplement (2013): 186.12. http://dx.doi.org/10.4049/jimmunol.190.supp.186.12.

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Abstract It has been demonstrated that Brucella abortus is capable to multiply into professional antigen presenting cells such as macrophages and dendritic cells. However, there are a few reports about Brucella infection into B cells. In this work, we evaluated the ability of B. abortus 2308 for infect the human B cell line, NALM6 R. B cells cultured in RPMI medium supplied with L-glutamine and 10% of fetal calf serum were infected with several MOIs of Brucella abortus 2308 transformed by electroporation with the pBBR1MCS-2-gfp-mut3 plasmid to evaluate the entry of green fluorescent Brucella.

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2

Tang, Yongmin, Lixia Li, Di Wang, et al. "Study on the Preparation of the Immunotoxin 2E8-NCTD and Its Targeting Killing Effect In Vitro." Blood 110, no. 11 (2007): 4186. http://dx.doi.org/10.1182/blood.v110.11.4186.4186.

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Abstract Objective: Monoclonal antibody (mAb) conjugated with certain toxin to generate immunotoxin bears an important and promising new therapy for patients with hematopoietic malignancies. However, most toxic moieties conjugated to antibody proteins reported were toxic proteins which presented immunogenicity to patients capable of producing anti-toxin antibody. Norcantharidin (NCTD) is a small molecule of toxin derived from a Chinese medicine Mylabris phalerata Pallas. The chemical name of this agent is 7-Oxabicyclo(2,2,1) heptane-2,3-dicarboxylic anhydride with a molecular weight of 168.15

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3

Iwasa, Masaki, Yasuo Miura, Aya Fujishiro, et al. "Bortezomib Attenuates Adhesion of B Cell Precursor Acute Lymphoblastic Lleukemia Cells to Bone Marrow Mesenchymal Stromal/Stem Cells Via Regulating SPARC Expression." Blood 126, no. 23 (2015): 786. http://dx.doi.org/10.1182/blood.v126.23.786.786.

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The prognosis of adults with B cell precursor acute lymphoblastic leukemia (BCP-ALL) is poor. Many cases in complete remission experience relapse of leukemia despite intensive chemotherapy or hematopoietic stem cell transplantation. This clinical observation suggests that minimal residual disease (MRD) still exists after these intensive therapies. Cell adhesion-mediated drug resistance (CAM-DR) is one of the mechanisms to support MRD in the bone marrow microenvironment (Clin Cancer Res 14:9, 2008). Mesenchymal stromal/stem cells (MSCs) are a cellular component of bone marrow (BM) and maintain

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4

Hermanova, Ivana, Karel Valis, Karel Fiser, Hana Nuskova, Jan Trka, and Julia Starkova. "L-Asparaginase Strongly Affects Bioenergetics in Leukemic Cells." Blood 120, no. 21 (2012): 779. http://dx.doi.org/10.1182/blood.v120.21.779.779.

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Abstract Abstract 779 L-asparaginase (L-asp) is an important component of childhood acute lymphoblastic leukemia (ALL) therapy. Its cytotoxic effect is based on the depletion of extracellular asparagine and glutamine. Leukemic cells are sensitive to this depletion due to the lower activity of asparagine synthetase compared to healthy cells. However, the mechanism of resistance development remains unclear. The aim of this study was to obtain further insights into the mechanisms underlying the cytotoxic effect of L-asp. We used two models: resistant preB ALL leukemic cells derived from the REH (

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Gu, Yan, Chunhua Song, Sinisa Dovat, Qinglong Guo, Qinyu Ge, and Zheng Ge. "Oncogenesis of CRLF2 Overexpression and Effect of JAK2 Inhibitor in CRLF2 Overexpressed B-Cell Acute Lymphoblastic Leukemia." Blood 134, Supplement_1 (2019): 2757. http://dx.doi.org/10.1182/blood-2019-125259.

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Backgroud: Cytokine receptor-like factor 2 (CRLF2) plays an important role in the development of normal B lymphocytes, which can mediate the proliferation of early B cells. However, the diect oncogenic effect of CRLF2 overexpression in acute lymhpoblastic leukemia (ALL) is far yet to be clarified. Here, we explored the effect of CRLF2 overexpression on cell proliferation and the effect of the novel JAK2 inhibitor on B-ALL cells with CRLF2 overexpression. Methods: The 83 patients with newly-diagnosed ALL (56 B-cell and 27 T-cell ALL; range from 14 to 77 years old) between June 2008 and June 201

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Barredo, Julio C., Sanja Altman-Hamandzic та Guy J. Leclerc. "Differences in Folylpoly-γ-Glutamate Synthetase (FPGS) Expression in Childhood ALL Result from Cell Lineage of Origin and Presence of Non-Random Translocations." Blood 104, № 11 (2004): 2087. http://dx.doi.org/10.1182/blood.v104.11.2087.2087.

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Abstract Methotrexate (MTX) is a universal component of chidlhood ALL therapies and its conversion to long chain polyglutamates (PG) by folylpoly-γ-glutamate synthetase (FPGS) is essential for its antileukemic acitivity. Expression of FPGS appears to be controlled by tissue/lineage specific and proliferation-dependent mechanisms. Levels of FPGS mRNA, protein, and enzyme activity are 2-3 fold higher in B-precursor (Bp) ALL cells when compared to T-lineage ALL, and these differences correlate with intracellular accumulation of long chain MTX-PG and lymphoblast sensitivity to MTX. To characterize

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Borges, Christopher M., Kevin Wasko, Jared M. Nasser, et al. "Preclinical Development of Edit-201, a Multigene Edited Healthy Donor NK Cell with Enhanced Anti-Tumor Function and Superior Serial Killing Activity in an Immunosuppressive Environment." Blood 136, Supplement 1 (2020): 33. http://dx.doi.org/10.1182/blood-2020-139988.

