Relevant bibliographies by topics / B-CLL

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Academic literature on the topic 'B-CLL'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "B-CLL"

1

Parker, Anton, Shilu Amin, Tricia Zwiefelhofer, Ben Gregory, Helen White, Oliver Giles Best, Nick Cross, Jelena Mann, Mathias Ehrich, and David Graham Oscier. "Epigenetic Regulation of ZAP70 in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (November 16, 2008): 2246. http://dx.doi.org/10.1182/blood.v112.11.2246.2246.

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Abstract ZAP70 expression has been shown to be involved in enhanced signalling and more aggressive disease in a subset of CLL. Mechanisms regulating ZAP70 expression are unknown. We have shown previously that despite the absence of a 5’ CpG island, the methylation status of a small region of CpG dinucleotides (CpGs) correlates with the transcriptional state of the gene in both normal lymphocytes and B cell leukemias. Quantitative methylation analysis of 605 CpGs across the 28kb genomic region spanning ZAP70 was performed by MassARRAY on a panel of 17 CLL tumor cell samples, 4 lymphoid cell lines and B cell, T cell and myeloid cell samples pooled from 3 normal individuals. All samples showed hypermethylation of the gene body and of the gene’s two 3’ CpG islands. However, there was variability between samples in the methylation of 12 consecutive CpGs within a 1kb predicted promoter region (PPR), spanning the transcription start site (TSS) and in the methylation of 24 consecutive CpGs in an adjacent 1kb differentially methylated region (DMR), downstream of the TSS. The methylation of the PPR and DMR, together with the expression status of the samples, suggested four different states for the gene (Table 1). Table 1 - ZAP70 gene states defined by ZAP70 expression status and methylation of the PPR and DMR. MEAN CpG METHYLATION (%) SAMPLE ZAP70 EXPRESSION STATUS PPR DMR GENE STATE NAMALWA − 65 82 I B CELLS − 48 82 I MYELOID − 53 80 I CLL6 − 4 86 II CLL7 − 5 75 II CLL8 − 12 78 II CLL10 − 12 62 II CLL11 − 4 62 II CLL12 − 21 77 II HBL2 − 18 60 II CLL13 + 4 40 III CLL14 + 5 46 III CLL15 + 7 45 III CLL16 + 9 43 III CLL17 + 5 56 III NALM6 + 8 52 III CLL1 + 3 4 IV CLL2 + 3 4 IV CLL9 + 4 6 IV CLL4 + 3 8 IV CLL5 + 4 16 IV CLL3 + 4 17 IV JURKAT + 3 4 IV T CELLS + 9 13 IV Bisulphite cloning and sequencing of a PCR amplicon spanning an exon1 C/A SNP (rs2276645) and the PPR/DMR junction was performed together with cDNA pyrosequencing of rs2276645 on the five CLL tumor samples identified with gene state III. All samples showed allele specific methylation (ASM) of the A allele within the DMR and almost complete restriction of ZAP70 expression to the hypomethylated C allele. Bisulphite pyrosequencing of two DMR CpGs in purified leukocyte populations from these cases showed that ASM appears restricted to CLL cells, with hypermethylation and hypomethylation of the myeloid and T cells respectively (Table2). This suggests that while methylation of the DMR is sufficient for allele restriction, ASM does not result from imprinting and may be restricted to CLL tumor cells. Table 2 – Mean methylation of 2 DMR CpGs in leukocyte populations from CLL patients with known ASM of the DMR in their tumor cells. MYELOID CELLS CLL CELLS T CELLS PATIENT CD15 (%) METHYLATION(%) CD19 (%) METHYLATION (%) CD2 (%) METHYLATION (%) CLL13 83 90 98 59 71 21 CLL14 98 99 98 50 88 10 CLL15 88 84 93 45 85 24 CLL16 99 96 99 52 82 18 CLL17 92 89 98 49 90 22 Native chromatin immunoprecipitation (N-ChIP) using anti-AcH3, H3K14Ac and H3K14Me2 antibodies was performed on the 4 cell lines and tumor cells from CLLs 1, 2, 6, 7, 13 and 14 from the MassARRAY series. PCR for amplicons across the PPR and DMR showed the presence of all 3 histone modifications in ZAP70 expressing JURKAT and NALM6 cells but these modifications were absent in the ZAP70 negative NAMALWA and HBL2 cells. In contrast, all 6 CLL samples showed enrichment for all 3 modifications, regardless of gene state, suggesting an open, active/permissive chromatin structure, despite clear differences in methylation of the DMR. Further bisulphite pyrosequencing and N-ChIP of NAMALWA and HBL2 cells cultured for 6 days in the presence of 0.5μM Decitibine showed concomitant DMR demethyaltion, increased AcH3 within the DMR and up regulation of ZAP70 expression, all of which were reversed when the drug stimulus was removed. Taken together this data suggests that ZAP70 is regulated by epigenetic mechanisms, with the methylation status of a small DMR playing a key role, sufficient to differentiate the transcriptional activity of two alleles within a single cell. It is apparent that the gene is primed for expression in all CLL cells and that methylation of the DMR is part of the key switching process between active transcription and silencing. The differences in DMR methylation between an individual’s expressing T cells and CLL cells, suggests that differences may exist in the mechanism of regulation between T and B cells and raises the possibility that such differences could be exploited as targets for therapy.
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Goodman, Alice. "B-CLL." Oncology Times &NA;, Supplement (August 2006): 21. http://dx.doi.org/10.1097/01.cot.0000316106.04463.a9.

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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.

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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.

