Relevant bibliographies by topics / Killer cells. Lymphocytic leukemia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Killer cells. Lymphocytic leukemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Killer cells. Lymphocytic leukemia"

1

Correia, Daniel V., Manuela Fogli, Kelly Hudspeth, Maria Gomes da Silva, Domenico Mavilio, and Bruno Silva-Santos. "Differentiation of human peripheral blood Vδ1+ T cells expressing the natural cytotoxicity receptor NKp30 for recognition of lymphoid leukemia cells." Blood 118, no. 4 (July 28, 2011): 992–1001. http://dx.doi.org/10.1182/blood-2011-02-339135.

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Abstract The success of cancer immunotherapy depends on productive tumor cell recognition by killer lymphocytes. γδ T cells are a population of innate-like lymphocytes endowed with strong, MHC-unrestricted cytotoxicity against tumor cells. This notwithstanding, we recently showed that a large proportion of human hematologic tumors is resistant to γδ peripheral blood lymphocytes (PBLs) activated with specific agonists to the highly prevalent Vγ9Vδ2 TCR. Although this probably constitutes an important limitation to current γδ T cell–mediated immunotherapy strategies, we describe here the differentiation of a novel subset of Vδ2− Vδ1+ PBLs expressing natural cytotoxicity receptors (NCRs) that directly mediate killing of leukemia cell lines and chronic lymphocytic leukemia patient neoplastic cells. We show that Vδ1+ T cells can be selectively induced to express NKp30, NKp44 and NKp46, through a process that requires functional phosphatidylinositol 3-kinase (PI-3K)/AKT signaling on stimulation with γc cytokines and TCR agonists. The stable expression of NCRs is associated with high levels of granzyme B and enhanced cytotoxicity against lymphoid leukemia cells. Specific gain-of-function and loss-of-function experiments demonstrated that NKp30 makes the most important contribution to TCR-independent leukemia cell recognition. Thus, NKp30+ Vδ1+ T cells constitute a novel, inducible and specialized killer lymphocyte population with high potential for immunotherapy of human cancer.
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2

García-Muñoz, Ricardo, María-Josefa Nájera, Jesús Feliu, Judith Antón-Remírez, Enrique Ramalle-Gómara, Raquel Marín-Gorricho, Raisa Peralta, et al. "Battle of Thermopylae: 300 Spartans (natural killer cells plus obinutuzumab) versus the immortal warriors (chronic lymphocytic leukemia cells) of Xerxes’ army." Future Science OA 5, no. 10 (December 1, 2019): FSO425. http://dx.doi.org/10.2144/fsoa-2019-0064.

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Aim: To analyze the effects of subcutaneous or intravenous rituximab + lymphokine-activated killer cells, obinutuzumab or ibrutinib on natural killer (NK) cell levels in chronic lymphocytic leukemia and follicular lymphoma patients. Patients & methods: The distribution of peripheral blood NK cells of 31 patients was analyzed by flow cytometry. Results: We detected a decrease of NK cells in peripheral blood below normal range after obinutuzumab treatment. During maintenance treatment with subcutaneous rituximab, an NK cell reduction was less pronounced than after intravenous rituximab treatment, despite lymphokine-activated killer cell infusions. Conclusion: After one dose of obinutuzumab, each NK cell in peripheral blood destroys 25 leukemic cells.
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Wallgren, A., R. Festin, C. Gidlof, M. Dohlsten, T. Kalland, and TH Totterman. "Efficient killing of chronic B-lymphocytic leukemia cells by superantigen-directed T cells." Blood 82, no. 4 (August 15, 1993): 1230–38. http://dx.doi.org/10.1182/blood.v82.4.1230.1230.

