Academic literature on the topic 'SET-2 cell lines'

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Journal articles on the topic "SET-2 cell lines"

1

Santamaria, P., T. Utsugi, B. J. Park, N. Averill, S. Kawazu, and J. W. Yoon. "Beta-cell-cytotoxic CD8+ T cells from nonobese diabetic mice use highly homologous T cell receptor alpha-chain CDR3 sequences." Journal of Immunology 154, no. 5 (1995): 2494–503. http://dx.doi.org/10.4049/jimmunol.154.5.2494.

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Abstract Insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice results from a cell-mediated autoimmune process against pancreatic beta-cells. We have shown that beta-cell-cytotoxic CD8+ T cell clones can transfer IDDM to irradiated NOD mice if co-injected with nondiabetogenic CD4+ spleen T cells. To determine whether CTLs recruited to pancreatic islets recognize a restricted set of local Ags, we sequenced TCR-alpha and TCR-beta cDNA generated by anchor PCR from CD8+ CTL lines and clones derived from islets of 10 different NOD mice. These CTL lines were oligoclonal, but did
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2

Quentmeier, Hilmar, Claudia Pommerenke, and Hans G. Drexler. "Epigenetic Modifier Mutations in the LL-100 Panel." Blood 132, Supplement 1 (2018): 5271. http://dx.doi.org/10.1182/blood-2018-99-110060.

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Abstract The NCI-60 human cell line panel, developed for use in drug development comprises sixty human cancer cell lines derived from nine different tissues. Only six cell lines of the NCI-60 were derived from blood cancers. Therefore, most forms and subtypes of leukemia and lymphoma are not represented in the NCI-60 panel. To respond to this apparent gap, we suggest the novel LL-100 panel, 100 leukemia and lymphoma cell lines representing the major leukemia/lymphoma entities, for basic research and drug development. Whole exome sequencing and RNA sequencing were performed to identify mutation
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3

Moudgil, Tarsem, Bernard Fox, and Hong-Ming Hu. "85 Detection of human angiotensin-converting enzyme 2 receptor (hACE2R) on human cancer cell lines." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A93. http://dx.doi.org/10.1136/jitc-2021-sitc2021.085.

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BackgroundSARS-CoV-2 infections have delayed administration of treatments for some patients with cancer, increasing the number of avoidable deaths. However, we hypothesized that infection of cancer cells with SARS-CoV-2 might increase the immunogenicity of those cancer cells. Here we sought to determine whether non-small cell lung cancer (NSCLC) and head and neck squamous cell cancer (HNSCC) cell lines could be a potential target of SARS-CoV-2, which binds and infects host cells via interactions between the viral spike glycoprotein and the human angiotensin-converting enzyme 2 receptor (hACE2)
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4

Nagai, T., H. Harigae, H. Ishihara, et al. "Transcription factor GATA-2 is expressed in erythroid, early myeloid, and CD34+ human leukemia-derived cell lines." Blood 84, no. 4 (1994): 1074–84. http://dx.doi.org/10.1182/blood.v84.4.1074.1074.

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Abstract To understand the functional roles that the GATA factors may play during hematopoietic cell differentiation, we examined the expression of GATA factor mRNAs and protein products in various human cell lines. Blot hybridization analyses demonstrated that GATA-1 and GATA-2 mRNAs are expressed abundantly in a set of cell lines established from human myelogenous leukemia cells, but the expression pattern of each factor is distinct. GATA-2 mRNA is expressed in all cell lines tested that express erythroid markers, and, in addition, the mRNA is also expressed in three CD34+ cell lines and two
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Nagai, T., H. Harigae, H. Ishihara, et al. "Transcription factor GATA-2 is expressed in erythroid, early myeloid, and CD34+ human leukemia-derived cell lines." Blood 84, no. 4 (1994): 1074–84. http://dx.doi.org/10.1182/blood.v84.4.1074.bloodjournal8441074.

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To understand the functional roles that the GATA factors may play during hematopoietic cell differentiation, we examined the expression of GATA factor mRNAs and protein products in various human cell lines. Blot hybridization analyses demonstrated that GATA-1 and GATA-2 mRNAs are expressed abundantly in a set of cell lines established from human myelogenous leukemia cells, but the expression pattern of each factor is distinct. GATA-2 mRNA is expressed in all cell lines tested that express erythroid markers, and, in addition, the mRNA is also expressed in three CD34+ cell lines and two early my
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6

Resar, Linda, Donna Marie Williams, Lingling Xian, et al. "High Mobility Group A1 Chromatin Remodeling Proteins Amplify Inflammatory Networks to Drive Leukemic Transformation in Chronic Myeloproliferative Neoplasia in Humans and JAK2V617F Transgenic Mouse Models." Blood 132, Supplement 1 (2018): 102. http://dx.doi.org/10.1182/blood-2018-99-119549.