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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., B. Degar, D. Costin, EW Newcomb, M. Mani, CR Rosenberg, L. Morse, JC Drygas, ZN Canellakis, and M. Potmesil. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (November 15, 1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.3440.

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Abstract Chemosensitivity of B lymphocytes, obtained from 65 patients with B- cell chronic lymphocytic leukemia (B-CLL), Rai stages 0 through IV, was determined using the MTT assay. The results were expressed by the drug concentration required for 50% inhibition of cell viability (IC50). The cytotoxicity of chlorambucil (CLB) was compared with that of fludarabine and the DNA topoisomerase I inhibitors, camptothecin, 9- aminocamptothecin, 10,11-methylenedioxy-20(S)-camptothecin (10,11-MDC) and 9-amino-10,11-methylenedioxy-20(S)-campthothecin (9-A-10,11-MDC), and topotecan. Considerable heterogeneity in sensitivity to CLB was observed, with a median IC50 of 40.5 mumol/L in untreated patients. B- CLL cells from patients treated with CLB had a significantly higher median IC50 of 86.0 mumol/L (P < .01). Untreated as well as CLB-treated patients were divided into two subsets. For the purpose of this study, B-CLL lymphocytes with an IC50 CLB of less than 61.0 mumol/L were designated as “sensitive” and those with an IC50 CLB of > or = 61.0 mumol/L were designated as “0resistant.” After baseline assays, 15 untreated patients received CLB; after treatment, the IC50 increased in B-CLL lymphocytes from 13 of 15 patients. The response to CLB treatment, determined by its effect on the absolute lymphocyte count and by the Eastern Cooperative Oncology Group clinical criteria, was significantly better in patients whose lymphocytes had an IC50 CLB of less than 61.0 mumol/L before therapy (P < .01). B-CLL lymphocytes also had a variable degree of sensitivity in vitro to each of the other drugs. There was significant cross-resistance between CLB and fludarabine (P < 0.01). Whereas only 29% of CLB-resistant B-lymphocyte specimens obtained from individual patients were sensitive to fludarabine in vitro, 52% and 67% of CLB-resistant lymphocyte samples were sensitive to 10,11-MDC and 9-A-10,11-MDC, respectively. We have previously reported that p53 gene mutations were associated with aggressive B-CLL and a poor prognosis. B lymphocytes from seven patients with these mutations were resistant to CLB, and five of six were resistant to fludarabine. Lymphocytes from four of seven were resistant to 10,11-MDC, and three of four were resistant to 9-A-10,11- MDC. This study implies that the MTT assay may be useful in identifying subsets of CLL patients resistant to conventional chemotherapy. However, definitive conclusions can not be drawn in view of the small number of patients studied prospectively. In addition, these results suggest the potential of camptothecin-based therapy for patients unresponsive to standard treatment.
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Silber, R., B. Degar, D. Costin, EW Newcomb, M. Mani, CR Rosenberg, L. Morse, JC Drygas, ZN Canellakis, and M. Potmesil. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (November 15, 1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.bloodjournal84103440.

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Chemosensitivity of B lymphocytes, obtained from 65 patients with B- cell chronic lymphocytic leukemia (B-CLL), Rai stages 0 through IV, was determined using the MTT assay. The results were expressed by the drug concentration required for 50% inhibition of cell viability (IC50). The cytotoxicity of chlorambucil (CLB) was compared with that of fludarabine and the DNA topoisomerase I inhibitors, camptothecin, 9- aminocamptothecin, 10,11-methylenedioxy-20(S)-camptothecin (10,11-MDC) and 9-amino-10,11-methylenedioxy-20(S)-campthothecin (9-A-10,11-MDC), and topotecan. Considerable heterogeneity in sensitivity to CLB was observed, with a median IC50 of 40.5 mumol/L in untreated patients. B- CLL cells from patients treated with CLB had a significantly higher median IC50 of 86.0 mumol/L (P < .01). Untreated as well as CLB-treated patients were divided into two subsets. For the purpose of this study, B-CLL lymphocytes with an IC50 CLB of less than 61.0 mumol/L were designated as “sensitive” and those with an IC50 CLB of > or = 61.0 mumol/L were designated as “0resistant.” After baseline assays, 15 untreated patients received CLB; after treatment, the IC50 increased in B-CLL lymphocytes from 13 of 15 patients. The response to CLB treatment, determined by its effect on the absolute lymphocyte count and by the Eastern Cooperative Oncology Group clinical criteria, was significantly better in patients whose lymphocytes had an IC50 CLB of less than 61.0 mumol/L before therapy (P < .01). B-CLL lymphocytes also had a variable degree of sensitivity in vitro to each of the other drugs. There was significant cross-resistance between CLB and fludarabine (P < 0.01). Whereas only 29% of CLB-resistant B-lymphocyte specimens obtained from individual patients were sensitive to fludarabine in vitro, 52% and 67% of CLB-resistant lymphocyte samples were sensitive to 10,11-MDC and 9-A-10,11-MDC, respectively. We have previously reported that p53 gene mutations were associated with aggressive B-CLL and a poor prognosis. B lymphocytes from seven patients with these mutations were resistant to CLB, and five of six were resistant to fludarabine. Lymphocytes from four of seven were resistant to 10,11-MDC, and three of four were resistant to 9-A-10,11- MDC. This study implies that the MTT assay may be useful in identifying subsets of CLL patients resistant to conventional chemotherapy. However, definitive conclusions can not be drawn in view of the small number of patients studied prospectively. In addition, these results suggest the potential of camptothecin-based therapy for patients unresponsive to standard treatment.
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Ponzoni, Maurilio, and Claudio Doglioni. "Prognostic factors in B-CLL." Advances in Anatomic Pathology 11, no. 3 (May 2004): 172–73. http://dx.doi.org/10.1097/00125480-200405000-00006.

