Log in

Relevant bibliographies by topics / B-CLL / Journal articles

To see the other types of publications on this topic, follow the link: B-CLL.

Journal articles on the topic 'B-CLL'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'B-CLL.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Parker, Anton, Shilu Amin, Tricia Zwiefelhofer, et al. "Epigenetic Regulation of ZAP70 in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (2008): 2246. http://dx.doi.org/10.1182/blood.v112.11.2246.2246.

Full text

Abstract:

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 lin

APA, Harvard, Vancouver, ISO, and other styles

2

Silber, R., CM Farber, E. Papadopoulos, et al. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

Silber, R., CM Farber, E. Papadopoulos, et al. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.

Full text

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

APA, Harvard, Vancouver, ISO, and other styles

4

Goodman, Alice. "B-CLL." Oncology Times &NA;, Supplement (2006): 21. http://dx.doi.org/10.1097/01.cot.0000316106.04463.a9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Silber, R., B. Degar, D. Costin, et al. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.3440.

Full text

Abstract:

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 heteroge

APA, Harvard, Vancouver, ISO, and other styles

6

Silber, R., B. Degar, D. Costin, et al. "Chemosensitivity of lymphocytes from patients with B-cell chronic lymphocytic leukemia to chlorambucil, fludarabine, and camptothecin analogs." Blood 84, no. 10 (1994): 3440–46. http://dx.doi.org/10.1182/blood.v84.10.3440.bloodjournal84103440.

Full text

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

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

Abstract:

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 detec

APA, Harvard, Vancouver, ISO, and other styles

8

Santiago-Schwarz, F., C. Panagiotopoulos, A. Sawitsky, and KR Rai. "Distinct characteristics of lymphokine-activated killer (LAK) cells derived from patients with B-cell chronic lymphocytic leukemia (B-CLL). A factor in B-CLL serum promotes natural killer cell-like LAK cell growth." Blood 76, no. 7 (1990): 1355–60. http://dx.doi.org/10.1182/blood.v76.7.1355.1355.

Full text

Abstract:

Abstract We show that lymphokine-activated killer (LAK) cell precursors derived from patients with B-cell chronic lymphocytic leukemia (B-CLL) and cultured in the presence of recombinant interleukin-2 and normal human serum (NHS), develop into primarily NK cell-like (CD 57+) LAK cells, whereas identically prepared LAK cell precursors from normal subjects develop into mainly T cell-like (CD 3+, CD 8+) LAK cells. B-CLL LAK cells exhibited greater proliferative capacity than did normal LAK cells. When normal LAK cells were grown in B-CLL serum instead of NHS, their proliferation increased; NK cel

APA, Harvard, Vancouver, ISO, and other styles

9

Santiago-Schwarz, F., C. Panagiotopoulos, A. Sawitsky, and KR Rai. "Distinct characteristics of lymphokine-activated killer (LAK) cells derived from patients with B-cell chronic lymphocytic leukemia (B-CLL). A factor in B-CLL serum promotes natural killer cell-like LAK cell growth." Blood 76, no. 7 (1990): 1355–60. http://dx.doi.org/10.1182/blood.v76.7.1355.bloodjournal7671355.

Full text

Abstract:

We show that lymphokine-activated killer (LAK) cell precursors derived from patients with B-cell chronic lymphocytic leukemia (B-CLL) and cultured in the presence of recombinant interleukin-2 and normal human serum (NHS), develop into primarily NK cell-like (CD 57+) LAK cells, whereas identically prepared LAK cell precursors from normal subjects develop into mainly T cell-like (CD 3+, CD 8+) LAK cells. B-CLL LAK cells exhibited greater proliferative capacity than did normal LAK cells. When normal LAK cells were grown in B-CLL serum instead of NHS, their proliferation increased; NK cell levels

APA, Harvard, Vancouver, ISO, and other styles

10

Tummala, Hemanth, Alexey Goltsov, Hilal S. Khalil, et al. "Advocating the need of a systems biology approach for personalised prognosis and treatment of B-CLL patients." BioDiscovery 6 (December 30, 2012): e8939. https://doi.org/10.7750/BioDiscovery.2012.6.4.

Full text

Abstract:

The clinical course of B-CLL is heterogeneous. This heterogeneity leads to a clinical dilemma: can we identify those patients who will benefit from early treatment and predict the survival? In recent years, mathematical modelling has contributed significantly in understanding the complexity of diseases. In order to build a mathematical model for determining prognosis of B-CLL one has to identify, characterise and quantify key molecules involved in the disease. Here we discuss the need and role of mathematical modelling in predicting B-CLL disease pathogenesis and suggest a new systems biology

APA, Harvard, Vancouver, ISO, and other styles

11

Buhmann, Raymund, Annette Nolte, Doreen Westhaus, Bertold Emmerich, and Michael Hallek. "CD40-Activated B-Cell Chronic Lymphocytic Leukemia Cells for Tumor Immunotherapy: Stimulation of Allogeneic Versus Autologous T Cells Generates Different Types of Effector Cells." Blood 93, no. 6 (1999): 1992–2002. http://dx.doi.org/10.1182/blood.v93.6.1992.406k23_1992_2002.

