Relevant bibliographies by topics / Chronic lymphocytic leukemia

Academic literature on the topic 'Chronic lymphocytic leukemia'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Chronic lymphocytic leukemia"

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Hrushik, Amin, Lisa Thomas, Qi Shi, Sudeep Ruparelia, Alfonso Zangardi, and Howard Nash. "Chronic Lymphocytic Leukemia with Bi-Nucleated Lymphocytes." Blood 126, no. 23 (December 3, 2015): 5285. http://dx.doi.org/10.1182/blood.v126.23.5285.5285.

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Abstract Introduction: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. It is very uncommon to find bi-nucleated lymphocytes as a morphological feature in this disorder. Our patient was diagnosed with CLL and was found to have bi-nucleated lymphocytes in the peripheral smear. The mechanism behind this type of morphological feature of lymphocytes is unknown in CLL, and whether it has prognostic value on disease outcome is undetermined. Case Description: 62 y/o man was referred to hematology oncology after diagnosis of small cell lymphocytic leukemia was made s/p a right inguinal lymph node biopsy. His CBC revealed a wbc count of 14,000, Rbc count of 4,360, Absolute lymphocyte count of 11,500 and Platelet count of 125,000. The patient did not have any B-symptoms. On physical exam, a pertinent finding was palpable right axillary adenopathy. The CT of abdomen /pelvic to evaluate these findings. This revealed extensive axillary, abdominal/pelvic lymphadenopathy, hepatosplenomegaly and cardio phrenic lymphadenopathy. The patient had a biopsy of the right inguinal lymph node as well as bone marrow biopsy. Biopsy results showed small lymphocytic cells, some of which show occasional large nucleoli were consistent with small lymphocytic lymphoma/chronic lymphocytic leukemia, and morphologic characteristics of the lymphocytes showed bi-nucleated lymphocytes in peripheral blood smear (figure A). Flow cytometric analysis confirmed a lymphocytic population with lambda light chain restriction, expressing CD5, CD19, CD20, and CD23 consistent with chronic lymphocytic leukemia/small lymphocytic lymphoma. Bone marrow biopsy showed a hypercellular marrow with 75 % cellularity mainly composed of mature lymphocytes with scattered macrophages and eosinophils, Flow cytometric analysis (Clarient FI11-041053) of the bone marrow is interpreted as chronic lymphocytic leukemia/small cell lymphoma with the abnormal B cells representing 56% of the viable white cells. FISH study showed deletion of the ATM gene (11q22-23), D13S319 (13q14) and TP53 (p53) were observed in 29%, 71% and 35.5% of the cells analyzed, respectively. A subset of cells with the 13q deletion (20.5% of the total cells) showed homozygous deletion of D13S319 (13q14). ATM deletion is associated with progressive disease and poor prognosis in cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).He did not have any other previous history of malignancy or hematologic disorder. Discussion: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. To make a diagnosis requires absolute lymphocyte count >4x10 9 and lymphoid cell morphology. In CLL, leukemic cells are small and mature appearing lymphocytes, which have regular nuclear and cytoplasmic outlines and scant weakly basophilic cytoplasm. Surface markers that define a CLL cell are proteins such as antibody light chains (kappa or lambda) and CD proteins (CD5, CD19, CD20, and CD23). In our patient absolute lymphocyte count was 11.5x109 and lymphocytic population showed surface marker lambda light chain and CD proteins CD5, CD19, CD20 and CD23 which was consistent with CLL/SLL on inguinal lymph node biopsy, but morphology of lymphocytes was small and mature bi-nucleated lymphocytes, which is very uncommon. Although bi-nucleated lymphocytes are described in a disorder "Polyclonal chronic B-cell lymphocytosis with bi-nucleated lymphocytes". Detection of an extra chromosome for the long arm of chromosome 3 +i(3)(q10) has been considered a specific marker of Polyclonal B-cell lymphocytosis with binucleated lymphocytes (PPBL),which was not present in our case. One case study by Amouroux et al, included four patients with B-cell CLL who were found to have bi-nucleated lymphocytes. Disease course was stable in one patient, one patient had an indolent course and only one required treatment due to rapid doubling time of lymphocytes. Our patient initiated chemotherapy with Rituxan and Fludara, as he had progressive disease with hepatosplenomegaly, lymph nodes and bone marrow involvement. Conclusion: Bi -nucleated lymphocytes in B-cell CLL are very rare. Explanations as to the etiology of this morphological feature in B-cell CLL is unknown. There is no sufficient evidence that bi-nucleated lymphocytes in CLL has any impact on disease progression. Disclosures No relevant conflicts of interest to declare.
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Fidan, Kemal. "Chronic lymphocytic leukemia." Journal of Current Hematology & Oncology Research 1, no. 3 (August 30, 2023): 59–67. http://dx.doi.org/10.51271/jchor-0014.