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Salomon-Nguyen, Florence, Francoise Valensi, Helene Merle-Beral, and Georges Flandrin. "A Scoring System for the Classification of CD5- B CLL versus CD5+ B CLL and B PLL." Leukemia & Lymphoma 16, no. 5-6 (January 1995): 445–50. http://dx.doi.org/10.3109/10428199509054432.

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Matvieieva, A. S., L. M. Kovalevska, and E. V. Kashuba. "The SMAD4 transcription factor shows cytoplasmic retention in B-cells of patients with chronic lymphocytic leukemia (CLL)." Faktori eksperimental'noi evolucii organizmiv 22 (September 9, 2018): 144–48. http://dx.doi.org/10.7124/feeo.v22.939.

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Aim. To illuminate the reason of inactivity of the TGFB-SMAD2/3 pathways in CLL cells. Methods. CLL cells were isolated from peripheral blood of CLL patients, using gradient centrifugation at the ficoll. Expression and cellular localization of SMAD2, 3 and 4 proteins were analyzed by fluorescence microscopy, using specific antibodies. Results. The SMAD2 protein was basically not expressed in CLL cells, in contrast to B cells, isolated from the peripheral blood of a healthy donor. Moreover, the SMAD3 and SMAD4 proteins were localized exclusively in the cytoplasm (a proportion of SMAD3 was detected in the membrane) of CLL cells. Conclusions. The TGFB-SMAD2/3 signaling pathway is not active in CLL cells. We have found that SMAD2 is not expressed. Also, the nuclear heterodimers that consisted of SMAD3 and SMAD4 proteins, were not detected. Keywords: chronic lymphocytic leukemia (CLA), acute myeloid leukemia (AML), peripheral blood B-cells, SMAD, the TGFB-SMAD2/3 signaling pathway.
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Paul, Santanu, Steven L. Allen, Kanti R. Rai, and Nicholas Chiorazzi. "Expression of Angiogenin in Normal B Lymphocytes and B-CLL Cells." Blood 106, no. 11 (November 16, 2005): 1188. http://dx.doi.org/10.1182/blood.v106.11.1188.1188.

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Abstract Angiogenesis is critical for the clinical progression of hematopoietic malignancies and depends on a series of angiogenic factors. Angiogenin is a potent angiogenic factor produced by the host microenvironment and certain neoplastic cells. The association between angiogenin, cancer progression and poor outcome in solid tumors has been documented, but its significance in B-CLL has not been defined. A previous study suggests that B-CLL patients in Rai stage O with higher angiogenin levels have a better clinical outcome. This is surprising in light of the association of angiogenin levels with progression in solid tumors. Therefore we analyzed angiogenin mRNA and protein expression by the leukemic cells of B-CLL patients in order to correlate the production of this molecule with disease progression in B-CLL. Angiogenin was expressed in B-CLL cells as well as in B cells of normal donors, although the expression in the former was much higher than in the latter. Q PCR revealed a 7-fold induction in angiogenin-specific mRNA transcription in B-CLL cells (n=10) in comparison to normal B cells (n=13). In addition, angiogenin protein was identified by confocal microscopy both within and on the cell surface of B-CLL cells. All B-CLL cases, regardless of IgV gene mutation status, express angiogenin as defined by FACS. Approximately 85% of the cells that comprise B-CLL clones (n=28) display angiogenin on their surface membranes (range: 55-98%). Furthermore approximately 13% of polyclonal B cells from normal subjects (n=12) also produce angiogenin (range: 1–33%). Using enzyme immunoassay, we also measured serum angiogenin levels and detected significant differences in 66 B-CLL patients (median: 381 ng/mL; range: 185–875) versus 24 age- and sex-matched healthy controls (median: 301 ng/mL; range: 192–536) (P = 0.0056). Surprisingly, there was no correlation between surface and serum angiogenin levels and the different V gene-defined B-CLL subgroups. Our results show for the first time that a small fraction of normal B cells and all cases of B-CLL express angiogenin transcripts as well as intracellular and surface membrane protein. Angiogenin levels do not correlate with IgV gene mutations status or expression of surface membrane CD38. The role of angiogenin in the pathogenesis and progression of B-CLL needs further study.
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Dissertations / Theses on the topic "B-CLL"

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Schlaak, Max Simon. "Differentielles Genexpressionsmuster in chronischen lymphatischen Leukämiezellen vom B-Zell-Typ (B-CLL-Zellen)." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=966320069.

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Schlaak, Max Simon. "Differentielles Genexpressionsmuster in chronischen lymphatischen Leukämiezellen vom B-Zell-Typ (B-CLL-Zellen)." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14817.