Full text

Abstract:

Although spontaneous remissions may rarely occur in B-cell chronic lymphocytic leukemia (B-CLL), T cells do generally not develop a clinically significant response against B-CLL cells. Because this T-cell anergy against B-CLL cells may be caused by the inability of B-CLL cells to present tumor-antigens efficiently, we examined the possibility of upregulating critical costimulatory (B7-1 and B7-2) and adhesion molecules (ICAM-1 and LFA-3) on B-CLL cells to improve antigen presentation. The stimulation of B-CLL cells via CD40 by culture on CD40L expressing feeder cells induced a strong upregulat

APA, Harvard, Vancouver, ISO, and other styles

12

Kay, Neil E., Ann K. Strege, Tait D. Shanafelt, Nancy D. Bone, and Yean K. Lee. "CLL B Cell Interaction with Bone Biopsy Generated Marrow Stromal Elements Enhances Their Apoptosis Resistance in Association with an Angiogenic Switch." Blood 104, no. 11 (2004): 1914. http://dx.doi.org/10.1182/blood.v104.11.1914.1914.

Full text

Abstract:

Abstract CLL B cells have significant opportunity to interact with multiple tissue sites that are critical to the leukemic cell’s ability to survive. The marrow stromal elements (MSE) in B-chronic lymphocytic leukemia (B-CLL) are very likely one of the most frequently involved in this important cell-cell interaction. We have utilized a novel bone marrow biopsy technique (Alvi S, Leuk Res, 2001) that consistently generates robust and long-lived marrow stromal elements from B-CLL patients in order to study CLL B cell apoptosis status in relation to angiogenic factors. The latter angiogenic param

APA, Harvard, Vancouver, ISO, and other styles

13

Wojdacz, Tomasz K., Harindra E. Amarasinghe, Latha Kadalayil, et al. "Clinical significance of DNA methylation in chronic lymphocytic leukemia patients: results from 3 UK clinical trials." Blood Advances 3, no. 16 (2019): 2474–81. http://dx.doi.org/10.1182/bloodadvances.2019000237.

Full text

Abstract:

Abstract Chronic lymphocytic leukemia patients with mutated immunoglobulin heavy-chain genes (IGHV-M), particularly those lacking poor-risk genomic lesions, often respond well to chemoimmunotherapy (CIT). DNA methylation profiling can subdivide early-stage patients into naive B-cell–like CLL (n-CLL), memory B-cell–like CLL (m-CLL), and intermediate CLL (i-CLL), with differing times to first treatment and overall survival. However, whether DNA methylation can identify patients destined to respond favorably to CIT has not been ascertained. We classified treatment-naive patients (n = 605) from 3

APA, Harvard, Vancouver, ISO, and other styles

14

Douglas, Raymond S., Renold J. Capocasale, Roberta J. Lamb, Peter C. Nowell та Jonni S. Moore. "Chronic Lymphocytic Leukemia B Cells Are Resistant to the Apoptotic Effects of Transforming Growth Factor-β". Blood 89, № 3 (1997): 941–47. http://dx.doi.org/10.1182/blood.v89.3.941.

Full text

Abstract:

Abstract Chronic lymphocytic leukemia (CLL) is the most common leukemia of the western world and is characterized by a slowly progressing accumulation of clonal CD5+ B cells. Our laboratory has investigated the role of transforming growth factor-β (TGF-β) and interleukin-4 (IL-4) in the pathogenesis of B-cell expansion in CLL. In vitro addition of TGF-β did not increase spontaneous apoptosis of B cells from most CLL patients, as determined using the TUNEL method, compared with a twofold increase observed in cultures of normal B cells. There was similar expression of TGF-β type II receptors on

APA, Harvard, Vancouver, ISO, and other styles

15

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 (2005): 1188. http://dx.doi.org/10.1182/blood.v106.11.1188.1188.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

16

Palena, Claudia, Loni McIntosh, Jeffrey Schlom, Kenneth Foon, Dennis Panicali, and Kwong Y. Tsang. "Modification of B-CLL Cells Via Infection with a Replication-Defective MVA Virus Encoding Three Costimulatory Molecules: A Potential Approach to Tumor Cell Immunotherapy of B-CLL." Blood 104, no. 11 (2004): 2516. http://dx.doi.org/10.1182/blood.v104.11.2516.2516.

Full text

Abstract:

Abstract Chronic lymphocytic leukemia of B-cell origin (B-CLL) is a lymphoproliferative disorder characterized by the accumulation of slowly dividing, apoptosis-defective, clonal CD5+ B cells that typically involve the bone marrow, lymph nodes, spleen and blood of affected individuals. New therapeutic approaches are necessary to be investigated for the treatment of B-CLL. Several characteristics of the neoplastic B cells make B-CLL a good candidate for immunotherapy; evidence exists that B-CLL cells can be recognized by autologous anti-tumor T cells in an MHC-restricted manner. B-CLL cells, ho

APA, Harvard, Vancouver, ISO, and other styles

17

Sonia Jaramillo, Andreas Agathangelidis, Christof Schneider, et al. "Prognostic impact of prevalent chronic lymphocytic leukemia stereotyped subsets: analysis within prospective clinical trials of the German CLL Study Group (GCLLSG)." Haematologica 105, no. 11 (2019): 2598–607. http://dx.doi.org/10.3324/haematol.2019.231027.