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Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is a mature B-cell neoplasm characterized by progressive accumulation of monoclonal B lymphocytes. CLL is considered being identical to SLL. Malignant cells seen in CLL and SLL have the same pathological and immunophenotypic features. The term CLL is used when the disease occurs mainly in the blood, while the term SLL is used when the involvement is mainly nodal.
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Klein, Ami, Michael Lishner, Barbara Bruser, John E. Curtis, Dominick J. Amato, and Aaron Malkin. "Cortisol catabolism by lymphocytes of patients with chronic lymphocytic leukemia." Biochemistry and Cell Biology 68, no. 4 (April 1, 1990): 810–13. http://dx.doi.org/10.1139/o90-118.

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A low rate of catabolism of cortisol by lymphocytes correlates with high sensitivity of the cells to the steroid and causes them to die at a greater rate than control samples. Since lymphocytes of patients with chronic lymphocytic leukemia respond to treatment with glucocorticosteroids and are cortisol sensitive, we attempted to see whether their capability to catabolize cortisol differs from that of normal lymphocytes. No difference was found between the two groups of cells with regard to the pattern of cortisol metabolites. However, the lymphocytes of the chronic lymphocytic leukemia groups showed a total cortisol catabolism per cell that was significantly lower than that of the control group. Patients with low lymphocyte count in peripheral blood showed a relatively higher cortisol metabolism by lymphocytes per cell than those with high counts.Key words: lymphocytes, cortisol, catabolism, chronic lymphocytic leukemia, morbidity.
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Kajtár, Béla, and Hajna Losonczy. "Chronic lymphocytic leukemia." Orvosi Hetilap 149, no. 17 (April 2008): 806–7. http://dx.doi.org/10.1556/oh.2008.28331.

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Vaisitti, Tiziana, Francesca Arruga, and Alessandra Ferrajoli. "Chronic Lymphocytic Leukemia." Cancers 12, no. 9 (September 3, 2020): 2504. http://dx.doi.org/10.3390/cancers12092504.

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Manoharan, A. "Chronic Lymphocytic Leukemia." CA: A Cancer Journal for Clinicians 39, no. 1 (January 1, 1989): 61. http://dx.doi.org/10.3322/canjclin.39.1.61.

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Jain, Preetesh, and Kanti R. Rai. "Chronic Lymphocytic Leukemia." Emerging Cancer Therapeutics 2, no. 2 (August 1, 2011): 329–46. http://dx.doi.org/10.5003/2151-4194.2.2.329.

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Brown, Jennifer R. "Chronic Lymphocytic Leukemia." Hematology/Oncology Clinics of North America 35, no. 4 (August 2021): i. http://dx.doi.org/10.1016/s0889-8588(21)00069-1.

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Rossi, Davide. "Chronic lymphocytic leukemia." HemaSphere 2 (June 2018): 44. http://dx.doi.org/10.1097/hs9.0000000000000133.

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Cheze, Stephane, and Michel Leporrier. "Chronic Lymphocytic Leukemia." American Journal of Cancer 1, no. 2 (2002): 127–43. http://dx.doi.org/10.2165/00024669-200201020-00006.

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Dissertations / Theses on the topic "Chronic lymphocytic leukemia"

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Matthews, Christine. "Molecular genetics of chronic lymphocytic leukemia." Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444515.