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Die B-CLL ist eine niedrigmaligne Erkrankung, die im höheren Lebensalter auftritt und für die es weiterhin keine dauerhaft kurative Therapie gibt. Die Erforschung der genetischen Grundlagen dieser Krankheit könnte Erkenntnisse über die Funktionsmechanismen und neue Diagnose- und Therapieansätze erbringen. Ziel dieser Arbeit war es, eine Genbank von CLL-Patienten bzw. gesunden Spendern zu erstellen, um Gene, die für die Entstehung der Erkrankung mitverantwortlich sein könnten, zu identifizieren. Die subtraktive suppressive Hybridisierung (SSH) wurde als Methode eingesetzt, um cDNA-Mischungen zu generieren, in denen differentielle Gene angereichert wurden. In dieser Arbeit wurden drei differentielle Gene identifiziert. Eines dieser Gene kodiert den Oberflächenmarker CD5, der bei CLL-Erkrankten stärker exprimiert wurde. Da CD5 ein für die B-CLL relativ spezifischer Marker ist, bestätigte dieses Ergebnis die Qualität der Genbank. Mit Hilfe der SSH wurde ein Verlust der Expression der cDNA für den Oberflächenmarker CD20 bei CLL-Erkrankten nachgewiesen. CD20 ist möglicherweise ein Kalziumkanal und wird als Ziel des anti-CD20-Antikörpers Rituximab verwendet. Der Verlust von CD20 im Verlauf der Erkrankung konnte in dieser Arbeit angedeutet werden. Weiterhin wurde eine verringerte Expression von cDNA für IkappaBa (Mad-3) bei CLL-Patienten entdeckt. Der Transkriptionsfaktor IkBa spielt im zellulären Ablauf der Apoptose eine wichtige Rolle. Phosphoryliertes IkBa inhibiert die Wirkung von NF-kB. Eine Reduktion von IkBa-cDNA könnte ebenfalls die Funktion von NF-kB beeinflussen. Dieses Ergebnis könnte auch für zukünftige immuntherapeutische Ansätze von Bedeutung sein. Weiterhin sind die nachgewiesenen Gene interessant für die Technik des "DNA-Microarrays". Diese schnelle Methode ermöglicht kostengünstige Diagnosen und könnte daher eine zukunftsweisende Alternative zu herkömmlichen Ansätzen bieten. In der vorliegenden Arbeit konnten differentielle Transkripte auf mRNA-Ebene bei B-CLL-Erkrankten und gesunden Kontrollen festgestellt und untersucht werden. Die Ergebnisse geben neue Einsichten über Onkogene und Tumorsurpressorgene in der B-CLL und eröffnen zukünftige immuntherapeutische Ansätze.
The B-CLL is a malignancy that appears in the higher age and for which it gives further no durably curative therapy. The investigation of the genetic bases of this illness could furnish understandings of the function mechanisms and new diagnosis and therapy extensions. It was the goal of this work of generating a gene bank of CLL-patients and healthy donors, in order to identify genes, that could be responsible for the origin of the disease. The subtractive suppressive hybridisation (SSH) was inserted as a method in order to generate cDNA-mixtures, in which differential genes were enriched. In this work, three differential genes were identified. One of these genes codes for CD5 that in CLL-patients was stronger expressed. Because CD5 is a marker relatively specific for the B-CLL, this result confirmed the quality of the gene bank. By means of the SSH, a loss of the Expression of the cDNA was proved for CD20 in CLL-patients. Possibly CD20 is a calcium canal and is used as a goal of the anti-CD20-antibody Rituximab. The loss of CD20 in the progress of the disease could be indicated in this work. Further a diminished expression was discovered by cDNA for IkBa (Mad-3) in CLL-patients. The transcription factor IkBa plays an important role in the cellular system of apoptosis. Phosphorylated IkBa is inhibiting the effect of NF-kB. A reduction of IkBa-cDNA could influence also the function of NF-kB. This result could be interesting for future immune therapeutic extension. Further the proved genes are interesting for the technology of the "DNA-Microarrays". This fast method enables favorable diagnoses and could offer therefore a leading-edge alternative to conventional extensions. In the existing work, differential transcripts could be assessed on mRNA-levels in B-CLL-patients and healthy donors. The results give new insights over oncogenes and tumor surpressing genes in the B-CLL and open future immune therapeutic extensions.
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Kurzeder, Christian. "Gentransfer in primäre B-CLL-Zellen mittels EBV abgeleiteter Genvektoren." [S.l.] : [s.n.], 2004. http://edoc.ub.uni-muenchen.de/archive/00004955.

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Kurzeder, Christian. "Gentransfer in primäre B-CLL-Zellen mittels EBV abgeleiteter Genvektoren." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-49552.

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Bund, Dagmar. "hTERT, CD23 und CD229 als Tumorantigene bei der B-CLL." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145282.

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Almond, Jason Baron. "Mechanisms of proteasome inhibitor-induced apoptosis of B-cell chronic lymphocytic leukaemia (B-CLL) cells." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/30761.

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Proteasome inhibitors, including lactacystin, LLnL (N-acetyl-N-leucinyl-L-leucinyl-L- norleucinal) and MG132 (carbobenzoxyl-leucinyl-leucinyl-leucinal), potently induce apoptosis in leukaemic B-cells from patients with B-cell chronic lymphocytic leukaemia (B-CLL). This pro-apoptotic effect occurs in cells from patients at all stages of the disease, including those resistant to conventional chemotherapy, suggesting that proteasome inhibitors may be useful for treatment of B-CLL. Following initial inhibition of proteasomal activity and an increase in ubiquitinated proteins, these agents induce mitochondrial cytochrome c release and caspase-dependent apoptosis, involving cleavage/activation of caspases -2, -3, -7, -8 and - 9. Pre-treatment with the cell permeable caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe)fluoromethyl ketone (Z-VAD.fmk), does not prevent the release of cytochrome c or partial processing of caspase-9 but prevents activation of effector caspases and induction of apoptosis. These results suggest that the release of cytochrome c is caspase independent and that caspase-9 is the initiator caspase in proteasome inhibitor-induced apoptosis of B-CLL cells. Activation of B-CLL lysates with dATP results in the formation of an -700 kDa caspase-activating apoptosome complex containing Apaf-1. A similar complex is formed in B-CLL cells induced to undergo apoptosis by proteasome inhibitors. Mechanisms of proteasome inhibitor-induced apoptosis vary between cell types, but often involve accumulation of short-lived proteins such as p53, p27 and pro-apoptotic Bcl-2 family members, activation of the stress kinase JNK, or inhibition of NF-kB transcriptional activity. Proteasome inhibitor-induced apoptosis in B-CLL cells is not triggered by alterations in the Bcl-2:Bax ratio, increase in pro-apoptotic t-Bid, or alterations in p27, XIAP, cIAPl or cIAP2. There is also no accumulation of IkB proteins that would inhibit NFkB survival signalling. Although proteasome inhibitors cause an accumulation of p53 and p21, this is not sufficient to induce apoptosis, as etoposide causes more pronounced increases in these molecules but is a less potent inducer of apoptosis. Activation of the stress kinases c-Jun N- terminal kinase (JNK) and p38 also does not appear to be involved. Therefore proteasome inhibitors induce mitochondrial perturbation in B-CLL cells by an apparently novel mechanism.
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Walton, Alexander James. "CD4+PF+ T Cells in B-CLL Patients & Normal Controls." Thesis, University of Westminster, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502405.