Full text

Abstract:

Almost one-third of all patients with chronic lymphocytic leukemia (CLL) express stereotyped B cell receptor immunoglobulins (BcR IG) and can be assigned to distinct subsets, each with a particular BcR IG. The largest stereotyped subsets are #1, #2, #4 and #8, associated with specific clinicobiological characteristics and outcomes in retrospective studies. We assessed the associations and prognostic value of these BcR IG in prospective multicenter clinical trials reflective of two different clinical situations: i) early-stage patients (watch-and-wait arm of the CLL1 trial) (n=592); ii) patient

APA, Harvard, Vancouver, ISO, and other styles

18

Lotz, M., E. Ranheim, and T. J. Kipps. "Transforming growth factor beta as endogenous growth inhibitor of chronic lymphocytic leukemia B cells." Journal of Experimental Medicine 179, no. 3 (1994): 999–1004. http://dx.doi.org/10.1084/jem.179.3.999.

Full text

Abstract:

Chronic lymphocytic leukemia (CLL) B cells are hyporesponsive or refractory to mitogens and growth factors in vitro. This study examined whether transforming growth factor beta (TGF-beta), a potent inhibitor of lymphocyte proliferation may play a role in the growth regulation of CLL B cells. CLL B cells from all donors treated expressed detectable TGF-beta 1 mRNA. In vitro release of TGF-beta by unstimulated cultures, or cultures stimulated by antibody to cell surface immunoglobulin (anti-mu) plus phorbol 12-myristate 13-acetate (PMA) was higher in CLL than in normal B cells. High levels of TG

APA, Harvard, Vancouver, ISO, and other styles

19

Seifert, Marc, Ludger Sellmann, Johannes Bloehdorn, et al. "Cellular origin and pathophysiology of chronic lymphocytic leukemia." Journal of Experimental Medicine 209, no. 12 (2012): 2183–98. http://dx.doi.org/10.1084/jem.20120833.

Full text

Abstract:

The cellular origin of chronic lymphocytic leukemia (CLL) is still debated, although this information is critical to understanding its pathogenesis. Transcriptome analyses of CLL and the main normal B cell subsets from human blood and spleen revealed that immunoglobulin variable region (IgV) gene unmutated CLL derives from unmutated mature CD5+ B cells and mutated CLL derives from a distinct, previously unrecognized CD5+CD27+ post–germinal center B cell subset. Stereotyped V gene rearrangements are enriched among CD5+ B cells, providing independent evidence for a CD5+ B cell derivation of CLL.

APA, Harvard, Vancouver, ISO, and other styles

20

Sinha, Sutapa, Charla R. Secreto, Justin C. Boysen, et al. "Enhanced Expression of Beta-Catenin and Axl Receptor Tyrosine Kinase (RTK) in Chronic Lymphocytic Leukemia (CLL) B-Cells with Co-Culture on Marrow Stromal Cells: Implications for Leukemic Cell Drug Resistance." Blood 132, Supplement 1 (2018): 3125. http://dx.doi.org/10.1182/blood-2018-99-110981.

Full text

Abstract:

Abstract Introduction CLL remains an incurable disease and represents a significant health problem in the western world. Increasing evidence highlights that the impact of marrow stromal cells is a key component influencing CLL B-cell survival. We have utilized an in vitro bone marrow stromal cell (BMSC) model system and found unique alterations in CLL B-cells with BMSC co-culture that point to previously unidentified biologic changes in the CLL B-cells that may influence CLL B-cell signaling and drug resistance. Methods Purified primary CLL B-cells (n= 39) from previously untreated CLL patient

APA, Harvard, Vancouver, ISO, and other styles

21

Liang, Xueqing, Veronika Bachanova, and Wei Chen. "Deletion and mutation of IL10RA gene on chromosome 11q23 to avert CpG-B oligodeoxynucleotides-induced apoptosis of human chronic lymphocytic leukemia B cells." Journal of Clinical Oncology 31, no. 15_suppl (2013): 3023. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3023.

Full text

Abstract:

3023 Background: Targeting TLR9 expressed on human CLL cells with CpG-B oligodeoxynucleotides leads to IL-10-induced tyrosine phosphorylation of STATs and apoptosis of B-CLL cells. However, B-CLL cells from a small subset of patients were resistant to CpG-B ODN treatment. Here, we investigated the molecular mechanism by which B-CLL cells are sensitive or resistant to CpG-B ODN treatment. Methods: Purified CD19+CD23+CD5+primary B-CLL cells were cultured for 5 days with/without CpG-B ODN (CpG 2006, CpG 685) or rh-IL-10. B-CLL cell apoptosis were determined by viable cell counts, Annexin V/PI and

APA, Harvard, Vancouver, ISO, and other styles

22

Hwang, Kwan-Ki, Xi Chen, Daniel M. Kozink, et al. "Enhanced outgrowth of EBV-transformed chronic lymphocytic leukemia B cells mediated by coculture with macrophage feeder cells." Blood 119, no. 7 (2012): e35-e44. http://dx.doi.org/10.1182/blood-2011-08-371203.

Full text

Abstract:

Abstract B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the clonal expansion of CD5-expressing B lymphocytes that produce mAbs often reactive with microbial or autoantigens. Long-term culture of B-CLL clones would permit the collection and characterization of B-CLL mAbs to study antigen specificity and of B-CLL DNA to investigate molecular mechanisms promoting the disease. However, the derivation of long-term cell lines (eg, by EBV), has not been efficient. We have improved the efficiency of EBV B-CLL transformation of CpG oligonucleotide-stimulated cells by incubating patient

APA, Harvard, Vancouver, ISO, and other styles

23

Baskar, Sivasubramanian, Jessica M. Suschak, Ivan Samija, et al. "A human monoclonal antibody drug and target discovery platform for B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic stem cell transplantation and phage display." Blood 114, no. 20 (2009): 4494–502. http://dx.doi.org/10.1182/blood-2009-05-222786.