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Natural killer (NK) cells distinguish tumor from healthy tissue via multiple mechanisms, including recognition of stress ligands and loss of MHC class I expression. For example, KIR mismatching enables allogenic NK cells to respond to MHC positive tumors in a similar manner to MHC negative tumors, making allogeneic NK cell therapy a promising approach for broad oncology indications. Accordingly, allogenic human HD-NK cells, including gene-modified cells, have demonstrated an impressive safety and efficacy profile when administered to patients with advanced hematologic malignancies. However, ef

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Wang, Lingyan, Yue Zhang, Eden Anderson, Rajesh Kumar, Adam J. Lamble, and Rimas J. Orentas. "CD22 CAR-T Induces Both CD19 and CD22 Surface Down-Modulation: Defining a Mechanism of Generalized Immune Evasion and the Effects of Epigenetic Modifiers." Blood 136, Supplement 1 (2020): 22–23. http://dx.doi.org/10.1182/blood-2020-134930.

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The success of chimeric antigen receptor modified T lymphocyte (CAR-T cell) therapy for pediatric and adult leukemia and lymphoma has been impressive, but far from universal. Even for the most responsive disease, pediatric pre-B-ALL, one-year remission rates are 50% or less. This brings fundamental questions as to how leukemia resists CAR-T activity front and center. CD19- and CD22-specific CAR-T escape mechanisms appear to differ. For CD19, antigen loss and RNA-splicing variants are common. For CD22, decreasing the number of target molecules on the surface of the leukemia appears to be a prim

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Barredo, Julio C., Tingting Kinser та Guy J. Leclerc. "TEL/AML1 and E2A/PBX1 Tranlsocations Lead to Altered Folylpoly-γ-Glutamate Synthetase (FPGS) Expression in ALL." Blood 106, № 11 (2005): 539. http://dx.doi.org/10.1182/blood.v106.11.539.539.

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Abstract Expression of the human folylpoly-γ-glutamate synthetase (FPGS) gene is controlled by tissue/lineage specific and proliferation-dependent mechanisms. Levels of FPGS mRNA, protein, and enzyme activity are 2–3 fold higher in B-precursor (Bp) ALL cell lines and primary cells when compared to T-lineage ALL. These differences correlate with intracellular accumulation of long chain methotrexate (MTX) polyglutamates (PG), and more important with clinical sensitivity to MTX. However, significant heterogeneity of FPGS expression exists within hematopoietic cells of the same lineage, suggesting

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Tukaramrao, Diwakar Bastihalli, Arati Sharma, Dhimant Desai та Sinisa Dovat. "Abstract 6052: Metabolic consequences of casein kinase 2α inhibition in lymphoid leukemia". Cancer Research 83, № 7_Supplement (2023): 6052. http://dx.doi.org/10.1158/1538-7445.am2023-6052.

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Abstract Overexpression of casein kinase 2α (CK2α) is a common feature in lymphoid leukemias. Constitutively active CK2α can disable transcriptional activity of lymphoid transcription factors like IKAROS that act as metabolic gatekeeper and limit the energy supply needed for oncogenic transformation of B cells. Our studies have shown that pharmacological inhibition of CK2α can restore the transcriptional activity of IKAROS and ablate leukemia. However, the role of CK2α in glucose metabolism has not been fully studied in B and T acute lymphoblastic leukemia (ALL). Therefore, in the present stud

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Benito, Juliana, Yuexi Shi, Barbara Szymanska, et al. "Targeting the Leukemia-Associated Hypoxic Microenvironment with Hypoxia-Activated Prodrug PR-104." Blood 116, no. 21 (2010): 868. http://dx.doi.org/10.1182/blood.v116.21.868.868.

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Abstract Abstract 868 Interactions between leukemia cells and the bone marrow (BM) microenvironment are known to promote leukemia cell survival and confer resistance to drugs commonly used in the management of this disease. We investigated the protective role of hypoxia in the BM microenvironment. We observed a marked expansion of hypoxic niches in the bone marrow of immunodeficient mice engrafted with the acute lymphoblastic leukemia (ALL) cell line Nalm6 and with primary ALL cells, as detected by the reductive 2-nitroimidazole compound pimonidazole (PIM), which forms stable adducts in hypoxi

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Tanaka, Yosuke, Masahito Kawazu, Satoshi Inoue, et al. "Chromatin Architecture Modulation in B-Cell Acute Lymphoblastic Leukemia Carrying DUX4 Fusions." Blood 134, Supplement_1 (2019): 1240. http://dx.doi.org/10.1182/blood-2019-125207.

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B-cell acute lymphoblastic leukemia (B-ALL) carrying DUX4 fusions is a novel cluster of B-ALL. DUX4 fusions are generated from insertions of wild- type (WT) DUX4, mainly into the IGH locus.The translocation replaces the 3′ end of the WT DUX4 coding region with a fragment of IGH or another gene, producing DUX4 out-of-frame fusion proteins devoid of the C terminus of WT DUX4. Usually, WT DUX4 is expressed in germ cells in testis, while its expression is epigenetically repressed in somatic tissues. Recently, it is identified to plays a critical role in transcriptional programs at the cleavage of

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Charkhizadeh, Samira, Mehdi Imani, Nematollah Gheibi, Fateme Shabaani, Akbar Nikpajouh, and Mohammad R. Rezvany. "In Vitro Inhibitory Effect of Recombinant Human Calprotectin on Nalm6 Leukemia Cell Line." Anti-Cancer Agents in Medicinal Chemistry 20, no. 8 (2020): 951–62. http://dx.doi.org/10.2174/1871520620666200331101209.