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Abstract In vitro studies have indicated that chronic lymphocytic leukemia of B- cell origin (B-CLL) is resistant to cytotoxic effector lymphocytes such as natural killer and lymphokine activated killer (LAK) cells. We show here that B-cell cells are sensitive to Staphylococcal enterotoxin (SE) A-directed T-cell killing. Activation of the target cells by phorbol ester (tetradecanoyl phorbol acetate, [TPA]) greatly enhances their sensitivity to lysis. In SE-dependent cellular cytotoxicity (SDCC), members of the SE superantigen family form a bridge between T cells and target cells expressing major histocompatability complex class II molecules. Binding of SEA to the T-cell-receptor V beta region induces a strong cytotoxic capacity and cytokine production. Cells from 9 B-CLL patients were cultured in the presence or absence of TPA and used as targets in a 4-hour SDCC assay using an allogeneic T-cell line as effector. At an effector:target cell ratio 30:1, 70% to 80% of TPA- induced B-CLL cells were killed. Even at the effector:target ratio of 3:1, 47% +/- 6% of TPA-activated B-cell cells were lysed compared with 13% +/- 2% of resting cells (P < .001). A T-cell line established from a B-CLL patient killed autologous tumor cells as efficiently as allogeneic effectors. SEA-directed T cells were far more lytic to B-CLL cells compared with LAK cells or lectin (phytohemagglutinin-directed T cells. Mechanisms of SDCC lysis were investigated. Effector plus target cell supernatants contained high levels of tumor necrosis factor (TNF)- alpha and interferon-gamma, but these supernatants were not directly toxic to B-CLL cells in short term culture. High concentrations of recombinant TNF-alpha or TNF-beta had no lytic effect. Addition of neutralizing anti-TNF-alpha and anti-TNF-beta antibodies into the SDCC assay did not inhibit SEA-directed T-cell killing. TPA-activated B-CLL cells showed a 1.2- to 13-fold increased expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen (LFA)-1, and LFA-3, whereas expression of HLA class II molecules increased up to 5 times. The expression of CD72, CD40, and BB-1/B7 increased 1.8 to 4.5 times. The role of these surface molecules in SDCC was analyzed in blocking experiments with monoclonal antibodies. Antibodies to ICAM-1, CD18, and HLA-DR abolished the cytotoxicity, and a substantial reduction was seen with antibody to CD72.(ABSTRACT TRUNCATED AT 400 WORDS)
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Wallgren, A., R. Festin, C. Gidlof, M. Dohlsten, T. Kalland, and TH Totterman. "Efficient killing of chronic B-lymphocytic leukemia cells by superantigen-directed T cells." Blood 82, no. 4 (August 15, 1993): 1230–38. http://dx.doi.org/10.1182/blood.v82.4.1230.bloodjournal8241230.

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In vitro studies have indicated that chronic lymphocytic leukemia of B- cell origin (B-CLL) is resistant to cytotoxic effector lymphocytes such as natural killer and lymphokine activated killer (LAK) cells. We show here that B-cell cells are sensitive to Staphylococcal enterotoxin (SE) A-directed T-cell killing. Activation of the target cells by phorbol ester (tetradecanoyl phorbol acetate, [TPA]) greatly enhances their sensitivity to lysis. In SE-dependent cellular cytotoxicity (SDCC), members of the SE superantigen family form a bridge between T cells and target cells expressing major histocompatability complex class II molecules. Binding of SEA to the T-cell-receptor V beta region induces a strong cytotoxic capacity and cytokine production. Cells from 9 B-CLL patients were cultured in the presence or absence of TPA and used as targets in a 4-hour SDCC assay using an allogeneic T-cell line as effector. At an effector:target cell ratio 30:1, 70% to 80% of TPA- induced B-CLL cells were killed. Even at the effector:target ratio of 3:1, 47% +/- 6% of TPA-activated B-cell cells were lysed compared with 13% +/- 2% of resting cells (P < .001). A T-cell line established from a B-CLL patient killed autologous tumor cells as efficiently as allogeneic effectors. SEA-directed T cells were far more lytic to B-CLL cells compared with LAK cells or lectin (phytohemagglutinin-directed T cells. Mechanisms of SDCC lysis were investigated. Effector plus target cell supernatants contained high levels of tumor necrosis factor (TNF)- alpha and interferon-gamma, but these supernatants were not directly toxic to B-CLL cells in short term culture. High concentrations of recombinant TNF-alpha or TNF-beta had no lytic effect. Addition of neutralizing anti-TNF-alpha and anti-TNF-beta antibodies into the SDCC assay did not inhibit SEA-directed T-cell killing. TPA-activated B-CLL cells showed a 1.2- to 13-fold increased expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen (LFA)-1, and LFA-3, whereas expression of HLA class II molecules increased up to 5 times. The expression of CD72, CD40, and BB-1/B7 increased 1.8 to 4.5 times. The role of these surface molecules in SDCC was analyzed in blocking experiments with monoclonal antibodies. Antibodies to ICAM-1, CD18, and HLA-DR abolished the cytotoxicity, and a substantial reduction was seen with antibody to CD72.(ABSTRACT TRUNCATED AT 400 WORDS)
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5

Fehniger, Todd A., Kazuhiro Suzuki, Anand Ponnappan, Jeffrey B. VanDeusen, Megan A. Cooper, Sorin M. Florea, Aharon G. Freud, Michael L. Robinson, Joan Durbin, and Michael A. Caligiuri. "Fatal Leukemia in Interleukin 15 Transgenic Mice Follows Early Expansions in Natural Killer and Memory Phenotype Cd8+ T Cells." Journal of Experimental Medicine 193, no. 2 (January 15, 2001): 219–32. http://dx.doi.org/10.1084/jem.193.2.219.