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Baliakas, Panagiotis. "Reappraising prognosis in chronic lymphocytic leukemia." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-280943.

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Chronic lymphocytic leukemia (CLL) exhibits remarkable clinical heterogeneity likely reflecting the underlying biological heterogeneity. The genetic landscape of CLL has been recently enriched with mutations within a number of genes proposed as novel prognostic markers. Mounting evidence also supports the pivotal role of the clonotypic B-cell receptor immunoglobulin (BcR IG) in the natural history of CLL. Interestingly, almost 30% of all CLL patients can be assigned to different patient subsets, each defined by expression of a distinct stereotyped BcR IG. Whether stereotyped subsets exhibit distinct clinical behavior is still an issue of debate. The aim of this thesis was to evaluate the prognostic relevance of recurrent gene mutations and to assess the clinicobiological associations and clinical impact of BcR IG stereotypy in CLL. In a cohort of 3490 patients, NOTCH1, SF3B1 and TP53 mutations were enriched within clinically aggressive cases carrying unmutated IGHV genes (U-CLL), frequently co-occurring with trisomy 12, del(11q) and del(17p), respectively. Of note, SF3B1 mutations increased in parallel with increasing timespan between diagnosis and mutational screening. NOTCH1 mutations, SF3B1 mutations and TP53 abnormalities (TP53abs, deletions and/or mutations) correlated with shorter time-to-first-treatment among early stage cases, while in multivariate analysis, only SF3B1 mutations and TP53abs retained independent significance. In a series of 8593 CLL patients, stereotyped subsets showed marked differences in demographics, clinical presentation, cytogenetic aberrations and gene mutational spectrum. Patients within a specific subset generally followed similar clinical courses, whereas patients in different stereotyped subsets—even when displaying similar IG somatic hypermutation status— experienced significantly different clinical outcome. In particular, subset #2 (IGHV3-21/IGLV3-21), the largest overall, was found to exhibit (i) a remarkably high incidence of SF3B1 mutations (44%), alluding to subset-biased acquisition of genomic aberrations, in the context of particular antigenic stimulation; and, (ii) a dismal clinical outcome, distinct from the remaining IGHV3-21 CLL. Our findings strongly support the adverse clinical impact of SF3B1 mutations in CLL in addition to TP53abs. BcR IG stereotypy also emerges as prognostically relevant, further highlighting that an immunogenetic sub-classification of CLL based on BcR IG configuration could refine patient risk stratification.
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Beckwith, Kyle Addison. "Novel Immunotherapeutic Strategies for Chronic Lymphocytic Leukemia." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461203257.

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Hing, Zachary Andrew. "Targeting Nuclear Export in Chronic Lymphocytic Leukemia." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523543484958313.

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Sevov, Marie. "RNA-based Prognostic Markers in Chronic Lymphocytic Leukemia." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-133250.

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Chronic lymphocytic leukemia (CLL) is a heterogeneous disease where a significant proportion of patients will develop an aggressive disease. Today, the mutational status of the immunoglobulin heavy variable (IGHV) genes is one of the strongest prognostic markers in CLL, where unmutated IGHV genes correlate with poor outcome. In addition, IGHV3-21 gene usage is associated with poor prognosis independent of mutational status. Recently, several genes were shown to be differently expressed between IGHV mutated and unmutated CLL and were suggested as prognostic markers. The aim of this thesis was to examine the applicability of these RNA-based prognostic markers in CLL. In papers I and II, the prognostic significance of LPL and TCL1A mRNA expression in CLL was investigated in 140 and 144 patients, respectively. High expression was found to be associated with inferior clinical outcome for both markers. However, CLL cases with mutated IGHV3-21 genes displayed low levels of LPL expression, indicating that LPL cannot identify this poor-risk patient group. In contrast, high TCL1A expression was detected in all IGHV3-21 cases. To elucidate the functionality of LPL in CLL, LPL lipase activity was measured in 33 cases. The lipase activity was found to be invariably low, implying an alternative function for LPL in CLL. In paper III, a comprehensive analysis of five RNA-based markers (LPL, TCL1A, ZAP70, CLLU1 and MCL1) was performed in 252 CLL patients. All RNA-based markers except MCL1 predicted clinical outcome, with LPL being the strongest. Moreover, LPL expression independently predicted overall survival when adjusted for established markers. All of the RNA-based markers added additional prognostic information to established markers, e.g. high LPL expression predicted an inferior outcome in patients with mutated IGHV genes or good-risk cytogenetics. For clinical application, over time stability of prognostic markers is crucial. In paper IV, the expression of LPL, TCL1A, ZAP70 and MCL1 was investigated in samples taken at diagnosis and at a follow-up of seven years in 104 CLL patients. LPL was found to be the most stable marker, displaying high correlation between the sequential samples, whereas ZAP70 and MCL1 varied significantly. TCL1A expression increased at follow-up, which may indicate disease progression as TCL1A promotes cell survival. In summary, this thesis highlights the applicability of RNA-based markers in CLL prognostication, both as single markers or in combination with established markers. In particular, LPL was shown to be the strongest RNA-based marker in terms of prognostic strength and stability.
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Ljungström, Viktor. "Exploring next-generation sequencing in chronic lymphocytic leukemia." Doctoral thesis, Uppsala universitet, Experimentell och klinisk onkologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-302026.