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Background & Purpose: In evaluating new drugs for the treatment of various types of cancer, investigations have been made to discover a variety of anti-tumor compounds with less side effects on normal cells. Investigations have shown that the heterodimers S100A8 and S100A9 inhibit the enzyme casein kinase 2 and then prevent the activation of the E7 oncoprotein. Therefore, the aim of this study was to evaluate the effect of calprotectin as an antitumor compound on the Nalm6 (B cell precursor leukemia cell line). Material & Methods: Transformation of genes encoding S100A8 and S100A9 huma

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Karalewitz, Andrew, Natalie Czeryba, Yewei Xing, et al. "Abstract 2835: Chimeric antigen receptor (CAR) T-cell generation for therapeutic testing in the disseminated NALM6 human B-cell acute lymphoblastic leukemia mouse model." Cancer Research 82, no. 12_Supplement (2022): 2835. http://dx.doi.org/10.1158/1538-7445.am2022-2835.

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Abstract Cancer immunotherapies reprogram the patient’s immune system to mount a coordinated response against a malignant target. T cells engineered to express Chimeric Antigen Receptors (CARs) through transduction with a lentiviral vector represent an effective strategy to specifically eliminate cancerous cells from a patient. Currently, five CAR T cell therapies are approved by the FDA for the treatment of hematological malignancies. With the recent clinical and regulatory success of CAR T cell therapies, the next generation of CAR T cells are undergoing preclinical development. Labcorp Drug

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Leclerc, Gilles M., Guy J. Leclerc, Jeffim N. Kuznetsov, and Julio C. Barredo. "PIM2 Upregulation Leads to Physiological Buffering of Metformin-Induced Cell Death Mediated by ER Stress/UPR in Acute Lymphoblastic Leukemia,." Blood 118, no. 21 (2011): 3496. http://dx.doi.org/10.1182/blood.v118.21.3496.3496.

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Abstract Abstract 3496 Acute Lymphoblastic Leukemia (ALL) is the most common malignancy in children and adolescents. Despite significant overall improvements in cure rates, outcome remains dismal for patients with resistant phenotypes or after relapse. Therefore, novel treatment strategies are warranted. Recently, we identified the AMP activated protein kinase (AMPK), a regulator of energy homeostasis in eukaryotic cells, as a potential target for ALL therapy due to its effects on cell growth, proliferation, and cell cycle regulation, as well as its crosstalk with critical metabolic and oncoge

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Kohler, M. Eric, Zachary Walsh, Kole Degolier, and Terry J. Fry. "Enhancing the Antigen-Sensitivity of the CD22 CAR through Modulation of the Affinity and Linker-Length of the Single-Chain Fragment Variable." Blood 136, Supplement 1 (2020): 41–42. http://dx.doi.org/10.1182/blood-2020-143372.

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The advent of chimeric antigen receptor (CAR) T cell therapy has revolutionized the treatment of relapsed/refractory acute lymphoblastic leukemia (r/r ALL). CD19 directed CAR T cells have demonstrated the ability to induce complete remissions in up to 90% of r/r ALL patients. Despite this remarkable upfront success, relapse after CAR T cell therapy remains a major obstacle to long term remissions. A major mechanism for relapse after CD19-directed CAR T cell therapy is the recurrence of antigen-negative ALL cells. In recent years, CD22 CAR T cell therapy has emerged as an effective salvage ther

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Leclerc, Guy J., Jianfeng Du, Joanna DeSalvo, Gilles M. Leclerc, and Julio C. Barredo. "The BCR-ABL Fusion Protein Sensitizes Acute Lymphoblastic Leukemia to Apoptotic Death Induced by the Dual Glycolytic and Glycosylation Inhibitor 2-Deoxy-D-Glucose." Blood 120, no. 21 (2012): 2439. http://dx.doi.org/10.1182/blood.v120.21.2439.2439.

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Abstract Abstract 2439 Tumor metabolism has emerged as a hallmark of cancer by which the oncogenic profile of cancer cells pairs energy availability with cell growth and survival. BCR-ABL positive acute lymphoblastic leukemia (BCR-ABL+ ALL) is a highly resistant phenotype, and the BCR-ABL fusion protein has been correlated with alterations in glucose metabolism. The glucose analogue 2-deoxy-D-glucose (2DG) has been found to be an effective antitumor agent in both animal models and human clinical trials for solid tumors based on the dependency of hypoxic tumor cells on anaerobic glycolysis to g

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Sipol, Alexandra, Thomas Grünewald, Guenther Richter та ін. "Overexpression of the Metabolic Stress Sensor and Proglycolytic Transcription Factor ΜLΧΙΡ Mediates Malignancy of Common Acute Lymphoblastic Leukemia in Vivo and Is Targetable By Allorestricted Peptide Specific T Cells". Blood 124, № 21 (2014): 2436. http://dx.doi.org/10.1182/blood.v124.21.2436.2436.

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Abstract Oncogene addiction provides ideal targets for successful immunotherapy. MLXIP (MAX like protein X interacting protein, also known as MondoA) is a metabolic stress sensor and a proglycolytic transcription factor potentially involved in metabolic addiction features of leukemia, the Warburg effect and anoikis. MLXIP dimerizes with MLX within the MYC interactome and promotes longevity in C. elegans (Johnson et al. 2014). The MYC interactome comprises the MYC/MAX/MAD/MLX/MLXIPtranscriptionfactornetwork: Its key players MYC, MAD and MLXIP differentially mediate proliferation, differentiatio

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Ueno, Shikiko, Jiayun Lu, He Jie, et al. "SALL4 Is a Key Survival Factor in Acute B-Cell Lymphoblastic Leukemia." Blood 118, no. 21 (2011): 2428. http://dx.doi.org/10.1182/blood.v118.21.2428.2428.