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Inflammation likely has a role in the early genesis of certain malignancies. Interleukin (IL)-15, a proinflammatory cytokine and growth factor, is required for lymphocyte homeostasis. Intriguingly, the expression of IL-15 protein is tightly controlled by multiple posttranscriptional mechanisms. Here, we engineered a transgenic mouse to overexpress IL-15 by eliminating these posttranscriptional checkpoints. IL-15 transgenic mice have early expansions in natural killer (NK) and CD8+ T lymphocytes. Later, these mice develop fatal lymphocytic leukemia with a T-NK phenotype. These data provide novel evidence that leukemia, like certain other cancers, can arise as the result of chronic stimulation by a proinflammatory cytokine.
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Helfand, SC, JF Modiano, PF Moore, SA Soergel, PS MacWilliams, RD Dubielzig, JA Hank, EW Gelfand, and PM Sondel. "Functional interleukin-2 receptors are expressed on natural killer-like leukemic cells from a dog with cutaneous lymphoma." Blood 86, no. 2 (July 15, 1995): 636–45. http://dx.doi.org/10.1182/blood.v86.2.636.bloodjournal862636.

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We identified a dog with large granular lymphocytic leukemia and cutaneous lymphoma that exhibited constitutive expression of interleukin-2 (IL-2) receptors by the leukemic peripheral blood lymphocytes. The leukemic cells phenotypically resembled natural killer (NK) cells, and their surface IL-2 receptors were functional, as determined by the capacity to bind human recombinant IL-2 with high- affinity resulting in the transduction of proliferation signals and in the development of lymphokine-activated killer cell activity. These cells produced IL-2 spontaneously, and they may have maintained their proliferative state through an IL-2-dependent autocrine growth pathway. Our results indicate that neoplastic lymphocytes of syndromes that involve circulating leukemic cells with dermotropism can originate from NK-like cells. Additionally, the data also suggest that proliferative conditions such as these may be the result of the aberrant production of IL-2. Further, this case illustrates the potential for the use of hematopoietic malignancies in the dog as a suitable animal model for immune targeting of IL-2 receptors as a novel treatment approach for similar malignancies of human beings.
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Ohmori, K., A. Takada, T. Yoneda, Y. Buma, K. Hirashima, K. Tsuyuoka, A. Hasegawa, and R. Kannagi. "Differentiation-dependent expression of sialyl stage-specific embryonic antigen-1 and I-antigens on human lymphoid cells and its implications for carbohydrate-mediated adhesion to vascular endothelium." Blood 81, no. 1 (January 1, 1993): 101–11. http://dx.doi.org/10.1182/blood.v81.1.101.101.

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Abstract Expression of two developmentally regulated carbohydrate antigens, the sialyl stage-specific embryonic antigen-1 (SSEA-1) and I-antigens, in human lymphocytes and lymphocytic leukemia cells was investigated using specific monoclonal antibodies. Sialyl SSEA-1 was expressed only on natural killer (NK) cells, and was essentially absent on resting mature T and B cells among normal peripheral lymphocytes. On the other hand, the I-antigen was strongly expressed on virtually all mature B cells, moderately expressed on most mature T cells, but not expressed on NK cells in normal donors. Expression of the two antigens on normal T and B cells was reversible; in vitro stimulation of normal lymphocytes with concanavalin A (Con A) resulted in the loss of I-antigen and appearance of sialyl SSEA-1 on CD3+ T blasts, whereas stimulation with pokeweed mitogen led to loss of I-antigen expression and appearance of sialyl SSEA-1 antigen on CD19+ B blasts. Among lymphocytic leukemia cells, sialyl SSEA-1 was detected primarily on leukemia cells having immature properties such as most common acute lymphocytic leukemia (cALL) blasts, while the I-antigen was frequently expressed on malignant cells having relatively mature properties, such as those found in adult T- cell leukemia or chronic lymphocytic leukemia, and only occasionally on cALL blasts. Among normal peripheral lymphocytes, the sialyl SSEA-1+I- antigen- NK cells selectively underwent E-selectin (ELAM-1, endothelial- leukocyte adhesion molecule-1)-dependent adhesion to endothelial cells, while the I-antigen+sialyl SSEA-1- mature T and B cells did not, in line with the recent finding that sialyl SSEA-1 serves as a specific ligand for E-selectin. Con A blasts, which are sialyl SSEA-1+I-antigen- , also exhibited significant E-selectin-dependent adhesion to endothelial cells. These results indicate that expression of the sialyl SSEA-1 and I-antigens varies alternately depending on the differentiation/activation status of the lymphocytes, and that this at least partly regulates the behavior of lymphocytes at the vessel wall.
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Ohmori, K., A. Takada, T. Yoneda, Y. Buma, K. Hirashima, K. Tsuyuoka, A. Hasegawa, and R. Kannagi. "Differentiation-dependent expression of sialyl stage-specific embryonic antigen-1 and I-antigens on human lymphoid cells and its implications for carbohydrate-mediated adhesion to vascular endothelium." Blood 81, no. 1 (January 1, 1993): 101–11. http://dx.doi.org/10.1182/blood.v81.1.101.bloodjournal811101.