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Our group has previously shown that CD4+Perforin (PFt T cells with cytotoxic potential are expanded in patients with B-CLL, accounting for up to 50% of CD4+ T cells in this disease. This study confinns the finding of increased percentages of CD4+PF+ T cells in a new cohort of B-CLL patients. However, the significance of this subset in B-CLL remains unclear. Evidence has accumulated for the potential role of CD4+ cytotoxic T cells in controlling cytomegalovirus (CMV). Therefore, a potential relationship between chronic CMV infection and CD4+PF+ T cell expansion in B-CLL was investigated. CMV seropositivity was found to be strongly associated with CD4+PF+ T cell expansion in both B-CLL patients and controls. This suggested that CD4+PF+ T cells from CMV seropositive (SP) patients and controls might contain clonally expanded populations of CMV-specific cells. To test this hypothesis, the CMV reactivity of CD4+PF+ and CD4+PF- T cells from B-CLL patients and controls was detennined using an intracellular cytokine staining flow cytometric assay. CD4+PF+ cells from untreated patients were enriched for CMV-reactive cells, as measured by . IFN-y production, compared to the CD4+PF- subset. In addition, the data indicated that CD4+ T cell immunity to CMV is dysregulated in B-CLL patients. CD4+PF+T cells from B-CLL patients are characterised by a highly differentiated CD2S-CD57+ phenotype. To further characterise the differentiation phenotype of these cells, the distribution of CD45RA and CCR7 was detennined on CD4+PF+ T cells from B-CLL patients and controls. CD4+PF+ T cells from B-CLL patients were both characterised by a highly differentiated T-effector memory TEM (CCRT) phenotype, but differed in the proportion of CD45RA expressing cells, which might reflect chronic T cell activation in the fonner group. ~inally, flowFISH analysis revealed that CD4+PF+ T cells had shorter telomeres compared CD4+PF- T cells in B-CLL patients, indicative of a more extensive replicative history. The results indicate that low, but persistent, antigenic exposure in CMVinfected individuals leads to the emergence of a CD4+PF+ T cell subset, characterised by a highly differentiated cell surface phenotype and shortened telomeres.
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Munoz-Ritchie, Varinia Graciela. "P-glycoprotein-associated anthracycline resistance in B-CLL : potential for cytokine modulation." Thesis, University of Plymouth, 2001. http://hdl.handle.net/10026.1/2809.

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The phenomenon of multidrug resistance (MDR) in cancer cells is generally associated with P-glycoprotein (P-gp) expression and presents an obstacle to successful chemotherapy. Attempts to overcome P-gp-associated MDR using P-gp modulators, such as verapamil, have been hindered by their intrinsic in vivo toxicity. In 1991, however, Scala et al. demonstrated the alteration of P-gp function by interferon-alpha (IFN-α) in vitro at non-toxic in vivo concentrations, suggesting a basis for the use of IFN-α clinically in patients exhibiting P-gp-associated MDR. Drug resistance in B-CLL has been linked to the phenomenon of MDR, however, publications regarding this have been conflicting. The contrasting results prompted further investigation of the role of P-gp-associated anthracycline resistance and, using isolated β-lymphocytes from B-CLL patients, this investigation examined P-gp expression, function and IFN-α modulation in vitro. Optimum conditions for in vitro analysis of P-gp-associated anthracycline resistance were determined by examining the stability of the anthracycline, daunorubicin, in varying cell culture conditions. The resulting system balanced conditions affecting drug stability with those affecting cell survival. While other investigations have neglected the issue of drug stability, this study demonstrates that the instability of daunorubicin may be a critical variable determining the outcome of drug sensitivity studies. In RPMI + 2mM L-glutamine and 10% (v/v) FBS, loss of drug concentration is due to both adsorption and degradation and these experiments show that the presumed availability of drug may be over-estimated in in vitro studies. Furthermore, the degradation products might interfere with P-gp function and modulation. MDRl gene mRNA was detected in the B-cells of forty-three out of fifty B-CLL patients analysed, whereas P-gp expression, as measured by flow cytometry, resulted in only sixteen patients out of fifty-five being classed as positive (> 10% increase in staining as compared to the control). P-gp functionality and modulation studies on the B-cells of eleven patients confirmed the existence of an efflux mechanism with identical characteristics to P-gp using verapamil, the dye rhodamine 123 (rho123) and daunorubicin. Four patients were classed as functional low expressers (functional P-gp with low P-gp expression (7-10% increase in staining)), six were classed as functional high expressors (functional P-gp with high P-gp expression (20-57% increase in staining)) and one as a non-functional high expressor (non-functional P-gp with high P-gp expression (13.4% increase in staining)). Verapamil modulated rho123 efflux in all ten patients classed as P-gp functional expressors, and daunorubicin efflux in eight of these patients. However, IFN-α modulated rho123 and daunorubicin efflux in only two and one patients, respectively, even at concentrations higher than 500I.U./ml. In contrast to Scala et al. (1991), this finding suggests that at a well tolerated concentration IFN-α may not be suitable for use as a P-gp modulating agent in vivo in B-CLL, although conclusive evidence would require a larger study.
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Hellqvist, Eva. "Antigen interaction with B cells in two proliferative disorders : CLL and MGUS." Doctoral thesis, Linköping : Department of Clinical and Experimental Medicine, Linköping University, 2010. http://www2.bibl.liu.se/liupubl/disp/disp2010/med1158s.pdf.