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Abstract Abstract 2428 SALL4 is a zinc-finger transcriptional factor and a member of the SALL gene family. It plays an essential role in the maintenance of ESC pluripotent and self-renewal properties by interacting with other two key regulators in ESCs, Nanog and Oct4. We previously have shown that stem cell factor SALL4 is aberrantly expressed in 75% of acute B-cell lymphoblastic leukemia (B-ALL). We have also shown that SALL4 is aberrantly expressed in AML, and down-regulation of SALL4 in AML leads to significant cell death. In this study, we focused on investigating the functional role of S

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Xu, Bing, Manman Deng, Zhiwu Jiang, Jie Li, Kai Chen, and Peng Li. "Role of Mitochondrial Apoptotic Pathway in Disulfiram/Copper Mixture-Induced Cell Apoptosis in Human B-Lineage Acute Lymphoblastic Leukemia in Vitro." Blood 126, no. 23 (2015): 4920. http://dx.doi.org/10.1182/blood.v126.23.4920.4920.

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Abstract Backgrounds: The long term prognosis of adult B-lineage acute lymphoblastic leukemia (B-ALL) is poor when compared with pediatric B-ALL. The current therapeutic regimen for adult B-ALL often results in refractory and relapsing diseases. Therefore, it is urgently needed to explore novel approaches to treat adult B-ALL. Disulfiram (DS) has been used clinically as a safe anti-alcoholism drug for over 6 decades. Recent studies demonstrated that disulfiram/cooper mixture (DS/Cu) was cytotoxic to multiple solid cancers, but its effects on B-ALL cells are still unclear. Moreover, the molecul

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Zanjirband, Maryam, Soheila Rahgozar, and Narges Aberuyi. "miR-16-5p enhances sensitivity to RG7388 through targeting PPM1D expression (WIP1) in Childhood Acute Lymphoblastic Leukemia." Cancer Drug Resistance 6, no. 2 (2023): 242–56. http://dx.doi.org/10.20517/cdr.2022.113.

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Aim: Given the encouraging results of the p53-Mdm2 inhibitor RG7388 in clinical trials and the vital function of miR-16-5p in suppressing cell proliferation, the aim of the present study was to investigate the combined impact of RG7388 and miR-16-5p overexpression on the childhood acute lymphoblastic leukemia (chALL). Methods: miRTarBase and miRDB, along with KEGG and STRING databases, were used to predict miR-16-5p target genes and explore protein-protein interaction networks, respectively. B- and T-lymphoblastic cell lines, in addition to patient primary cells, were treated with RG7388. Ecto

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Mansilla-Soto, Jorge, Justin Eyquem, Sascha Haubner, et al. "132 HLA-independent T cell receptors effectively target low abundance antigens." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A142. http://dx.doi.org/10.1136/jitc-2021-sitc2021.132.

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BackgroundChimeric antigen receptors (CARs) engage antigen independently of HLA and enable sustained T cell proliferation when they are endowed with both activating and costimulatory functions. While remission rates have been noticeably elevated in numerous clinical trials targeting CD19, CD22 or BCMA, relapses are common. One of the several underlying relapse mechanisms is antigen escape, which refers to a relapsing tumor that is either negative for the targeted antigen or expresses the latter at a low level. Failure to eliminate antigen-low tumors raises questions about the sensitivity of CA

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Kawamata, Norihiko, Fabienne Isken, Stefanie Goellner, C. Müller-Tidow, and H. Phillip Koeffler. "ChIP-on-Chip Analysis Using Dominant Negative Form of PAX5 Fusion Gene Revealed Genes Associated with Tumorigenesis Were Directly Regulated by PAX5 in a Human B Cell Line, NALM6." Blood 112, no. 11 (2008): 3585. http://dx.doi.org/10.1182/blood.v112.11.3585.3585.

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Abstract PAX5 is a transcriptional factor playing an important role in B-cell development. Overexpression of PAX5 induced by translocation to the enhancer region of immunoglobulin heavy chain gene occurs in non-Hodgkin lymphomas (NHL), suggesting that PAX5 can be also associated with development of NHL. To identify genes associated with tumorigenesis in malignancies overexpressing PAX5, we performed ChIP-on-chip analysis using PAX5 specific antibody. Non-specifically immunoprecipitated DNA by antibodies can cause false positive results using ChIP-on-chip analysis (background). To reduce the ba

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Mladenov, Emil, Katja Paul-Konietzko, Veronika Mladenova, Martin Stuschke, and George Iliakis. "Increased Gene Targeting in Hyper-Recombinogenic LymphoBlastoid Cell Lines Leaves Unchanged DSB Processing by Homologous Recombination." International Journal of Molecular Sciences 23, no. 16 (2022): 9180. http://dx.doi.org/10.3390/ijms23169180.

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In the cells of higher eukaryotes, sophisticated mechanisms have evolved to repair DNA double-strand breaks (DSBs). Classical nonhomologous end joining (c-NHEJ), homologous recombination (HR), alternative end joining (alt-EJ) and single-strand annealing (SSA) exploit distinct principles to repair DSBs throughout the cell cycle, resulting in repair outcomes of different fidelity. In addition to their functions in DSB repair, the same repair pathways determine how cells integrate foreign DNA or rearrange their genetic information. As a consequence, random integration of DNA fragments is dominant

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Xing, Dongxia, Wendy Fang, William K. Decker, et al. "Ex Vivo Expansion of Cord Blood NK Cell Have In Vivo Efficacy Against Leukemia." Blood 110, no. 11 (2007): 2741. http://dx.doi.org/10.1182/blood.v110.11.2741.2741.