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Expression of two developmentally regulated carbohydrate antigens, the sialyl stage-specific embryonic antigen-1 (SSEA-1) and I-antigens, in human lymphocytes and lymphocytic leukemia cells was investigated using specific monoclonal antibodies. Sialyl SSEA-1 was expressed only on natural killer (NK) cells, and was essentially absent on resting mature T and B cells among normal peripheral lymphocytes. On the other hand, the I-antigen was strongly expressed on virtually all mature B cells, moderately expressed on most mature T cells, but not expressed on NK cells in normal donors. Expression of the two antigens on normal T and B cells was reversible; in vitro stimulation of normal lymphocytes with concanavalin A (Con A) resulted in the loss of I-antigen and appearance of sialyl SSEA-1 on CD3+ T blasts, whereas stimulation with pokeweed mitogen led to loss of I-antigen expression and appearance of sialyl SSEA-1 antigen on CD19+ B blasts. Among lymphocytic leukemia cells, sialyl SSEA-1 was detected primarily on leukemia cells having immature properties such as most common acute lymphocytic leukemia (cALL) blasts, while the I-antigen was frequently expressed on malignant cells having relatively mature properties, such as those found in adult T- cell leukemia or chronic lymphocytic leukemia, and only occasionally on cALL blasts. Among normal peripheral lymphocytes, the sialyl SSEA-1+I- antigen- NK cells selectively underwent E-selectin (ELAM-1, endothelial- leukocyte adhesion molecule-1)-dependent adhesion to endothelial cells, while the I-antigen+sialyl SSEA-1- mature T and B cells did not, in line with the recent finding that sialyl SSEA-1 serves as a specific ligand for E-selectin. Con A blasts, which are sialyl SSEA-1+I-antigen- , also exhibited significant E-selectin-dependent adhesion to endothelial cells. These results indicate that expression of the sialyl SSEA-1 and I-antigens varies alternately depending on the differentiation/activation status of the lymphocytes, and that this at least partly regulates the behavior of lymphocytes at the vessel wall.
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Moignet, Aline, and Thierry Lamy. "Latest Advances in the Diagnosis and Treatment of Large Granular Lymphocytic Leukemia." American Society of Clinical Oncology Educational Book, no. 38 (May 2018): 616–25. http://dx.doi.org/10.1200/edbk_200689.

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Large granular lymphocyte (LGL) leukemia has been recognized in the World Health Organization classifications among mature T cell and natural killer cell neoplasms and is divided into three categories. Chronic T cell leukemia and natural killer cell lymphocytosis can be considered as a similar spectrum of an indolent disease characterized by cytopenias and autoimmune conditions. The last category, aggressive natural killer cell LGL leukemia is very rare, related to Epstein-Barr virus, and seen mainly in young Asian people. Clonal LGL expansion arises from chronic antigenic stimulation sustained by interleukin-15 and platelet-derived growth factor cytokine signal. Those leukemic cells are resistant to apoptosis, mainly because of constitutive activation of survival pathways including Jak/Stat, MapK, Pi3k-Akt, RasRaf-1, MEK1/ERK, sphingolipid, and NFκB. Stat3 constitutive activation is the hallmark of this lymphoproliferative disorder. Socs3 is downregulated, but no mutation could be found to explain this status. However, several somatic mutations, including Stat3, Stat5b, and tumor necrosis factor alpha–induced protein 3, have been demonstrated recently in LGL leukemia; they are identified in half of patients and cannot explain by themselves LGL leukemogenesis. Recurrent infections as a result of chronic neutropenia, anemia, and autoimmune disorders are the main complications related to LGL leukemia. Despite an indolent presentation, 10% of patients die, mainly because of infectious complications. Current treatments are based on immunosuppressive therapies. A better mechanistic understanding of LGL leukemia will allow future consideration of a personalized therapeutic approach perhaps based on Jak/Stat inhibitors, which may offer better results than current immunosuppressive therapy.
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Fricke, William. "CD11b Is Useful in the Diagnosis of Chronic Lymphocytic Leukemia/Prolymphocytic Leukemia, Mixed Chronic Lymphocytic Leukemia, and Prolymphocytic Leukemia." Blood 104, no. 11 (November 16, 2004): 4806. http://dx.doi.org/10.1182/blood.v104.11.4806.4806.