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Next-generation sequencing (NGS) techniques have led to major breakthroughs in the characterization of the chronic lymphocytic leukemia (CLL) genome with discovery of recurrent mutations of potential prognostic and/or predictive relevance. However, before NGS can be introduced into clinical practice, the precision of the techniques needs to be studied in better detail. Furthermore, much remains unknown about the genetic mechanisms leading to aggressive disease and resistance to treatment. Hence, in Paper I, the technical performance of a targeted deep sequencing panel including 9 genes was evaluated in 188 CLL patients. We were able to validate 143/155 (92%) selected mutations through Sanger sequencing and 77/82 mutations were concordant in a second targeted sequencing run, indicating that the technique can be introduced in clinical practice. In Paper II we screened 18 NF-κB pathway genes in 315 CLL patients through targeted deep sequencing which revealed a recurrent 4 base-pair deletion in the NFKBIE gene. Screening of NFKBIE in 377 additional cases identified the mutation in ~6% of all CLL patients. We demonstrate that the lesion lead to aberrant NF-κB signaling through impaired interaction with p65 and is associated with unfavorable clinical outcome. In Paper III we sought to delineate the genetic lesions that leads to relapse after fludarabine, cyclophosphamide, and rituximab treatment. Through whole-exome sequencing of pre-treatment and relapse samples from 41 cases we found evidence of frequent selection of subclones harboring driver mutations and subsequent clonal evolution following treatment. We also detected mutations in the ribosomal protein RPS15 in 8 cases (19.5%) and characterization of the mutations through functional assays point to impaired p53 regulation in cells with mutated RPS15. Paper IV aimed at characterizing 70 patients assigned to three major subsets (#1, #2, and #4) through whole-genome sequencing. Besides recurrent exonic driver mutations, we report non-coding regions significantly enriched for mutations in subset #1 and #2 that may facilitate future molecular studies. Collectively, this thesis supports the potential of targeted sequencing for mutational screening of CLL in clinical practice, provides novel insight into the pathobiology of aggressive CLL, and demonstrates the clinical outcome and cellular effects of NFKBIE and RPS15 mutations.
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Cortese, Diego. "Genomic and transcriptomic sequencing in chronic lymphocytic leukemia." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-303703.