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Abstract Introduction: Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell (HSC) disorders characterized by overproduction of mature blood cells and increased risk of transformation to myelofibrosis (MF) and acute myeloid leukemia (AML), although molecular mechanisms driving disease progression remain elusive. While most patients who acquire a JAK2V617F mutation in CD34+ cells present with chronic, indolent Polycythemia Vera (PV), ~25% will progress to MF or AML. High Mobility Group A1/2 (HMGA1/2) genes encode oncogenic chromatin remodeling proteins which are overexpressed in
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7

Lindhout, E., A. Lakeman, M. L. Mevissen, and C. de Groot. "Functionally active Epstein-Barr virus-transformed follicular dendritic cell-like cell lines." Journal of Experimental Medicine 179, no. 4 (1994): 1173–84. http://dx.doi.org/10.1084/jem.179.4.1173.

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Follicular dendritic cells (FDC) are unique nonlymphoid cells found only in germinal centers. FDC can be distinguished from other accessory cells based on a characteristic set of cell surface markers. It is known that FDC are able to rescue germinal center B cells from apoptosis. To investigate the role of FDC in the process of selection and maturation of B cells during germinal center reactions, we tried to establish factor-independent immortalized FDC-like cell lines. Because freshly isolated FDC express the Epstein-Barr Virus (EBV) receptor CD21, we attempted EBV transformation on isolated
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8

Troeger, Anja, Pascal-David Johann, Mumine Senturk, Michael D. Milsom, and David A. Williams. "Intact Rac Signaling Is Important for Leukemia Cell Survival." Blood 116, no. 21 (2010): 2885. http://dx.doi.org/10.1182/blood.v116.21.2885.2885.

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Abstract Abstract 2885 Rho GTPases, Ras-related small G proteins, regulate multiple cell processes in hematopoietic cells. There is growing evidence that acute myeloid leukemia (AML) blasts and particularly MLL-rearranged AML blasts, rely on Rac activity (Mulloy JC et al, Blood, 2010). However, little is known about the role of these GTPases in acute lymphoblastic leukemia (ALL) and particularly precursor B cell ALL. To investigate the role of Rac and potential compensation by other GTPases in ALL, we first assessed the protein expression and activation of Rac in a number of B-ALL cell lines (
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9

Verheul, C., T. V. Kers, A. Van Der Ploeg, et al. "P11.47 Generation, characterisation and drug screening of patient-derivedIDH1-mutated glioma cell lines." Neuro-Oncology 21, Supplement_3 (2019): iii54. http://dx.doi.org/10.1093/neuonc/noz126.193.

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Abstract BACKGROUND Despite considerable scientific efforts, endogenous in vitro isocitrate dehydrogenase (IDH)-mutated glioma models remain scarce. Availability of these models is key to understanding underlying molecular mechanisms and vital for the development of new therapeutic interventions. We established and characterized a set of seven cell lines derived from IDH1-mutated gliomas and utilized them to investigate IDH-mutant glioma drug-response in vitro. MATERIAL AND METHODS Fresh tumor material was collected directly from the operating room, mechanically and enzymatically dissociated a
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10

Gozgit, Joseph M., Geraldine A. Bebernitz, Pankaj Patil, et al. "Effects of a Novel, Selective Jak2 Inhibitor, AZ60, on STAT5 Signaling and Cellular Growth in Jak2 V617F Cell Lines." Blood 110, no. 11 (2007): 3549. http://dx.doi.org/10.1182/blood.v110.11.3549.3549.

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Abstract A role for Jak2 in the etiology of the myeloproliferative diseases (MPDs) was discovered with the identification of a single activating point mutation, V617F, in the pseudokinase domain of JAK2. We have developed a Jak2 inhibitor, AZ60, which inhibits in vitro JAK2 enzyme activity with a Ki of 0.45 nM. AZ60 demonstrates inhibition of STAT5 phosphorylation and proliferation in a Tel-Jak2 engineered cell line with IC50 values of 18 and 23 nM, respectively. To understand the selectivity versus other Jak kinase family members we engineered three additional cell lines containing Tel fusion
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