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Abstract CD11b is well known as an integrin, Mac-1, is often complexed with CD18, and is found on monocytes, granulocytes, and natural killer cells. It also serves as a receptor for iC3b. However, its occurrence in B cell chronic lymphoproliferative disorders is not generally recognized and has not been fully evaluated. To address this issue, a series of B cell leukemias and lymphomas referred for primary diagnosis was evaluated for the presence of CD11b. The purpose was to determine the frequency of its expression on these tumors and to evaluate its diagnostic value. Consecutive cases referred for flow cytometry as possible lymphoproliferative disease were analyzed. Included were bone marrow, peripheral blood, and lymph nodes. All cases were diagnosed according to the WHO classification based on immunophenotypic, morphologic, and clinical findings. The morphologic criteria of Melo (1986) and Bennett (1989) were used for classification of chronic lymphocytic leukemia (CLL), CLL/prolymphocytic leukemia (CLL/PLL), mixed CLL, and PLL. Cases identified as not related to chronic lymphocytic leukemia or prolymphocytic leukemia were recorded but not further analyzed. Similarly, lymph node and spleen-based tumors were excluded from the final analysis. CD11b was present on cells from 32 of 123 cases, including occasional follicular lymphoma, (5/35); mantle cell lymphoma, (1/8); diffuse large B cell lymphoma, (3/9); hairy cell leukemia, (3/5); multiple myeloma, (1/2); lymphoplasmacytic lymphoma, (2/2); nodal marginal zone lymphoma, 0/1); and splenic marginal zone lymphoma, (1/1). However, it was most consistently expressed on CLL that contained increased numbers of prolymphocytes or large cells and on PLL. A total of 16 such cases were found. Morphologic assessment showed them to include 8 CLL/PLL, 3 mixed CLL, 4 PLL, and 1 typical CLL. The typical CLL case included both large cells and prolymphocytes but did not have more than 10% PLs. Five of the 16 cases (31%) were negative for CD5, CD23, and CD38 but were positive for FMC-7. In contrast, the other 11 cases were all CD5(+) and CD23(+); 3/11 were positive for CD38; and 5/11 were positive for FMC-7. Forty-five CLLs also were identified during the study, of which 27 had sufficient data for comparison. Twenty-six of the 27 CLLs were morphologically typical. The remaining case was mixed CLL. All of the CLLs were CD11b(−), CD5(+) and CD23(+); 15/43 were CD38(+), and 6/43 were FMC-7(+). The findings show that CD11b is expressed on chronic B cell lymphoproliferative disorders. In particular, it is expressed on almost all CLL cases that contain large cells or prolymphocytes and on PLL. Inclusion of CD11b in routine screening panels of possible chronic B cell leukemiaa will improve diagnosis of these disorders.
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Dissertations / Theses on the topic "Killer cells. Lymphocytic leukemia"

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黃傑煇 and Kit-fai Wong. "CD56-positive: natural killer cell lymphoma/leukaemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B3198177X.

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Wong, Kit-fai. "CD56-positive natural killer cell lymphoma/leukaemia /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23736197.

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Vyas, Maulik [Verfasser], Peter [Gutachter] Nürnberg, and Von Strandmann Elke [Gutachter] Pogge. "Development of novel trispecific immunoligands (triplebodies) to retarget natural killer cells against chronic lymphocytic leukemia / Maulik Vyas ; Gutachter: Peter Nürnberg, Elke Pogge von Strandmann." Köln : Universitäts- und Stadtbibliothek Köln, 2016. http://d-nb.info/1140164694/34.

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Chu, Peter P. "Immune-mediated apoptosis of chronic lymphocytic leukemia cells /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3031939.

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Suck, Garnet, Yeh Ching Linn, and Torsten Tonn. "Natural Killer Cells for Therapy of Leukemia." Karger, 2016. https://tud.qucosa.de/id/qucosa%3A71644.