Full text

Abstract:

Abstract Allogeneic hematopoietic stem cell transplantation (alloHSCT) is the only potentially curative treatment available for patients with B-cell chronic lymphocytic leukemia (B-CLL). Here, we show that post-alloHSCT antibody repertoires can be mined for the discovery of fully human monoclonal antibodies to B-CLL cell-surface antigens. Sera collected from B-CLL patients at defined times after alloHSCT showed selective binding to primary B-CLL cells. Pre-alloHSCT sera, donor sera, and control sera were negative. To identify post-alloHSCT serum antibodies and subsequently B-CLL cell-surface a

APA, Harvard, Vancouver, ISO, and other styles

24

Maiti, Guru P., Sutapa Sinha, Justin C. Boysen, Neil E. Kay, and Asish K. Ghosh. "Epigenetic Silencing of Catalase Induces Accumulation of Reactive Oxygen Species in Chronic Lymphocytic Leukemia B Cells Leading to Activation of Axl: An Escape Strategy?" Blood 128, no. 22 (2016): 4363. http://dx.doi.org/10.1182/blood.v128.22.4363.4363.

Full text

Abstract:

Abstract Background: A challenge for novel therapeutic strategies will be the fine tuning of intracellular reactive oxygen species (ROS) signaling in order to effectively deprive cells from ROS-induced tumor promoting events and subsequent tipping the balance to ROS-induced apoptotic signaling. ROS plays a critical role in regulation of the pro-survival receptor tyrosine kinase (RTK) signaling pathways in human cancers. Studies have identified mitochondrial metabolism as the key source for abundant ROS in chronic lymphocytic leukemia (CLL). Unlike in other malignant cells, increased oxidative

APA, Harvard, Vancouver, ISO, and other styles

25

Sinha, Sutapa, Zhiquan Wang, Weiguo Han, et al. "Abstract 1252: Role of purine and pyrimidine metabolism in CLL B cell survival and drug resistance mediated via interaction with bone marrow microenvironment." Cancer Research 83, no. 7_Supplement (2023): 1252. http://dx.doi.org/10.1158/1538-7445.am2023-1252.

Full text

Abstract:

Abstract Multiple studies including ours have shown that the interaction of chronic lymphocytic leukemia (CLL) B cells with the bone marrow (BM) microenvironment promotes cell survival and protects these cells from the cytotoxic effects of therapy. A detailed understanding of this interaction will help better understand CLL leukemic cell survival and drug resistance mechanisms. We performed RNA-seq in paired CLL B cells isolated from untreated blood and BM (n=6) and in untreated CLL B cells (n=4) cultured alone or co-cultured with bone marrow stromal cells (BMSCs) derived from either normal in

APA, Harvard, Vancouver, ISO, and other styles

26

Yasukawa, M., T. Shiroguchi, A. Inatsuki, and Y. Kobayashi. "Antigen presentation in an HLA-DR-restricted fashion by B-cell chronic lymphocytic leukemia cells." Blood 72, no. 1 (1988): 102–8. http://dx.doi.org/10.1182/blood.v72.1.102.102.

Full text

Abstract:

Abstract The ability of B-cell chronic lymphocytic leukemia (B-CLL) cells to present antigen to antigen-specific T cells was investigated. B-CLL cells present herpes simplex virus (HSV) antigen and purified protein derivative (PPD) to HSV- and PPD-specific, interleukin-2-dependent T- cell lines in an antigen-specific manner. Treatment of B-CLL cells with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) induced markedly increased levels of HLA-DR expression. TPA-treated B-CLL cells showed substantially more effective presentation, especially at low antigen concentrations, than did u

APA, Harvard, Vancouver, ISO, and other styles

27

Yasukawa, M., T. Shiroguchi, A. Inatsuki, and Y. Kobayashi. "Antigen presentation in an HLA-DR-restricted fashion by B-cell chronic lymphocytic leukemia cells." Blood 72, no. 1 (1988): 102–8. http://dx.doi.org/10.1182/blood.v72.1.102.bloodjournal721102.

Full text

Abstract:

The ability of B-cell chronic lymphocytic leukemia (B-CLL) cells to present antigen to antigen-specific T cells was investigated. B-CLL cells present herpes simplex virus (HSV) antigen and purified protein derivative (PPD) to HSV- and PPD-specific, interleukin-2-dependent T- cell lines in an antigen-specific manner. Treatment of B-CLL cells with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) induced markedly increased levels of HLA-DR expression. TPA-treated B-CLL cells showed substantially more effective presentation, especially at low antigen concentrations, than did untreated

APA, Harvard, Vancouver, ISO, and other styles

28

Jurlander, Jesper, Chun-Fai Lai, Jimmy Tan, et al. "Characterization of Interleukin-10 Receptor Expression on B-Cell Chronic Lymphocytic Leukemia Cells." Blood 89, no. 11 (1997): 4146–52. http://dx.doi.org/10.1182/blood.v89.11.4146.