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Abstract Introduction Allogeneic stem cell transplantation has demonstrated the ability to prevent leukemic relapse via an immune-mediated graft-vs.-leukemia effect. Natural killer (NK) cells have been shown to comprise a significant component of this anti-leukemia effect and have been reported to enhance engraftment and reduce graft-vs.-host disease. Ex-vivo expansion of peripheral blood-derived NK cells has been demonstrated. Cord blood (CB) is a promising alternate source of NK cells with enhanced cytokine/antigen-responsiveness, proliferation and increasing availability. We studied expansi

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Ma, Xiao-Tong, Ya-Kun Mou, Yang-Yang Zhao, et al. "Set7 Is Highly Expressed in B-Lineage Acute Lymphoblastic Leukemia Cells and Overexpression of Set7 Exhibits Antileukemia Effect." Blood 128, no. 22 (2016): 5088. http://dx.doi.org/10.1182/blood.v128.22.5088.5088.

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Abstract Set7 is a member of protein lysine methyltransferase family that is highly conserved in vertebrates. Set7 can regulate the maintenance of chromosome structure, cell cycle and apoptosis, and plays an important role in many kinds of cancer, metabolism and inflammatory process. However, studies concerning its pathogenic role in leukemia are scarce. We analyzed the expression of Set7 in different types of leukemia and healthy human bone marrow cells or peripheral blood from the Oncomine databases (http://www.oncomine.org), and showed that Set7 was highly expressed in acute lymphoid leukem

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Mardiana, Sherly, Olga Shestova, Stephan A. Grupp, Marco Ruella, David M. Barrett, and Saar Gill. "Repurposing Bi-Specific Chimeric Antigen Receptor (CAR) Approach to Enhance CAR T Cell Activity Against Low Antigen Density Tumors." Blood 138, Supplement 1 (2021): 1727. http://dx.doi.org/10.1182/blood-2021-146995.

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Abstract BACKGROUND Chimeric antigen receptor (CAR) T cell therapy has revolutionized the treatment of relapsed/refractory B-cell malignancies, as highlighted by high complete remission rates and FDA approval of CD19-specific CAR T cell products. However, depth and duration of remission are limited by antigen loss/downregulation on tumors, as observed in clinical trials using CAR T cells targeting the CD19 or CD22 in leukemia and lymphoma, BCMA in multiple myeloma, and EGFRvIII in glioblastoma. This observation forms the basis of current efforts to develop multi-targeting CAR T cells to preven

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Hlozkova, Katerina, Alpesh Thakker, Natividad Alquézar-Artieda, et al. "Separate Roles of Asparagine and Glutamine in Cytostatic Effect of L-Asparaginase - Stable Isotope Tracing Approach." Blood 134, Supplement_1 (2019): 2575. http://dx.doi.org/10.1182/blood-2019-127911.

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L-asparaginase (ASNase) is one of the crucial components of acute lymphoblastic leukemia (ALL) therapy. Although we have previously shown that ASNase triggers metabolic reprogramming of leukemic cells, the significance and interconnections of the changes have not yet been elucidated. Metabolic reprogramming is an accompanying feature in therapy response and is also triggered by commonly used cytostatic drugs. ASNase hydrolyzes two non-essential amino acids asparagine (Asn) and glutamine (Gln). Therapeutic ASNase concentration used in vitro transforms all Asn and Gln to aspartate (Asp) and glut

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Du, Jianfeng, Joanna DeSalvo, and Julio C. Barredo. "Mechanisms of Sensitivity of B-Precursor, T-Lineage and BCR/ABL Positive Acute Lymphoblastic Leukemia (ALL) to the Glycolytic Inhibitor 2-Deoxy-D-Glucose (2-DG)." Blood 114, no. 22 (2009): 3081. http://dx.doi.org/10.1182/blood.v114.22.3081.3081.

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Abstract Abstract 3081 Poster Board III-18 Novel treatment strategies are needed for patients with ALL diagnosed with resistant phenotypes or after relapse. The glucose analogue 2-deoxy-D-glucose (2-DG) is a glycolytic inhibitor that induces growth arrest and cell death by inhibiting the key glycolytic enzymes phosphoglucose isomerase (PGI) and hexokinase (HK). Cancer cells and hypoxic cells are more sensitive to 2-DG due to their reliance on glycolysis for ATP generation. In this study, we evaluated the antileukemic activity of 2-DG in T- and Bp-ALL subtypes characterized by non-random transl

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Qin, Haiying, Sang M. Nguyen, Sneha Ramakrishna, et al. "Novel CD19/CD22 Bicistronic Chimeric Antigen Receptors Outperform Single or Bivalent Cars in Eradicating CD19+CD22+, CD19-, and CD22- Pre-B Leukemia." Blood 130, Suppl_1 (2017): 810. http://dx.doi.org/10.1182/blood.v130.suppl_1.810.810.

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Abstract Treatment of pre-B cell acute lymphoblastic leukemia (ALL) using chimeric antigen receptor expressing T cells (CART) targeting CD19 have demonstrated impressive clinical results in children and young adults with up to 70-90% complete remission rate in multiple clinical trials. However, about 30% of patients relapse due to loss of the targeted epitope on CD19 or CART failure. Our CD22-targeted CAR trial has generated promising results in relapsed/refractory ALL, including CD19 antigen negative ALL, but relapse associated with decreased CD22 site density has occurred. Thus, developing s

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Schramm, Joseph W., Melanie Ehudin, Bing He, et al. "Abstract 3833: Leonurine derivatives as a potential novel therapeutic approach to acute lymphoblastic leukemias (ALL)." Cancer Research 83, no. 7_Supplement (2023): 3833. http://dx.doi.org/10.1158/1538-7445.am2023-3833.