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Clinical application of natural killer (NK) cells against leukemia is an area of intense investigation. In human leukocyte antigen-mismatched allogeneic hematopoietic stem cell transplantations (HSCT), alloreactive NK cells exert powerful anti-leukemic activity in preventing relapse in the absence of graft-versus-host disease, particularly in acute myeloid leukemia patients. Adoptive transfer of donor NK cells post-HSCT or in non-transplant scenarios may be superior to the currently widely used unmanipulated donor lymphocyte infusion. This concept could be further improved through transfusion of activated NK cells. Significant progress has been made in good manufacturing practice (GMP)-compliant large-scale production of stimulated effectors. However, inherent limitations remain. These include differing yields and compositions of the end-product due to donor variability and inefficient means for cryopreservation. Moreover, the impact of the various novel activation strategies on NK cell biology and in vivo behavior are barely understood. In contrast, reproduction of the thirdparty NK-92 drug from a cryostored GMP-compliant master cell bank is straightforward and efficient. Safety for the application of this highly cytotoxic cell line was demonstrated in first clinical trials. This novel ‘off-theshelf’ product could become a treatment option for a broad patient population. For specific tumor targeting chimeric-antigen-receptor-engineered NK-92 cells have been designed.
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Reed, Reiss. "Investigating the role of T-cells in chronic lymphocytic leukemia." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/73613/.

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T-cells appear to have multiple conflicting roles in CLL. On the one hand tumour-specific T-cells could be used to deliver effective immunotherapy; on the other hand, certain T-cell populations may enhance CLL survival and disease progression. The aim of this thesis was to address these contradictory aspects and to provide a deeper understanding of the role of T-cells in CLL. Firstly, candidate peptides from the pro-apoptotic protein Bax were used to activate potential CLL specific T-cells from HLA-A2+ patients. A CD8+ T-cell clone (6C5) was isolated and it’s specificity was initially mapped to (Bax161-170; LLSYFGTPT) and(Bax160–170; GLLSYFGTPT). However, 6C5 failed to recognise HLA-A2+ CLL cells in vitro, and failed to recognise highly purified forms of the peptides. Further characterisation, involving mass spectrometry and HPLC, mapped T-cell specificity to a modified peptide (LLSY(3-tBu)FGTPT). A second strand of this project involved detailed phenotypic analysis of T-cells from CLL patients (n=97) in order to investigate the basis for immune dysfunction. This analysis indicated that patients with an inverted CD4:CD8 ratio (CLLIR), displayed a skewing towards a highly differentiated T-cell phenotype, as well as expression of markers associated with replicative senescence (CD57+, CD27-) within CD4+ and CD8+ T-cell compartments. In addition, CD4+ T-cells expressing markers associated with immunosuppression (PD-1+, TIM-3+) were also increased in CLLIR. Importantly, the inversion of the CD4:CD8 ratio was associated with shorter progression-free survival. Furthermore, the frequencies of distinct T-cell populations were also shown to haveprognostic impact in both univariate analysis (CD4+PD-1+, CD4+CD57+, CD8+CD57+ and CD8+CD27-) and multivariate analysis (CD4+CD27-PD-1+LAG-3+ and CD8+CD27- CD57+PD-1+). To further evaluate the differences between CLLIR and CLLNR patients, preliminary transcriptional analysis was performed, focusing on genes associated with T-cell function. By contrast, transcriptional analysis suggested that genes associated with activation rather than suppression were enriched in CLLIR.
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Wang, Qiao. "Analysis of the role of invariant V[alpha]24+NKT cells in the pathogenesis of chronic lymphocytic leukaemia /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16185.pdf.

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Imam, Hasan. "Effects of protein kinase inhibitors on chronic lymphocytic leukemia (CLL) cells." Thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-73883.

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B cell Chronic lymphocytic leukemia (B-CLL) is a neoplastic disorder characterized by accumulation of B lymphocytes due to uncontrolled growth and resistance to apoptosis. Src family kinases (SFKs) are non receptor tyrosine kinases present in the cytosol, which couple with downstream B cell receptor signaling and thus mediate growth, survival, proliferation and antiapoptosis. In CLL cells SFKs are remarkably overexpressed, especially Lyn kinase. This gives the rational to use SFKs inhibitor to treat CLL. Addition of the specific pharmacological inhibitors of SFKs, bosutinib and saracatinib, inhibited the global tyrosine phosphorylation as well as the basal auto-phosphorylation of SFKs. Mechanistically, inhibition of SFKs is coupled to apoptosis induction via decreased protein levels of the anti-apoptotic proteins Bcl-2, Mcl-1 and survivin, which were demonstrated by Western blotting. To assess apoptosis induction, annexin V binding to freshly isolated CLL cells with or without treatment with kinase inhibitors was measured flow cytometrically. Using the inhibitors at a concentration of 10 μM the average percentages of annexin V-positive, apoptotic cells in 11 CLL samples increased from 24 % in untreated controls to 55 %, 45 % and 37 % after treatment with bosutinib, saracatinib and dasatinib, respectively. The response to each of the inhibitors showed a high but comparable degree of variation among the investigated CLL samples. On the average bosutinib induced apoptosis with significantly higher efficiency than dasatinib, which calls for further investigation of its pre-clinical potential for treatment of CLL.
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Bento, Rui Pedro Garcia de Oliveira. "CAR-modified T cells targeted to CD19 antigen for lymphocytic leukemia." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13445.