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Gorgone, Ausilia Giuseppa. "Correlazione tra dati biologici e prognosi in pazieti affetti da B-CLL." Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1138.

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Gli studi di questi anni hanno dimostrato che i fattori biologici giocano un ruolo fondamentale per la stratificazione del rischio come elementi predittivi del treatment-free survival e dell' overall survival nei pazienti affetti da CLL in stadio iniziale.La maggioranza di questi markers prognostici ,anche se ormai in uso quotidiano nella pratica clinica, non è ancora incluso nelle linee guida internazionali che si basano ancora su criteri esclusivamente clinici e individuano la valutazione biologica da usare in combinazione ai parametri clinici.Il loro impiego può certamente contribuire al miglioramento del clinical management dei pazienti affetti da CLL .
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Books on the topic "B-CLL"

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Sztuka Fabryka (Group of artists). B/W - CLR. Ireland: Redfoxpress, 2010.

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Dawson, Alma. Development of a core library collection for library automation: Report to the Council on Library Resources on Project CLR #4026-B. [Baton Rouge, La.]: Produced at the Research Center Annex, School of Library and Information Science, Louisiana State University, 1989.

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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Leukaemia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0004.

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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Hassan Al-Sader. Leukaemia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0004_update_001.

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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.

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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodysplastic syndromes (MDS), follicular lymphoma, diffuse large B-cell lymphoma, Burkitt’s lymphoma (BL), extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), mantle cell lymphoma, classical Hodgkin’s lymphoma (cHL), lymphoplasmacytic lymphoma (LPL), plasma cell myeloma, primary amyloidosis, and mature T-cell non-Hodgkin’s lymphomas.
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Steensma, David P. Malignant Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0296.

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The hematologic neoplasms include lymphoproliferative disorders (eg, chronic lymphocytic leukemia [CLL]/small lymphocytic lymphoma [SLL], large granular lymphocyte leukemia, hairy cell leukemia [HCL], Hodgkin lymphoma, non-Hodgkin lymphoma), plasma cell disorders (multiple myeloma, light chain amyloidosis, Waldenström macroglobulinemia, POEMS syndrome, heavy chain disease, plasmacytoma), chronic myeloid neoplasms (chronic myeloid leukemia, the BCR/ABL-negative myeloproliferative neoplasms, myelodysplastic syndromes), and acute leukemia (acute myeloid leukemia, acute lymphocytic leukemia). In addition, clonal but not overtly malignant conditions are common in the general population, including monoclonal gammopathy of undetermined significance (MGUS) and monoclonal B lymphocytosis (MBL).
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B. Bird's Clr Collection Super. Golden books, 1990.

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Little, Jean. A-B-C Mammoth Clr Merrigld. Golden Books, 1990.

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House, Happy. HH-RAGDY ANN ABC CLR B. Random House Books for Young Readers, 1987.

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Adams, Ansel. Photographs of Southwest Hb B Clb. Little, Brown Book Group Limited, 1999.

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Book chapters on the topic "B-CLL"

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Stilgenbauer, Stephan, Hartmut Döhner, and Peter Lichter. "Chronisch lymphatische Leukämie vom B-Zell-Typ (B-CLL)." In Molekularmedizinische Grundlagen von hämatologischen Neoplasien, 393–410. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59343-7_13.

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Agathangelidis, Andreas, Stavroula Ntoufa, and Kostas Stamatopoulos. "B Cell Receptor and Antigens in CLL." In Advances in Experimental Medicine and Biology, 1–24. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8051-8_1.

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Faguet, Guy B. "Clonal Evolution and Second Malignancies in B-CLL." In Chronic Lymphocytic Leukemia, 377–86. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_21.

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Hamblin, Terry. "The Heterogeneous Origin of the B-CLL Cell." In Chronic Lymphocytic Leukemia, 95–107. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_4.

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Genetet, Noelle, Dominique Bourel, Bernard Grosbois, Genevieve Merdrignac, Michele Marty, Renee Fauchet, Francois Lancelin, Robert Leblay, and Bernard Genetet. "Heterogeneity of B-CLL Cells Defined by Monoclonal Antibodies." In Leukocyte Typing II, 385–89. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4848-4_32.

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Lanza, F., and G. L. Castoldi. "Flow Cytochemical Analysis of Lymphoid Cells in B-Chronic Lymphocytic Leukemia (B-CLL)." In Leukemias, 319–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77083-8_56.

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Phipps, R. P., S. J. Pollock, K. Kaur, J. Kaufman, M. A. Borrello, B. A. Graf, D. Nazarenko, et al. "Expression of Cyclooxygenase-2 and Prostaglandins by B-1 Cells and B-CLL Cells." In Current Topics in Microbiology and Immunology, 293–300. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_30.