Full text

Abstract:

Abstract B-cell chronic lymphocytic leukemia (B-CLL) cells accumulate in vivo in the G0/G1 phase of the cell cycle, suggesting that their malignant expansion is due, at least in part, to a delay in cell death. However, the cellular or molecular factors responsible for a delay in B-CLL cell death are unknown. B-CLL cells do express receptors for interferon-α (IFN-α) and IFN-γ, and activation of both has been shown to promote B-CLL survival in vitro by preventing apoptosis. The interleukin-10 (IL-10) receptor is another member of the IFN receptor family, but its ligand, IL-10, has been reported

APA, Harvard, Vancouver, ISO, and other styles

29

Xing, Dongxia, Alan G. Ramsay, Simon Robinson, et al. "Lenalidomide Treatment Enhances Immunological Synapse Formation of Cord Blood Natural Killer Cells with B Cells Derived From Chronic Lymphocytic Leukemia." Blood 118, no. 21 (2011): 1794. http://dx.doi.org/10.1182/blood.v118.21.1794.1794.

Full text

Abstract:

Abstract Abstract 1794 Immune dysfunction is a hallmark of chronic lymphocytic leukemia (CLL) including suppressed humoral and cell-mediated immune responses. The immunomodulatory agent lenalidomide has shown effective clinical activity against CLL, but its mechanism of action is poorly understood. Previous work has demonstrated that the T cell immunological synapse and functional defects in CLL can be reversed following lenalidomide treatment (J Clin Invest. 2008; 118). Polymerization of F-actin at the NK cell immunological synapse with tumor cells is required for signaling molecules to assem

APA, Harvard, Vancouver, ISO, and other styles

30

Lankester, AC, GM van Schijndel, CE van der Schoot, MH van Oers, CJ van Noesel, and RA van Lier. "Antigen receptor nonresponsiveness in chronic lymphocytic leukemia B cells." Blood 86, no. 3 (1995): 1090–71. http://dx.doi.org/10.1182/blood.v86.3.1090.1090.

Full text

Abstract:

Abstract B chronic lymphocytic leukemia (B-CLL) are clonal populations of mIgM+ or mIgM+/mIgD+ CD5+ B cells that appear to be arrested in the follicular mantle-zone B-cell stage. Functional analyses have shown two groups of B-CLL that can be distinguished based on their capacity to proliferate in response to B-cell antigen receptor complex (BCR) cross- linking. To investigate the molecular basis for this phenomenon, we have analyzed both architecture and functional properties of BCR complexes on these two groups of B-CLL. Both groups were found to express structurally similar BCR. However, pro

APA, Harvard, Vancouver, ISO, and other styles

31

Lankester, AC, GM van Schijndel, CE van der Schoot, MH van Oers, CJ van Noesel, and RA van Lier. "Antigen receptor nonresponsiveness in chronic lymphocytic leukemia B cells." Blood 86, no. 3 (1995): 1090–71. http://dx.doi.org/10.1182/blood.v86.3.1090.bloodjournal8631090.

Full text

Abstract:

B chronic lymphocytic leukemia (B-CLL) are clonal populations of mIgM+ or mIgM+/mIgD+ CD5+ B cells that appear to be arrested in the follicular mantle-zone B-cell stage. Functional analyses have shown two groups of B-CLL that can be distinguished based on their capacity to proliferate in response to B-cell antigen receptor complex (BCR) cross- linking. To investigate the molecular basis for this phenomenon, we have analyzed both architecture and functional properties of BCR complexes on these two groups of B-CLL. Both groups were found to express structurally similar BCR. However, protein tyro

APA, Harvard, Vancouver, ISO, and other styles

32

Hegde, Ganapati V., Katie J. Peterson, Katy Emanuel, et al. "GLI1 Transcription Factor: A Potential Therapeutic Target in B-CLL." Blood 110, no. 11 (2007): 3100. http://dx.doi.org/10.1182/blood.v110.11.3100.3100.

Full text

Abstract:

Abstract B-cell Chronic Lymphocytic Leukemia (B-CLL) is characterized by accumulation of clonal lymphocytes resistant to apoptosis. Therefore, identification of molecules responsible for the increased resistance to apoptosis is warranted. The identified molecules could be further targeted to develop effective therapy. Emerging evidence on the mechanism of resistant to apoptosis in several cancers suggests that GLI1 transcription factor, target of hedgehog signaling, may have a potential role in the increased resistance to apoptosis in B-CLL. However such studies have not been reported for B-CL

APA, Harvard, Vancouver, ISO, and other styles

33

Lee, Yean K., Ann K. Strege, Nancy D. Bone та ін. "Hypoxia Inducible Factor-1α Is over Expressed in CLL B Cells Because of an Impaired Proteasome Pathway Associated with Defective Interaction with von Hippel-Landau Protein." Blood 106, № 11 (2005): 2115. http://dx.doi.org/10.1182/blood.v106.11.2115.2115.

Full text

Abstract:

Abstract We have found that CLL B cells spontaneously secrete vascular endothelial growth factor (VEGF) and that a VEGF autocrine pathway can induce apoptosis resistance in these cells. Recently, we also found that hypoxia-inducible factor-1 alpha (HIF-1α) is highly expressed in CLL B cells. Since this protein is a potent transcription factor for the induction of VEGF, we were interested in further definition of HIF-1α regulation and its function in CLL B cells. CLL blood B cells overexpress HIF-1α protein but not mRNA for HIF-1α compared to normal blood and splenic B cells. Immunohistochemist

APA, Harvard, Vancouver, ISO, and other styles

34

Cro, Lilla, Luca Baldini, Lucia Nobili, et al. "The Cytofluorimetric/FISH Diagnostic Approach Define a B-Cell Variant-CLL with Peculiar Clinico-Biological Features." Blood 110, no. 11 (2007): 2077. http://dx.doi.org/10.1182/blood.v110.11.2077.2077.