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Mestrado em Biomedicina Farmacêutica
Cellular immunotherapies, or Advanced Therapy Medicinal Products (ATMPs), are emerging as novel and specific therapeutic approaches to treat diseases, such as certain types of leukemias, which are difficult or impossible to treat with today’s biopharmaceutical products. Breakthroughs in basic, preclinical, and clinical science spanning cellular immunology, and cellprocessing technologies has allowed clinical applications of chimeric antigen receptor–based therapies. A recent example is CTL019, a lentivirus-based gene therapy for autologous T cells, acquired by Novartis in 2012 through a global alliance with the University of Pennsylvania. Although this technology is still in its infancy, clinical trials have already shown clinically significant antitumor activity in chronic lymphocytic leukemia and acute lymphocytic leukemia. Trials targeting a variety of other adult and pediatric malignancies are under way. The potential to target essentially any tumor-associated cell-surface antigen for which a monoclonal antibody can be made opens up an entirely new arena for targeted therapy of cancer. The regulatory environment for these Advanced Therapies Medicinal Products is complex and in constant evolution. Many challenges lie ahead in terms of manufacturing process, non-conventional supply chain logistics, business models, intellectual property, funding and patient access.
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Merchand, Reyes Giovanna. "Targeting myeloid cells as a potential Chronic Lymphocytic Leukemia therapeutic strategy." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595259890785332.

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Books on the topic "Killer cells. Lymphocytic leukemia"

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Symposium, Takamatsu no Miya Hi Gan Kenkyū Kikin International. Retroviruses in human lymphoma/leukemia: Proceedings of the 15th International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, 1984. Tokyo: Japan Scientific Societies Press, 1985.

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2

Volman, Gail Phyllis Nixon. Analysis of asparagine-linked oligosaccharide structures of chronic lymphocytic leukemia cells. 1986.

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Haas, David Gerard. Cytotoxic T lymphocyte and natural killer cell responses following chemoimmunotherapy of murine L1210 leukemia. 1986.

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4

Graham, Bird Angus, and Calvert Jane E, eds. B lymphocytes in human disease. Oxford: Oxford University Press, 1988.

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(Editor), M. Potter, and F. Melchers (Editor), eds. B1 Lymphocytes in B Cell Neoplasia: 16th Workshop on the Mechanisms of B Cell Neoplasia 1999 (Current Topics in Microbiology and Immunology). Springer, 2000.

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Cerhan, James R., Claire M. Vajdic, and John J. Spinelli. The Non-Hodgkin Lymphomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0040.

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Abstract:
The non-Hodgkin lymphomas (NHL) are a heterogeneous group of over forty lymphoid neoplasms that have undergone a major redefinition over the last twenty-five years, in part due to advances in immunology and genetics as well as implementation of the WHO classification system. NHLs are considered clonal tumors of B-cells, T-cells, or natural killer (NK) cells arrested at various stages of differentiation, regardless of whether they present in the blood (lymphoid leukemia) or lymphoid tissues (lymphoma). In the United States, the age-standardized NHL incidence rate (per 100,000) doubled from 1973 (10.2) to 2004 (21.4) and then stabilized, while five-year relative survival rates improved from 42% in 1973 to 70% in 2004. Established risk factors for NHL or specific NHL subtypes include infectious agents (HTLV-1, HIV, EBV, HHV8, HCV, H. pylori), immune dysregulation (primary immunodeficiency, transplantation, autoimmunity, and immunosuppressive drugs), family history of lymphoma, and common genetic variants identified by genome-wide association studies.
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Book chapters on the topic "Killer cells. Lymphocytic leukemia"

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Ziegler-Heitbrock, H. W. L., B. Emmerich, H. Theml, W. Siegert, and G. Riethmüller. "Killer Cells in Leukemia." In Modern Trends in Human Leukemia VI New Results in Clinical and Biological Research Including Pediatric Oncology, 508–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70385-0_102.

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Valkova, Veronika. "Chronic Lymphocytic Leukemia: Allogeneic Stem Cell Transplantation." In Stem Cells and Cancer Stem Cells, Volume 6, 353–64. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2993-3_31.

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Aslan, Burcu, Mary L. Ayres, and Varsha Gandhi. "Ex Vivo Pharmacological Profiling in Chronic Lymphocytic Leukemia Cells." In Methods in Molecular Biology, 19–25. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8876-1_2.