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Abstract Background: Pre-B cell Acute lymphoblastic leukemia (B ALL) high risk (HR) subgroups continue to result in significant mortality and morbidity of pediatric oncology patients. T cell ALL is higher risk and therapy has made less improvement than B ALL with a higher rate of significant poor outcomes. Novel treatment strategies are required to overcome chemotherapy resistance and improve mortality/morbidity for HR B ALL. Leonurine is a bioactive alkaloid that is naturally occurring only in Herbra Leonuri which has been used in traditional herbal medicine. Traditionally, it has been used f

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Jain, Nayan, Zeguo Zhao, Richard Koche, et al. "SUV39H1 disruption imparts functional persistence to CD28-costimulated human CAR T cells." Journal of Immunology 208, no. 1_Supplement (2022): 122.05. http://dx.doi.org/10.4049/jimmunol.208.supp.122.05.

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Abstract Retrovirally encoded CD19-specific CARs that incorporate CD28 and CD3z signaling motifs (Rv-1928z) have induced remarkable responses in patients with refractory leukemia and lymphoma. These CARs, however, induce a strong effector differentiation program in T cells that can limit their persistence and result in T cell dysfunction. Multiple studies have shown that effector differentiation and eventual dysfunction are associated with transcriptional and epigenetic changes. In this study, we examine the effect of disrupting the histone methyl transferase, SUV39H1 on the functional persist

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Singh, Nathan, Noelle V. Frey, Boris Engels, et al. "Single Chain Variable Fragment Linker Length Regulates CAR Biology and T Cell Efficacy." Blood 134, Supplement_1 (2019): 247. http://dx.doi.org/10.1182/blood-2019-131024.

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We recently conducted a clinical trial of CD22-directed chimeric antigen receptor (CAR) T cells in children and adults with relapsed or refractory B-cell acute lymphoblastic leukemia (ALL). While we did observe some transient responses, overall outcomes were inferior to another recent trial of CD22 CAR T cells in ALL performed at the NCI (Fry, T.J. et al. Nat Med, 2018). Intriguingly, these trials used a CAR that employed the same antigen-binding and intracellular signaling domains, and differed only in the length of linker connecting the variable regions of the single chain variable fragment

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Singh, Nathan, Olga Shestova, Katharina Hayer, et al. "CAR T Cell Cytotoxicity Is Dependent on Death Receptor-Driven Apoptosis." Blood 132, Supplement 1 (2018): 698. http://dx.doi.org/10.1182/blood-2018-99-117328.

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Abstract Background: T cells engineered to express chimeric antigen receptors targeting the B-cell antigen CD19 (CART19) have demonstrated impressive results in the treatment of lymphoid cancers. Despite these promising outcomes, a significant subset of patients relapse after initial response. To investigate the molecular pathways that drive relapse, we performed an unbiased, CRISPR/Cas9-mediated genome-wide knockout screen in the acute lymphoblastic leukemia (ALL) cell line Nalm6, and found that loss of CD19 was the primary driver of relapse after initial response. This finding is consistent

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35

Kitanaka, Akira, Hiroyuki Mano, Mary Ellen Conley, and Dario Campana. "Expression and Activation of the Nonreceptor Tyrosine Kinase Tec in Human B Cells." Blood 91, no. 3 (1998): 940–48. http://dx.doi.org/10.1182/blood.v91.3.940.

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Abstract The tyrosine kinase Tec belongs to a new group of structurally related nonreceptor tyrosine kinases that also includes Btk and Itk. Previous studies have suggested that these kinases have lineage-specific roles, with Tec being involved mainly in the regulation of cytokine-mediated myeloid cell growth and differentiation. In this study, we investigated expression and activation of Tec in human B-lymphoid cell lines representing different stages of B-cell maturation, including pro-B (RS4;11, 380, REH), pre-B (NALM6), and mature B (Ramos, and one Epstein-Barr virus [EBV]-transformed lymp

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Kitanaka, Akira, Hiroyuki Mano, Mary Ellen Conley, and Dario Campana. "Expression and Activation of the Nonreceptor Tyrosine Kinase Tec in Human B Cells." Blood 91, no. 3 (1998): 940–48. http://dx.doi.org/10.1182/blood.v91.3.940.940_940_948.

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The tyrosine kinase Tec belongs to a new group of structurally related nonreceptor tyrosine kinases that also includes Btk and Itk. Previous studies have suggested that these kinases have lineage-specific roles, with Tec being involved mainly in the regulation of cytokine-mediated myeloid cell growth and differentiation. In this study, we investigated expression and activation of Tec in human B-lymphoid cell lines representing different stages of B-cell maturation, including pro-B (RS4;11, 380, REH), pre-B (NALM6), and mature B (Ramos, and one Epstein-Barr virus [EBV]-transformed lymphoblastoi

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37

Jain, Nayan, Zeguo Zhao, Richard Koche, et al. "Abstract 5583: SUV39H1 disruption enhances the persistence and anti-tumor efficacy of CD28-costimulated human CAR T cells." Cancer Research 82, no. 12_Supplement (2022): 5583. http://dx.doi.org/10.1158/1538-7445.am2022-5583.

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Abstract Retrovirally encoded CD19-specific CARs that incorporate CD28 and CD3z signaling motifs (Rv-1928z) have induced remarkable responses in patients with refractory leukemia and lymphoma. These CARs induce a strong effector differentiation program in T cells that can limit their persistence and result in T cell dysfunction. This induction of terminal effector differentiation is accompanied by transcriptional and epigenetic changes resulting in induction of effector transcriptional factors, inhibitory receptors, and suppression of memory associated genes. In this study, we examine the effe

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38

Saunders, Philip O., Kenneth F. Bradstock, and Linda J. Bendall. "Dose Escalated RAD001 (Everolimus) Enhances Chemosensitivity in Precursor-B Acute Lymphoblastic Leukemia, through a JNK Dependent Suppression of Cell Cycle Checkpoint Regulation." Blood 112, no. 11 (2008): 1604. http://dx.doi.org/10.1182/blood.v112.11.1604.1604.