Full text

Abstract:

Abstract In the present study, we describe the clinico-biological features of 63 cases of variant B-CLL (v-B-CLL) defined according to a previously described diagnostic algorithm for CD5+ mature B-cell leukemias, based on the combined use of Cytofluorimetric (CFM) analysis and t(11;14)(q13;q32) detection by means of fluorescence in situ hybridisation (FISH). These leukemias were characterized by SIgbright/CD23+ or CD23+/− , CD79b/CD20 bright, and negativity for t(11;14)(q13;q32). A historical series of 112 classical B-CLL was used as comparison. The mean age was 61 years (33–85) and M/F ratio

APA, Harvard, Vancouver, ISO, and other styles

35

Kikushige, Yoshikane, Fumihiko Ishikawa, Toshihiro Miyamoto, and Koichi Akashi. "Hematopoietic Stem Cells Are Primarily Involved In Pathogenesis of Chronic Lymphocytic Leukemia." Blood 116, no. 21 (2010): 4604. http://dx.doi.org/10.1182/blood.v116.21.4604.4604.

Full text

Abstract:

Abstract Abstract 4604 Chronic lymphocytic leukemia (CLL) is characterized by consistent expansion of B cells in peripheral lymphoid organs. CLL B cells express CD5 antigen, and have clonal rearrangement of immunoglobulin heavy chain (IGH) genes with the restricted usage of VH genes. CLL has thus been believed to represent retention or proliferation of abnormal B cell clones presumably with anti-apoptotic potential, or with deregulated response to auto-antigens. In this study, we extensively search for CLL-initiating cells by utilizing the xenogeneic transplantation system, in which human hema

APA, Harvard, Vancouver, ISO, and other styles

36

Hallaert, Delfine Y. H., Laura A. Smit, Rene Spijker, et al. "Increased Expression Level of Noxa in Peripheral Versus Lymph Node Chronic Lymphocytic Leukemia Cells Is Correlated with Survival Capacity." Blood 108, no. 11 (2006): 4972. http://dx.doi.org/10.1182/blood.v108.11.4972.4972.

Full text

Abstract:

Abstract Background: The gradual accumulation of chronic lymphocytic leukemia (B-CLL) cells is presumed to derive from proliferation centers in lymph nodes and bone marrow. To what extent these cells possess the purported anti-apoptotic phenotype of peripheral B-CLL cells is unknown. Recently, we have described that in B-CLL samples from peripheral blood, aberrant apoptosis gene expression was not limited to protective changes but also included increased levels of pro-apoptotic BH3-only member Noxa. The functional consequence of this finding is not known, nor whether this aberrant apoptosis ge

APA, Harvard, Vancouver, ISO, and other styles

37

Tinhofer, Inge, Ingrid Marschitz, Marion Kos, et al. "Differential Sensitivity of CD4+ and CD8+T Lymphocytes to the Killing Efficacy of Fas (Apo-1/CD95) Ligand+ Tumor Cells in B Chronic Lymphocytic Leukemia." Blood 91, no. 11 (1998): 4273–81. http://dx.doi.org/10.1182/blood.v91.11.4273.411k25_4273_4281.

Full text

Abstract:

B-chronic lymphocytic leukemia (B-CLL) is characterized by cellular and humoral immune defects resulting in increased rates of infection and disturbed immune surveillance against cancer cells as well as by the expansion of slowly proliferating tumor cells. We found increased Fas receptor (FasR) expression in peripheral blood CD4+and CD8+ cells of B-CLL patients compared with the equivalent cells of healthy donors. Although increased Fas receptor expression was significant in both T-lymphocytic subsets, only CD4+ cells from B-CLL patients underwent apoptosis after treatment with the agonistic F

APA, Harvard, Vancouver, ISO, and other styles

38

Sinha, Sutapa, Charla R. Secreto, Justin C. Boysen та ін. "Β-Catenin and Axl Receptor Tyrosine Kinase Modulation in CLL B-Cells with Co-Culture on Marrow Stromal Cells: Implications for Drug Resistance". Blood 134, Supplement_1 (2019): 1739. http://dx.doi.org/10.1182/blood-2019-121772.

Full text

Abstract:

Introduction: Bone marrow stromal cells (BMSCs), a major component of CLL microenvironment influences CLL B-cell survival. We have utilized an in vitro BMSC model system and found unique alterations in CLL B-cells with short term BMSC co-culture that point to previously unidentified biologic changes in the CLL B-cells that may influence CLL B-cell signaling and their drug resistance. Methods: Purified primary CLL B-cells (n=41) from previously untreated CLL patients were cultured alone or co-cultured with primary BMSCs from either normal individuals (n=24) or CLL patients (n=18) at a 50:1 rati

APA, Harvard, Vancouver, ISO, and other styles

39

Ghosh, Asish K., Debabrata Mukhopadhyay, and Neil E. Kay. "Bosutinib, a Src/Abl Kinase Inhibitor Induces Apoptosis in CLL B Cells by Targeting Multiple Tyrosine Kinases and Overcomes Stroma Protection." Blood 114, no. 22 (2009): 2368. http://dx.doi.org/10.1182/blood.v114.22.2368.2368.