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Teichmann, J. V., W. D. Ludwig, H. Seibt-Jung, G. Sieber, and E. Thiel. "Induction of Lymphokine-Activated Killer (LAK) Cells Against Human Leukemia Cells." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 449–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74621-5_78.

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Sanchez-Correa, Beatriz, Rafael Solana, and Raquel Tarazona. "Aging of Natural Killer Cells in Acute Myeloid Leukemia." In Geriatric Oncology, 1–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44870-1_75-1.

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Sanchez-Correa, Beatriz, Rafael Solana, and Raquel Tarazona. "Aging of Natural Killer Cells in Acute Myeloid Leukemia." In Geriatric Oncology, 153–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-57415-8_75.

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Bernabei, P. A., I. Landini, B. Bartolozzi, I. Banchelli, A. Degli Innocenti o Nocentini, and V. Santini. "Activity of Vinorelbine on B-Chronic Lymphocytic Leukemia Cells In Vitro." In Drug Resistance in Leukemia and Lymphoma III, 473–76. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4811-9_51.

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Caligaris-Cappio, F., L. Bergui, G. Corbascio, L. Tesio, F. Malavasi, P. C. Marchisio, and F. Gavosto. "Membrane-Microfilament Interactions in the Cells of B-Chronic Lymphocytic Leukemia." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 195–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72624-8_43.

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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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Patel, Ashwin, and Somsuvra Ghatak. "Pediatric Leukemia of Natural Killer Cells: Diagnosis and Multi-Agent Chemotherapy." In Pediatric Cancer, Volume 4, 139–51. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6591-7_14.

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Conference papers on the topic "Killer cells. Lymphocytic leukemia"

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Yang, Lin, Sara Beiggi, Yunli Zhang, Robert Schmidt, Spencer B. Gibson, and James B. Johnston. "Abstract 4624: Clinical impact of telomere shortening in normal and leukemia cells in chronic lymphocytic leukemia." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4624.

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Klitgaard, Josephine L., Christian Geisler, and Mikkel W. Pedersen. "Abstract 4585: Targeting of CD5 on chronic lymphocytic leukemia cells with antibody mixtures." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4585.

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Paggetti, Jerome, Guy Berchem, and Etienne Moussay. "Abstract 144: Leukemic exosomes stimulate cells from the microenvironment to promote chronic lymphocytic leukemia." 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.am2014-144.

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Patel, Viralkumar M., Kumudha Balakrishnan, William Wierda, and Varsha Gandhi. "Abstract 3338: Novel caspase-3 activator, L14R8, induces apoptosis in chronic lymphocytic leukemia cells." 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.am2013-3338.

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Gibson, Spencer, WenYan Xiao, Ju Yoon Yoon, Edward Noh, Michelle Brown, and James B. Johnston. "Abstract 5232: Tyrosine kinase inhibitor, gefitinib targets ZAP-70 over expressing chronic lymphocytic leukemia cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5232.

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Bouchard, Eric DJ, Edgard M. Mejia, Iris Gehrke, Armando G. Poeppl, Donna Hewitt, James B. Johnston, Spencer B. Gibson, Grant M. Hatch, and Versha Banerji. "Abstract 3052: NAMPT inhibition induces mitochondrial dysfunction leading to apoptosis in chronic lymphocytic leukemia cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3052.

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Zhang, Suping, Christina Wu, Jessie Farrah-Fecteau, Bing Cui, Liguang Chen, Ling Zhang, Rongrong Wu, et al. "Abstract 5472: Targeting chronic lymphocytic leukemia cells with a humanized monoclonal antibody specific for CD44." 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.am2013-5472.

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Mendez, Mariana T., Hasan Mahmud, Sara K. Vesely, Jennifer Holter-Chakrabarty, and Asish K. Ghosh. "Abstract 3749: MER receptor tyrosine kinase overexpression potentiates survival signal in chronic lymphocytic leukemia cells." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3749.

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Walter, Roland, Khouloud Kouidri, Jessica Peter, Martine Pape, Laura Merschen, Bjoern Haeupl, Carmen Doebele, et al. "Abstract 2692: Elucidation of the pre-B-cell receptor signaling network in acute lymphocytic leukemia 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.am2018-2692.

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Pei, Lirong, Jeong-Hyeon Choi, Jimei Liu, Gerald Arthur, Jennifer L. Schnabel, Kristen H. Taylor, Charles W. Caldwell, Xinguo Wang, and Huidong Shi. "Abstract 4791: Genome-wide DNA methylation maps in chronic lymphocytic leukemia cells determined by next-generation sequencing." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4791.

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