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Okkenhaug, Klaus, and Jan A. Burger. "PI3K Signaling in Normal B Cells and Chronic Lymphocytic Leukemia (CLL)." In Current Topics in Microbiology and Immunology, 123–42. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/82_2015_484.

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Gorczyca, Wojciech. "Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL) and B-Cell Prolymphocytic Leukemia (B-PLL)." In Atlas of Differential Diagnosis in Neoplastic Hematopathology, 206–25. 4th ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003120445-09.

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Warnke, R. A. "Morphologic, immunologic and genetic features of B cell CLL/SLL and immunocytoma." In Human Lymphoma: Clinical Implications of the REAL Classification, 23–28. London: Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-0857-3_5.

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Conference papers on the topic "B-CLL"

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Andrianopoulou, S., M. Schmitt, V. Grüßinger, B. Lippert, and U. Martens. "Simultanes kutanes Plattenepithelkarzinom und B-CLL: Grenzen innovativer Therapiekonzepte." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685815.

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Deng, Jiusheng, Jonathon Cohen, Andrea Pennati, Yuanqiang Wu, Shala Yuan, Christopher Flowers, and Jacques Galipeau. "Abstract A11: GIFT4-reprogrammed leukemic B cells for CLL immunotherapy." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-a11.

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Davis, Joanne, Kylie Mason, Chia Sharpe, Rachel Koldej, Brendon Chua, David Jackson, Paul Neeson, Constantine Tam, and David Ritchie. "Abstract B054: Can CLL-B cells treated with novel combination therapies be used to promote anti-CLL immune responses?" In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b054.

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Santanam, Urmila, Nicola Zanesi, Alexey Efanov, Alexey Palamarchuk, Stefan Costinean, John Hagan, Carlo Croce, and Yuri Pekarsky. "Abstract LB-352: B-CLL phenotype in Eµ-miR-29 transgenic mice." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-352.

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Lai, Hsien, Suping Zhang, Christina Wu, Liguang Chen, Grace Liu, RongRong Wu, Fitzgerlad Lao, et al. "Abstract 950: Selective cytotoxicity of A6 peptide against ZAP-70 expressing CLL B-cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-950.

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Peltier, Cheryl, Eileen McMillan-Ward, Elizabeth Henson, Nabanita Chatterje, Donna Hewitt, Danielle Desautels, Matthieu Bourrier, et al. "Abstract 3515: Down the rabbit hole with structural effects of FK866 in primary CLL B cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3515.

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Filippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol, and Pr Y. Carcassonne. "PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.

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Plasminogen activators (PA) are thought to play a role in the invasive and metastatic properties of many types of cancer cells. Though, discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells have been described.In this study, we evaluated both tissue type (tPA) and urokinase type (UK) cellular PA activities in different mononuclear cell types : normal T and B human peripheral lymphocytes, B cells from patients with chronic lymphocytic leukemia (CLL), human blood monocytes, alveolar macrophages, U 937, RAJI and JM cell 1ines.Mononuclear cells were isolated by Ficoll-hypaque gradients and monocytes by plastic adhesion. T and B cells were separated by a rosetting technique using sheep red blood cells. Cellular extracts were prepared by 0.5 % Triton X 100 buffer treatment followed by sonication and centrifugation 10 ' at 2000 g. PA assays were performed on the supernatants.UK-type PA was evaluated by a liquid-phase assay in presence of human plasminogen (Kabi) and chromogenic substrate S 2251 (Kabi).tPA was determinated using a solid-phase fibrin activity assay which involves an affinity separation step and thus allows selective detection of tPA.In both cases, results were reported in international units by reference to standard curves of UK (Choay) or tPA (Kabi).In all cell types tested, PA detected was essentially urokinase-type. Highest PA activity was found in U 937 cells (0.7 IU/5×l06 cells). In normal blood lymphocytes, mean PA activity was 0.08 IU/5×l06 cells. Examination of lymphocytes from patients with CLL revealed a marked decrease in UK activity as compared to normals (< 0.01 IU/5×106 cells in more than 50 % cases).The function of PA in normal lymphocyte physiology and the potential pathogenic role of diminished PA in CLL lymphocytes remains to be investigated.
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Wang, Lili, Rutendo Gambe, Jean Fan, Angela N. Brooks, Jing Sun, Donna Neuberg, Peter Kharchenko, et al. "Abstract 669: Compound heterozygous Sf3b1-K700E mutation and Atm deletion in B cells leads to CLL in mice." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-669.

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Amrein, Lilian, May Shawi, Jeremy Grenier, Raquel Aloys, and Lawrence Panasci. "Abstract 932: Predictive markers of thein vitroanticancer effect of the pan class I PI3K inhibitor BKM120 in primary B-CLL lymphocytes." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-932.

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Parikh, Sameer A., Sara J. Achenbach, Kari G. Chaffee, Neil E. Kay, Connie E. Lesnick, James R. Cerhan, Curtis A. Hanson, Tait D. Shanafelt, and Susan L. Slager. "Abstract 3256: The prevalence of non-chronic lymphocytic leukemia (CLL) phenotype monoclonal B-cell lymphocytosis (MBL) in a population-based cohort of U.S. adults." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3256.

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Reports on the topic "B-CLL"

1

CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test MIL-M-9977J. Appendix J. NATO Stage B Cross-Servicing Checklist (CL2) Document Type Definition. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada306309.

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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test MIL-M-9977J. Appendix I. NATO Stage B Cross-Servicing Checklist (CL1) Document Type Definition. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada306310.

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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. TMSS Parsing Test, MIL-M-9977J, Appendix J, NATO Stage B Cross-Servicing Checklist (CL2), Document Type Definition. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada309304.