Full text

Abstract:

Abstract Abstract 2368 Poster Board II-345 Background: B-cell chronic lymphocytic leukemia (CLL) is characterized by the progressive accumulation of CD5+ B lymphocytes in the peripheral blood, lymphoid organs and bone marrow. Despite aggressive therapy, CLL is still incurable partly because of intrinsic defect in apoptosis induction. A novel therapeutic agent, Bosutinib, was initially developed as an inhibitor of Src and Abl kinases and is currently in phase II clinical trials for the treatment of several human malignancies. Recently, Bosutinib has been shown to inhibit phosphorylation of a no

APA, Harvard, Vancouver, ISO, and other styles

40

Tiribelli, Mario, Elisa Barbarotto, Claudio Celeghini, et al. "Aberrant Expression of Trail in B Chronic Lymphocytic Leukemia (B-CLL) Cells." Blood 106, no. 11 (2005): 4976. http://dx.doi.org/10.1182/blood.v106.11.4976.4976.

Full text

Abstract:

Abstract Chronic lymphocytic leukemia (CLL) is a quintessential example of human malignancies that are caused primarily by defect in apoptosis. Defects in apoptotic pathways contribute also to chemoresistance and can promote resistance to cellular immune responses. TNF-related apoptosis inducing ligand (TRAIL), interacts with four high affinity membrane receptors (TRAIL-R1 – R4): R1 and R2 are thought to transducer apoptotic signals, while R3 and R4 may act as “decoy” receptors, protecting cells from apoptosis. Despite its potential anti–cancer activity, TRAIL alone has a low cytotoxic activit

APA, Harvard, Vancouver, ISO, and other styles

41

Knauf, Wolfgang Ulrich, Toshko Lissichkov, Ali Aldaoud, et al. "Bendamustine Versus Chlorambucil in Treatment-Naive Patients with B-Cell Chronic Lymphocytic Leukemia (B-CLL): Results of an International Phase III Study." Blood 110, no. 11 (2007): 2043. http://dx.doi.org/10.1182/blood.v110.11.2043.2043.

Full text

Abstract:

Abstract Introduction: Bendamustine (BEN) is a purine analog / alkylator hybrid agent with a particular mechanisms of action that provides effective treatment for a number of hematologic and non-hematologic malignancies. It is used primarily for chemo-naïve, relapsed or refractory B-CLL as well as for other types of non-Hodgkin’s lymphomas. The aim of this randomized phase III, open-label, multicenter study was to compare the efficacy and safety of BEN versus chlorambucil (CLB) in treatment-naïve patients (pts) with B-CLL Binet stage B/C. Patients and Methods: Pts with untreated B-CLL were r

APA, Harvard, Vancouver, ISO, and other styles

42

Farren, Timothy W., Feng-Ting Liu, Claire Stephens, et al. "CD160 Expression in B-Cell Lymphoproliferative Disorders: Derivation and Validation of a New Three-Antigen Scoring System Improving Diagnostic Precision in B-Cell Malignancies." Blood 114, no. 22 (2009): 4382. http://dx.doi.org/10.1182/blood.v114.22.4382.4382.

Full text

Abstract:

Abstract Abstract 4382 The diagnosis of many chronic B-cell lymphoproliferative disorders (B-LPD) is based on the integration of characteristic morphology, immunophenotype and cytogenetic analysis. Atypical B-cell chronic lymphocytic leukaemia (CLL), mantle cell lymphoma (MCL) and monoclonal B cell lymphocytosis (MBL) share many features. which can lead to diagnostic confusion. Throughout the past decade, considerable progress has been achieved in defining new prognostic markers and treatment options in B-cell malignancies. However, over the same period, there has been only limited work perfor

APA, Harvard, Vancouver, ISO, and other styles

43

Tiwari, Sanjay, Kyriacos Felekkis, Eun-Yi Moon, Amanda Flies, David H. Sherr, and Adam Lerner. "Among circulating hematopoietic cells, B-CLL uniquely expresses functional EPAC1, but EPAC1-mediated Rap1 activation does not account for PDE4 inhibitor-induced apoptosis." Blood 103, no. 7 (2004): 2661–67. http://dx.doi.org/10.1182/blood-2003-06-2154.

Full text

Abstract:

Abstract Type 4 cyclic adenosine monophosphate (cAMP) phosphodiesterase (PDE4) inhibitors and other agents that raise intracellular cAMP levels induce apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) but not in T-CLL or peripheral blood T cells. Two principal effector proteins for cAMP are protein kinase A (PKA) and EPAC (exchange protein directly activated by cAMP), a Rap guanosine 5′-diphosphate (GDP) exchange factor. We here examine whether varying expression of EPAC accounts for the discrepant sensitivity of B-CLL and T cells to PDE4 inhibitor-induced apoptosis. B-CLL and periphera

APA, Harvard, Vancouver, ISO, and other styles

44

Ghosh, Asish K., Charla Secreto, Justin Boysen, et al. "The novel receptor tyrosine kinase Axl is constitutively active in B-cell chronic lymphocytic leukemia and acts as a docking site of nonreceptor kinases: implications for therapy." Blood 117, no. 6 (2011): 1928–37. http://dx.doi.org/10.1182/blood-2010-09-305649.