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Identification of recurrent mutations through next-generation sequencing (NGS) has given us a deeper understanding of the molecular mechanisms involved in chronic lymphocytic leukemia (CLL) development and progression and provided novel means for risk assessment in this clinically heterogeneous disease. In paper I, we screened a population-based cohort of CLL patients (n=364) for TP53, NOTCH1, SF3B1, BIRC3 and MYD88 mutations using Sanger sequencing, and confirmed the negative prognostic impact of TP53, SF3B1 or NOTCH1 aberrations, though at lower frequencies compared to previous studies. In paper II, we assessed the feasibility of targeted NGS using a gene panel including 9 CLL-related genes in a large patient cohort (n=188). We could validate 93% (144/155) of mutations with Sanger sequencing; the remaining were at the detection limit of the latter technique, and technical replication showed a high concordance (77/82 mutations, 94%). In paper III, we performed a longitudinal study of CLL patients (n=41) relapsing after fludarabine, cyclophosphamide and rituximab (FCR) therapy using whole-exome sequencing. In addition to known poor-prognostic mutations (NOTCH1, TP53, ATM, SF3B1, BIRC3, and NFKBIE), we detected mutations in a ribosomal gene, RPS15, in almost 20% of cases (8/41). In extended patient series, RPS15-mutant cases had a poor survival similar to patients with NOTCH1, SF3B1, or 11q aberrations. In vitro studies revealed that RPS15mut cases displayed reduced p53 stabilization compared to cases wildtype for RPS15. In paper IV, we performed RNA-sequencing in CLL patients (n=50) assigned to 3 clinically and biologically distinct subsets carrying stereotyped B-cell receptors (i.e. subsets #1, #2 and #4) and revealed unique gene expression profiles for each subset. Analysis of SF3B1-mutated versus wildtype subset #2 patients revealed a large number of splice variants (n=187) in genes involved in chromatin remodeling and ribosome biogenesis. Taken together, this thesis confirms the prognostic impact of recurrent mutations and provides data supporting implementation of targeted NGS in clinical routine practice. Moreover, we provide evidence for the involvement of novel players, such as RPS15, in disease progression and present transcriptome data highlighting the potential of global approaches for the identification of molecular mechanisms contributing to CLL development within prognostically relevant subgroups.
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Dielschneider, Rebecca. "Targeting Susceptible Signaling Pathways in Chronic Lymphocytic Leukemia." Cell Death and Disease, 2014. http://hdl.handle.net/1993/31681.

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Chronic lymphocytic leukemia (CLL) is a cancer of B cells and is the most common leukemia in North America. Current therapies are fraught with challenges, and drug resistance and disease relapse remain common occurrences. Therefore, novel therapies and novel therapeutic strategies are needed to improve CLL therapy. Better yet, therapies targeted at specific weaknesses of CLL cells will ensure maximum efficacy and minimum adverse toxicity. To this end, this thesis focuses on targeting the susceptible BCR pathway and lysosome-mediated cell death pathway using gefitinib and lysosomotropic agents, respectively. Firstly, the novel use of the tyrosine kinase inhibitor gefitinib was explored. This drug was most effective in aggressive ZAP-70+ CLL cells and cell lines. A similar inhibitor, erlotinib, had no effect in CLL. Gefitinib inhibited phosphorylation of Syk and ZAP-70, prevented downstream kinase activation, and supressed the pro-survival BCR response. ZAP-70 is implicated in the mechanism of action of gefitinib as introduction of ZAP-70 into a B cell line increased their sensitivity to gefitinib. Secondly, the novel strategy of targeting lysosomes was explored. The lysosomotropic drugs siramesine, nortriptyline, desipramine, mefloquine, and tafenoquine were all found to induce cytotoxicity and lysosome permeabilization. Lysosome permeabilization was accompanied with lipid peroxidation and followed by loss of mitochondrial membrane potential. Compared with healthy B cells, CLL cells were more sensitive to this cell death pathway. This was potentially due to the overexpression of SPP1 and overproduction of sphingosine, which destabilized lysosomes. Lastly, this thesis explored the clinical utility of these targeted therapies. Both gefitinib and siramesine were more effective in CLL cells than patient T cells. Furthermore, they retained efficacy amid protective stromal cells. Clinical correlations revealed that gefitinib and siramesine were effective in CLL cells with poor prognostic features. Siramesine was more effective in male cells and in previously-treated cells. Gefitinib was most effective in young patients. Overall, work presented herein demonstrates the efficacy of the tyrosine kinase inhibitor gefitinib and lysosomotropic agents in primary CLL cells. This work investigates the altered biology of the BCR pathway and lysosomes in CLL cells, and takes advantage of these weaknesses using targeted therapies.
October 2016
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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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Fogelson, Ben. "Mathematical Model of the Chronic Lymphocytic Leukemia Microenvironment." Scholarship @ Claremont, 2009. https://scholarship.claremont.edu/hmc_theses/219.