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Abstract Five year survival for patients with relapsed pre-B ALL remains less than 10%, requiring new approaches to therapy. We sought to evaluate the potential of mTOR inhibitor RAD001 to enhance pre-B ALL cell killing by agents that induce DNA damage or microtubule disruption and identify interactions that may indicate novel approaches to therapy. Combining 16μM RAD001 with agents that cause DNA damage or microtubule disruption in vitro, enhanced caspase-dependent killing (p&lt;0.05) of pre-B ALL cells. We observed 16μM RAD001 suppressed p53 and markedly attenuated p21 responses to DNA d

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Morisot, Nadege, Sarah Wadsworth, Tina Davis, et al. "127 Preclinical evaluation of NKX019, a CD19-targeting CAR NK Cell." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A140. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0127.

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BackgroundNatural killer (NK) cells are highly effective and fast-acting cytolytic cells capable of eradicating target cells with limited adverse effects such as cytokine release syndrome (CRS) or graft-versus-host disease. Chimeric antigen receptors (CARs)-engineered NK cells have been recently used against leukemia with encouraging clinical outcomes.1 The surface antigen CD19, expressed by B-lymphoblasts, represents an ideal CAR target against B cell acute lymphoblastic leukemia (B-ALL). We developed a highly potent CD19 -directed CAR NK cell therapy, NKX019, with an extended in vivo half-li

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Ito, Chihiro, Takuya Matsui, Eri Noda, Nijsiri Ruangrungsi, and Masataka Itoigawa. "Biphenyl Derivatives from Garcinia Schomburgkiana and the Cytotoxicity of the Isolated Compounds." Natural Product Communications 8, no. 9 (2013): 1934578X1300800. http://dx.doi.org/10.1177/1934578x1300800921.

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Study of the chemical constituents of the stems of Garcinia schomburgkiana Pierre (Guttiferae), collected in Thailand, led to the isolation and identification of five known compounds and two new biphenyl derivatives, schomburgbiphenyl A (1) and B (2). Six phenolic compounds isolated from this plant were screened for their cell growth inhibition activity using several human leukemia cell lines. One compound, oblongifolin C (7), showed significant cytotoxic activity towards Jurkat, NALM6, K562 and HPB-ALL cells.

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Sarno, Jolanda, Pablo Domizi, Yuxuan Liu, et al. "Glucocorticoid-Resistant B-Cell Acute Lymphoblastic Leukemic Cells Can be Targeted By BCR-Signaling Inhibition." Blood 138, Supplement 1 (2021): 617. http://dx.doi.org/10.1182/blood-2021-150356.

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Abstract Glucocorticoids (GCs) remain a backbone component of therapeutic regimens for childhood B-cell acute lymphoblastic leukemia (B-ALL). GCs resistance is a strong prognostic marker of relapse making its understanding an important challenge to be addressed to improve overall patients outcome. Healthy B-cell development is characterized by checkpoints where critical regulatory signaling influences the fate of developing B-cells. These stages are vulnerable for leukemic transformation and as we previously demonstrated, the developmental and functional state of B-ALL cells are of critical im

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Jain, Nayan, Zeguo Zhao, Archana S. Iyer, et al. "Loss of TET2 Uncouples Proliferative and Effector Functions in CAR T Cells." Blood 136, Supplement 1 (2020): 1. http://dx.doi.org/10.1182/blood-2020-142957.

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Chimeric antigen receptor (CAR) T cells have opened a new paradigm for the treatment of leukemia and lymphoma. Their production, however, is laborious, requiring tens of millions of CAR T cells per infusion. This constraint could be significantly alleviated if safe and more efficacious T cells could be generated. In a patient with chronic lymphocytic leukemia, treated with anti-CD19 CAR T cells, a recent report described the emergence of a single T cell clone that at its expansion peak accounted for 94% of circulating CAR T cells, coinciding with the development of cytokine release syndrome an

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Arnaud, Marie-Pierre, Audrey Vallée, Guillaume Robert, et al. "Disruption Of CD9 Expression Affects Adhesion, Migration and Engraftment Of Pre-B Lymphocytes." Blood 122, no. 21 (2013): 1222. http://dx.doi.org/10.1182/blood.v122.21.1222.1222.

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Abstract Introduction CD9 is a membrane protein, member of the tetraspanin family. Recent publications have reported the role of CD9 on engraftment of hematopoietic stem cells, and on cancer stem cell potential. The expression of CD9 has been correlated to the risk of metastases and to a poor clinical outcome in various types of cancer. Surprisingly, CD9 protein is downregulated in ETV6/RUNX1 pre-B acute lymphoblastic leukemia. The purpose of our study is to investigate the effect of CD9 expression on migration and engraftment abilities of pre-B lymphocytes. Materials and Methods The CD9-posit

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Iwanski, Gabriela B., Nils H. Thoennissen, Joy Nakitandwe, et al. "Dominant-Negative Impact of PAX5/TEL on Downstream Targets of PAX5 and Essential Pre-B Cell Receptor Genes." Blood 116, no. 21 (2010): 3231. http://dx.doi.org/10.1182/blood.v116.21.3231.3231.