Full text

Abstract:

Abstract Recently, we detected that chronic lymphocytic leukemia (CLL) B-cell–derived microvesicles in CLL plasma carry a constitutively phosphorylated novel receptor tyrosine kinase (RTK), Axl, indicating that Axl was acquired from the leukemic B cells. To examine Axl status in CLL, we determined the expression of phosphorylated-Axl (P-Axl) in freshly isolated CLL B cells by Western blot analysis. We detected differential levels of P-Axl in CLL B cells, and further analysis showed that expression of P-Axl was correlated with the other constitutively phosphorylated kinases, including Lyn, phos

APA, Harvard, Vancouver, ISO, and other styles

45

Jung, Byeongho, Anita Ng, Pui Yan Chiu, Barbara Sherry та Nicholas Chiorazzi. "Skewing Towards Effector Memory Cells in CLL Is Associated with IGHV -Mutation Status and IFNγ and IL-4". Blood 142, Supplement 1 (2023): 4625. http://dx.doi.org/10.1182/blood-2023-190595.

Full text

Abstract:

Memory T cells are a small, heterogenous population of T cells that remain following pathogen clearance and provide long-lasting protection. They are generally characterized as either central memory (T CM) or effector memory (T EM) based on differences in their surface and intracellular markers, anatomic location, effector function, and cytokine production. It is well known that patients with chronic lymphocytic leukemia (CLL) display differences in both T cell function and population compared to healthy individuals. Previous studies have shown that CLL patients skew towards the CD4 + memory c

APA, Harvard, Vancouver, ISO, and other styles

46

Burger, Jan A., Meike Burger, and Thomas J. Kipps. "Chronic Lymphocytic Leukemia B Cells Express Functional CXCR4 Chemokine Receptors That Mediate Spontaneous Migration Beneath Bone Marrow Stromal Cells." Blood 94, no. 11 (1999): 3658–67. http://dx.doi.org/10.1182/blood.v94.11.3658.

Full text

Abstract:

Abstract Chemokines play a central role for lymphocyte trafficking and homing. The mechanisms that direct the tissue localization of B cells from patients with chronic lymphocytic leukemia (B-CLL) are unknown. We found that CLL B cells express functional CXCR4 receptors for the chemokine stromal cell-derived factor-1 (SDF-1), as demonstrated by receptor endocytosis, calcium mobilization, and actin polymerization assays. Moreover, CLL B cells displayed chemotaxis to this chemokine that could be inhibited by monoclonal antibodies (MoAbs) against CXCR4, pertussis toxin, or Wortmannin, a phosphati

APA, Harvard, Vancouver, ISO, and other styles

47

Burger, Jan A., Meike Burger, and Thomas J. Kipps. "Chronic Lymphocytic Leukemia B Cells Express Functional CXCR4 Chemokine Receptors That Mediate Spontaneous Migration Beneath Bone Marrow Stromal Cells." Blood 94, no. 11 (1999): 3658–67. http://dx.doi.org/10.1182/blood.v94.11.3658.423k11_3658_3667.

Full text

Abstract:

Chemokines play a central role for lymphocyte trafficking and homing. The mechanisms that direct the tissue localization of B cells from patients with chronic lymphocytic leukemia (B-CLL) are unknown. We found that CLL B cells express functional CXCR4 receptors for the chemokine stromal cell-derived factor-1 (SDF-1), as demonstrated by receptor endocytosis, calcium mobilization, and actin polymerization assays. Moreover, CLL B cells displayed chemotaxis to this chemokine that could be inhibited by monoclonal antibodies (MoAbs) against CXCR4, pertussis toxin, or Wortmannin, a phosphatidylinosit

APA, Harvard, Vancouver, ISO, and other styles

48

Perri, RT. "Impaired expression of cell surface receptors for B cell growth factor by chronic lymphocytic leukemia B cells." Blood 67, no. 4 (1986): 943–48. http://dx.doi.org/10.1182/blood.v67.4.943.943.

Full text

Abstract:

Abstract Normal human B cell proliferation is controlled by various immunoregulatory signals including the T cell-derived lymphokine B cell growth factor (BCGF). The role of BCGF in the regulation of malignant B cell proliferation is unclear. Therefore, we studied the proliferative response of purified chronic lymphocytic leukemia (CLL) B cells to BCGF. For all CLL patients studied, CLL B cells showed a decreased proliferative response as compared with control B cells for BCGF- induced B cell proliferation (patient 291 +/- 59 cpm v control 3,942 +/- 622, mean +/- SEM). This impaired proliferat

APA, Harvard, Vancouver, ISO, and other styles

49

Perri, RT. "Impaired expression of cell surface receptors for B cell growth factor by chronic lymphocytic leukemia B cells." Blood 67, no. 4 (1986): 943–48. http://dx.doi.org/10.1182/blood.v67.4.943.bloodjournal674943.

Full text

Abstract:

Normal human B cell proliferation is controlled by various immunoregulatory signals including the T cell-derived lymphokine B cell growth factor (BCGF). The role of BCGF in the regulation of malignant B cell proliferation is unclear. Therefore, we studied the proliferative response of purified chronic lymphocytic leukemia (CLL) B cells to BCGF. For all CLL patients studied, CLL B cells showed a decreased proliferative response as compared with control B cells for BCGF- induced B cell proliferation (patient 291 +/- 59 cpm v control 3,942 +/- 622, mean +/- SEM). This impaired proliferative respo

APA, Harvard, Vancouver, ISO, and other styles

50

Ponzoni, Maurilio, and Claudio Doglioni. "Prognostic factors in B-CLL." Advances in Anatomic Pathology 11, no. 3 (2004): 172–73. http://dx.doi.org/10.1097/00125480-200405000-00006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!