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A mathematical model of the interaction between chronic lymphocytic leukemia (CLL) and CD4+ (helper) T cells was developed to study the role of T cells in cancer survival. In particular, a system of four nonlinear advection diffusion reaction partial differential equations were used to simulate spatial effects such as chemical diffusion and chemotaxis on CLL survival and proliferation.
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Books on the topic "Chronic lymphocytic leukemia"

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Malek, Sami N., ed. Chronic Lymphocytic Leukemia. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8876-1.

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Hallek, Michael, Barbara Eichhorst, and Daniel Catovsky, eds. Chronic Lymphocytic Leukemia. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11392-6.

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Faguet, Guy B., ed. Chronic Lymphocytic Leukemia. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2.

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Kaur, Prabhjot. Chronic Lymphocytic Leukemia. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70603-0.

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1939-, Polliack Aaron, and Catovsky D, eds. Chronic lymphocytic leukemia. Chur, Switzerland: Harwood Academic Publishers, 1988.

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Malek, Sami, ed. Advances in Chronic Lymphocytic Leukemia. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8051-8.

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B, Moreau Inès, ed. Chronic lymphocytic leukemia: New research. New York: Nova Science Publishers, 2008.

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Chadi, Nabhan, ed. Chronic lymphocytic leukemia research focus. New York: Nova Science Publishers, 2006.

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1946-, Cheson Bruce D., ed. Chronic lymphoid leukemias. 2nd ed. New York: Marcel Dekker, 2001.

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1946-, Cheson Bruce D., ed. Chronic lymphocytic leukemia: Scientific advances and clinical developments. New York: Dekker, 1993.

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Book chapters on the topic "Chronic lymphocytic leukemia"

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Marti, Gerald E., and Vincent Zenger. "The Natural History of CLL." In Chronic Lymphocytic Leukemia, 3–54. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_1.

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Rai, Kanti R., and Niraj Gupta. "Staging of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 193–99. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_10.

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Bosch, Francesc, and Emili Montserrat. "Prognostic Indicators of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 201–15. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_11.

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Dighiero, Guillaume. "Guidelines for Clinical Management of CLL." In Chronic Lymphocytic Leukemia, 219–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_12.

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Ferrajoli, Alessandra, Michael J. Keating, and Susan M. O’Brien. "Chemotherapy of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 241–54. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_13.

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Michallet, Mauricette. "Autologous and Allogeneic Transplantations for Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 255–68. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_14.

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Lin, Thomas S., Margaret S. Lucas, and John C. Byrd. "Monoclonal Antibody Therapy in Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 269–98. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_15.

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Frankel, Arthur E., and Robert J. Kreitman. "Immunotoxin Therapy of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 299–314. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_16.

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Hegde, Upendra P., and Wyndham H. Wilson. "New Treatment Strategies in Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 315–28. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_17.

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Castro, Januario E., and Thomas J. Kipps. "Gene Therapy of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 329–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_18.

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Conference papers on the topic "Chronic lymphocytic leukemia"

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Kundu, Abhisek, Hatice Gulcin Ozer, Tara Borlawsky, Kristin C. Circle, Kun Huang, and Philip Payne. "Clinical Attribute Network for Chronic Lymphocytic Leukemia." In 2009 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2009. http://dx.doi.org/10.1109/bibm.2009.77.

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Wand, Ori, Dovev Cohen, Alexandra Osadchy, Lilach Israeli-Shani, Keren Cohen-Hagai, and David Shitrit. "Bronchiectasis in Patients with Chronic Lymphocytic Leukemia." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa387.

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Wand, O., D. Cohen, A. Osadchy, L. Israeli-Shani, K. Cohen-Hagai, and D. Shitrit. "Bronchiectasis in Patients With Chronic Lymphocytic Leukemia." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2154.