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Reid, M. S., X. Wang, N. Utting, and C. Jiang. Comparison of water chemistry of hydraulic-fracturing flowback water from two geological locations at the Duvernay Formation, Alberta, Canada. Natural Resources Canada/CMSS/Information Management, 2021. http://dx.doi.org/10.4095/329276.

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We analyzed and compared the water chemistry between 17 Fox Creek region samples, each from a different well, and 23 Three Hills region samples from a single well. Overall, the two regions were similar in chemical composition but showed small differences in some lower abundance dissolved elements. Additionally, we investigated changes in water chemistry of FPW over time from a single well. The majority of water quality parameters and water chemistry remained constant over the 7-month sampling time. Major ion chemistry showed increasing concentrations of Ca and Mg, and a decreasing concentration of SO4. Several trace elements also showed small trends of both increasing and decreasing concentrations over time. There was a strong correlation between Ca and Mg concentrations in both the Fox Creek region samples and Three Hills region samples, which is an indication of the mixing of formation water. However, the correlation between B and Sr was different among two region samples, which is likely due to the delayed mixing of formation water with the fracturing fluids during the flowback at different time periods of post fracturing. Likewise, Fox Creek region samples showed correlations between concentrations of Cl and Ca, Na and Ca, and Na and Mg, but these correlations were not seen in the Three Hills region samples. Geochemical modeling demonstrates that there are potential scales formed in the flowback water, but most of the minerals are still in the dissolution state in the formation. Stable isotopic analysis confirmed the mixing of injection water and the formation water.
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Guy, Charles, Gozal Ben-Hayyim, Gloria Moore, Doron Holland, and Yuval Eshdat. Common Mechanisms of Response to the Stresses of High Salinity and Low Temperature and Genetic Mapping of Stress Tolerance Loci in Citrus. United States Department of Agriculture, May 1995. http://dx.doi.org/10.32747/1995.7613013.bard.

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The objectives that were outlined in our original proposal have largely been achieved or will be so by the end of the project in February 1995 with one exception; that of mapping cold tolerance loci based on the segregation of tolerance in the BC1 progeny population. Briefly, our goals were to 1) construct a densely populated linkage map of the citrus genome: 2) map loci important in cold and/or salt stress tolerance; and 3) characterize the expression of genes responsive to cold land salt stress. As can be seen by the preceding listing of accomplishments, our original objectives A and B have been realized, objective C has been partially tested, objective D has been completed, and work on objectives E and F will be completed by the end of 1995. Although we have yet to map any loci that contribute to an ability of citrus to maintain growth when irrigated with saline water, our very encouraging results from the 1993 experiment provides us with considerable hope that 1994's much more comprehensive and better controlled experiment will yield the desired results once the data has been fully analyzed. Part of our optimism derives from the findings that loci for growth are closely linked with loci associated with foliar Cl- and Na+ accumulation patterns under non-salinization conditions. In the 1994 experiment, if ion exclusion or sequestration traits are segregating in the population, the experimental design will permit their resolution. Our fortunes with respect to cold tolerance is another situation. In three attempts to quantitatively characterize cold tolerance as an LT50, the results have been too variable and the incremental differences between sensitive and tolerant too small to use for mapping. To adequately determine the LT50 requires many plants, many more than we have been able to generate in the time and space available by making cuttings from small greenhouse-grown stock plants. As it has turned out, with citrus, to prepare enough plants needed to be successful in this objective would have required extensive facilities for both growing and testing hardiness which simply were not available at University of Florida. The large populations necessary to overcome the variability we encountered was unanticipated and unforeseeable at the project's outset. In spite of the setbacks, this project, when it is finally complete will be exceedingly successful. Listing of Accomplishments During the funded interval we have accomplished the following objectives: Developed a reasonably high density linkage map for citrus - mapped the loci for two cold responsive genes that were cloned from Poncirus - mapped the loci for csa, the salt responsive gene for glutathione peroxidase, and ccr a circadian rhythm gene from citrus - identified loci that confer parental derived specific DNA methylation patterns in the Citrus X Poncirus cross - mapped 5 loci that determine shoot vigor - mapped 2 loci that influence leaf Na+ accumulation patterns under non-saline conditions in the BC1 population - mapped 3 loci that influence leaf Na+ accumulation paterns during salt sress - mapped 2 loci that control leaf Cl- accumulation patterns under non-saline conditions - mapped a locus that controls leaf Cl- accumulation patterns during salt stress Screened the BC1 population for growth reduction during salinization (controls and salinized), and cold tolerance - determined population variation for shoot/root ratio of Na+ and Cl- - determined levels for 12 inorganic nutrient elements in an effort to examine the influence of salinization on ion content with emphasis on foliar responses - collected data on ion distribution to reveal patterns of exclusion/sequestration/ accumulation - analyzed relationships between ion content and growth Characterization of gene expression in response to salt or cold stress - cloned the gene for the salt responsive protein csa, identified it as glutathione peroxidase, determined the potential target substrate from enzymatic studies - cloned two other genes responsive to salt stress, one for the citrus homologue of a Lea5, and the other for an "oleosin" like gene - cold regulated (cor) genes belonging to five hybridization classes were isolated from Poncirus, two belonged to the group 2 Lea superfamily of stress proteins, the others show no significant homology to other known sequences - the expression of csa during cold acclimation was examined, and the expression of some of the cor genes were examined in response to salt stress - the influence of salinization on cold tolerance has been examined with seedling populations - conducted protein blot studies for expression of cold stress proteins during salt stress and vice versa
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