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Abstract Abstract 3231 B cell lineage acute lymphoblastic leukemia (ALL) is a common malignancy in childhood, and the pre-B cell receptor (pre-BCR) signalling pathway was previously demonstrated to function as a tumor suppressor. The transcription factor PAX5, a key regulator of B cell development, is frequently involved in chromosomal rearrangements of leukemic blasts. Using high resolution single nucleotide polymorphism (SNP) genomic microarray by us and other groups, several candidate partner genes fused to PAX5 have been detected in samples of pediatric ALL, such as TEL, FOXP1, AUTS2, and

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Park, S., A. Register, H. Y. Lee, et al. "POS0007 KYV-101, A FULLY HUMAN CD19 CAR T CELL GENERATED FROM AUTOIMMUNE PATIENT LYMPHOCYTES, DEMONSTRATES CAR-MEDIATED AND CD19-DEPENDENT ACTIVITY AGAINST AUTOLOGOUS B CELLS." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 208.2–209. http://dx.doi.org/10.1136/annrheumdis-2023-eular.6228.

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BackgroundA significant unmet medical need remains in the treatment of relapsed and/or refractory B cell-driven autoimmune diseases, including lupus nephritis (LN). The presence of autoantibodies is a hallmark of such diseases and implicates dysregulated B cell function in their pathogenesis. The central role of B cells in these diseases is also supported by the presence of B cells in diseased tissues and the efficacious responses reported with biologic therapies that target B cells. KYV-101 is an autologous CD19 CAR-T cell therapy that depletes pathogenic B cells. Importantly, the CD19 CAR ut

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Khan, Naveed I., Kenneth Francis Bradstock, and Linda J. Bendall. "The Wnt Pathway Modulates Expression of Growth and Survival Genes in Acute Lymphoblastic Leukemia Cells." Blood 108, no. 11 (2006): 1850. http://dx.doi.org/10.1182/blood.v108.11.1850.1850.

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Abstract Wnt proteins are important bone marrow-derived growth factors known to support normal hematopoietic progenitor and stem cell development. Here we report that B cell progenitor acute lymphoblastic leukemia (pre-B ALL) cells express Wnt proteins, including Wnt-2b in 33%, Wnt-5a in 42%, Wnt-10b in 58% and Wnt-16b in 25% of cases. The Wnt receptors, Frizzled (Fz)-7 and -8 were also expressed in most cases while Fz-3, -4 and -9 were occasionally detected. Stimulation of pre-B ALL cells with Wnt-3a activated canonical Wnt signaling with increased expression and nuclear translocation of β-ca

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Liu, Xiaojun, David M. Barrett, Shuguang Jiang, et al. "Improved Anti-Leukemia Activities of Adoptively Transferred T Cells Expressing Bites." Blood 126, no. 23 (2015): 4431. http://dx.doi.org/10.1182/blood.v126.23.4431.4431.

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Abstract Bispecific T cell engagers (BiTEs) that are specific for both a surface target antigen on cancer cells and CD3 on T cells have been used to engage T cells for cancer therapies. However, the development of BiTEs to treat cancer patients still faces enormous challenges. BiTEs need to penetrate well into tumor tissue, where the reactivate tumor resident T cells might have already been tolerized or energized by tumor microenvironments. In addition, the therapeutic potential of exogenously administered BiTEs could be limited by their short half-life and their dissociation from the triggeri

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Draper, David W., Derrik Germain, Stacey Roys, Olivia Nelson, and Scott Wise. "Abstract 2749: Preclinical assessment of chimeric antigen receptor (CAR) T persistence and functionality in the disseminated NALM6-Luc human B cell acute lymphoblastic leukemia (ALL) model." Cancer Research 83, no. 7_Supplement (2023): 2749. http://dx.doi.org/10.1158/1538-7445.am2023-2749.

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Abstract Preclinical in vivo models are used to profile or refine CAR T therapies before advancing to human studies. Establishing long-term CAR T persistence and efficacy continues to challenge progress in the CAR T space, thus development of robust platforms that can provide longitudinal assessments of CAR T persistence and functionality is paramount. To this end, we used the NALM6-Luc ALL model to develop a flow cytometry platform that provides quantitative analysis of CAR T cells over time as well as surface markers that are documented to correlate with sustained T cell persistence and acti

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Dolinski, Brian, Vandana Chaturvedi, Daryl Humes, et al. "Abstract 2734: Modulation of resting T cell status to enhance transduction and CAR T expansion following exposure to CD8-targeted fusosomes." Cancer Research 83, no. 7_Supplement (2023): 2734. http://dx.doi.org/10.1158/1538-7445.am2023-2734.

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Abstract Introduction: Fusosomes are novel viral vectors pseudotyped with a modified paramyxovirus envelope targeting specific cell types. We have generated a CD8-targeted fusosome to deliver a CD19-directed chimeric antigen receptor (CAR) transgene to CD8+ T cells in vivo following intravenous (i.v.) injection. Although fusosomes are capable of genetically modifying resting T cells, modulation with chemical or biological agents may increase transduction and facilitate CAR T expansion. Here, we demonstrate that rapamycin and IL-7 enhance resting T cell transduction, and IL-7 supports the expan

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Leclerc, Guy J., and Julio C. Barredo. "Histone Deacetylase Inhibitor Induces FPGS mRNA Expression in Childhood B-Precursor and T Acute Lymphoblastic Leukemia: Implication of Combination Therapy with Methotrexate To Enhance Cytotoxicity." Blood 110, no. 11 (2007): 864. http://dx.doi.org/10.1182/blood.v110.11.864.864.

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Abstract Methotrexate (MTX) is an antifolate widely used to treat childhood acute lymphoblastic leukemia (ALL). MTX is retained within cells as long-chain polyglutamates (MTX-PGs), after metabolism by the enzyme folylpoly-γ-glutamate synthetase (FPGS). Intracellular retention of MTX-PGs results in enhanced cytotoxicity due to prolonged inhibition of dihydrofolate reductase (DHFR), and the additional inhibition of thymidylate synthetase (TS). The FPGS gene was shown to be regulated by the transcription factors Sp1 and NFY. We performed DNaseI hypersensitive assays and identified a hypersensitiv

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