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Moskalets, O. V. "The incidence of anti-rituximab antibodies in patients with chronic lymphocytic leukemia." In Global science. Development and novelty. L-Journal, 2020. http://dx.doi.org/10.18411/gsdn-25-12-2020-05.

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The aim of this study was to investigate the incidence of antibodies to rituximab, a chimeric monoclonal antibody targeted against the pan-B-cell marker CD20, in patients with chronic lymphocytic leukemia. Serum concentrations of anti-rituximab antibodies were determined in patients with B-chronic lymphocytic leukemia (newly diagnosed and resistant / recurrent forms, previously treated by rituximab) and healthy controls. Results: none of the patients with newly diagnosed disease have antibodies to rituximab. Positive results were recorded in 8 (33%) patients who received rituximab earlier.
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Brahmandam, S., S. Brahmandam, and K. El-Kersh. "Pseudohyperkalemia Associated with Chronic Lymphocytic Leukemia: Diagnostic Dilemma." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2989.

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Thota, V., S. Konduru, M. Paravathaneni, R. Chaudhari, B. Baralo, S. Iqbal, and J. Nair. "Recurrent Post-Obstructive Pneumonia in Chronic Lymphocytic Leukemia." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3977.

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Ajibola, O., S. Ramineni, P. Rani, R. Mazurkiewicz, and T. Collins. "Chronic Lymphocytic Leukemia an Unusual Cause of Hydropneumothorax." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1948.

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Villegas, Antonio, and Konstantin E. Starkov. "Global Dynamics of one Chronic Lymphocytic Leukemia Model." In 2015 International Conference on Mechatronics, Electronics and Automotive Engineering (ICMEAE). IEEE, 2015. http://dx.doi.org/10.1109/icmeae.2015.49.

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Moskalets, O. V. "Anti-rituximab antibodies in refractory / relapsing cases of chronic lymphocytic leukemia." In General question of world science. L-Journal, 2020. http://dx.doi.org/10.18411/gq-30-11-2020-02.

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Rituximab, a chimeric monoclonal antibody targeted against the pan-B-cell marker CD20, is widley used for treatment of lymphomas, rheumatologic diseases and other – 8 – General question of world science disorders. It is known that many monoclonal antibodies such as rituximab can elicit anti-drug antibodies, which may interfere with therapeutic response. The aim of this study was to investigate the incidence of antibodies to rituximab in patients with chronic lymphocytic leukemia. Serum concentrations of anti-rituximab antibodies was determined in blood serum of patients with B-chronic lymphocytic leukemia (newly diagnosed and resistant / recurrent forms, previously treated by rituximab) and healthy controls. Results: none of the patients with newly diagnosed disease have antibodies to rituximab. Positive results were recorded in 8 (33%) patients who received rituximab earlier
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Lau, J., M. Cecchini, E. S. Yi, and H. R. Cajigas. "More Than Meets the Eye: Bronchopulmonary Leukemic Infiltrates in Chronic Lymphocytic Leukemia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5864.

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Reports on the topic "Chronic lymphocytic leukemia"

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Cui, Di, Weiwei Zheng, Wenjing Zhang, Jie Zhou, and Chuanzhong Mei. A meta-analysis of the association between trisomy 12 and prognosis of chronic lymphocytic leukemia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0031.

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Singer, Ralfi. Insect bite-like reaction showing features of panniculitis in a patient with chronic lymphocytic leukemia. Science Repository OÜ, March 2019. http://dx.doi.org/10.31487/j.cor.2019.01.101.

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Pullarkat, Vinod. Phenotype and Function of Bone Marrow Infiltrating Lymphocytes in Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada486408.

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Pullarkat, Vinod. Phenotype and Function of Bone Marrow Infiltrating Lymphocytes in Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada471557.

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Cui, Di, Jie Zhou, Chuanzhong Mei, Weiwei Zheng, and Erhu Heng. The impact of BIRC3 gene mutation on the prognosis of chronic lymphocytic leukemia：A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0099.

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Report of public meeting to seek input on gaps in chronic lymphocytic leukemia (CLL) radiogenicity research held July 21, 2004. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, October 2005. http://dx.doi.org/10.26616/nioshpub2006100.

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