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Journal articles on the topic 'Chronic lymphocytic leukemia'

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Published: 4 June 2021
Last updated: 6 July 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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

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10

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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11

GALE, ROBERT PETER. "Chronic Lymphocytic Leukemia." Annals of Internal Medicine 103, no. 1 (July 1, 1985): 101. http://dx.doi.org/10.7326/0003-4819-103-1-101.

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12

Chiorazzi, Nicholas, Kanti R. Rai, and Manlio Ferrarini. "Chronic Lymphocytic Leukemia." New England Journal of Medicine 352, no. 8 (February 24, 2005): 804–15. http://dx.doi.org/10.1056/nejmra041720.

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13

Munir, Talha. "Chronic lymphocytic leukemia." Hematology 20, no. 4 (April 23, 2015): 245–46. http://dx.doi.org/10.1179/1024533215z.000000000356.

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14

Robak, Tadeusz. "Chronic lymphocytic leukemia." HemaSphere 3 (June 2019): 36. http://dx.doi.org/10.1097/hs9.0000000000000248.

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15

Kay, Neil E., Terry J. Hamblin, Diane F. Jelinek, Gordon W. Dewald, John C. Byrd, Sherif Farag, Margaret Lucas, and Thomas Lin. "Chronic Lymphocytic Leukemia." Hematology 2002, no. 1 (January 1, 2002): 193–213. http://dx.doi.org/10.1182/asheducation-2002.1.193.

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Abstract This update of early stage B-cell chronic lymphocytic leukemia (B-CLL) embraces current information on the diagnosis, biology, and intervention required to more fully develop algorithms for management of this disease. Emphasis on early stage is based on the rapid advancement in our understanding of the disease parameters and our increasing ability to predict for a given early stage patient whether there is a need for more aggressive management. In Section I, Dr. Terry Hamblin addresses the nature of the disease, accurate diagnostic procedures, evidence for an early “preclinical” phase, the use of newer prognostic features to distinguish who will be likely to progress or not, and whether it is best to watch or treat early stage disease. In Section II, Dr. Neil Kay and colleagues address the biologic aspects of the disease and how they may relate to disease progression. Review of the newer insights into gene expression, recurring genetic defects, role of cytokines/autocrine pathways, and the interaction of the CLL B cell with the microenvironment are emphasized. The relationship of these events to both trigger disease progression and as opportunities for future therapeutic intervention even in early stage disease is also considered. In Section III, Dr. John Byrd and colleagues review the historical and now current approaches to management of the previously untreated progressive B-CLL patient. They discuss what decision tree could be used in the initial decision to treat a given patient. The use of single agents versus newer combination approaches such as chemoimmunotherapy are discussed here. In addition, the place of marrow transplant and some of the newer antibodies available for treatment of B-CLL are considered. Finally, a challenge to utilize our growing knowledge of the biology of B-CLL in the early stage B-CLL is proffered.
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16

Byrd, John C., Stephan Stilgenbauer, and Ian W. Flinn. "Chronic Lymphocytic Leukemia." Hematology 2004, no. 1 (January 1, 2004): 163–83. http://dx.doi.org/10.1182/asheducation-2004.1.163.

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Abstract Chronic lymphocytic leukemia (CLL) is one of the most commonly diagnosed leukemias managed by practicing hematologists. For many years patients with CLL have been viewed as similar, with a long natural history and only marginally effective therapies that rarely yielded complete responses. Recently, several important observations related to the biologic significance of VH mutational status and associated ZAP-70 overexpression, disrupted p53 function, and chromosomal aberrations have led to the ability to identify patients at high risk for early disease progression and inferior survival. Concurrent with these investigations, several treatments including the nucleoside analogues, monoclonal antibodies rituximab and alemtuzumab have been introduced. Combination of these therapies in clinical trials has led to high complete and overall response rates when applied as initial therapy for symptomatic CLL. Thus, the complexity of initial risk stratification of CLL and treatment has increased significantly. Furthermore, when these initial therapies do not work, approach of the CLL patient with fludarabine-refractory disease can be quite challenging. This session will describe the natural history of a CLL patient with emphasis on important decision junctures at different time points in the disease. In Section I, Dr. Stephan Stilgenbauer focuses on the discussion that occurs with CLL patients at their initial evaluation. This includes a review of the diagnostic criteria for CLL and prognostic factors utilized to predict the natural history of the disease. The later discussion of risk stratification focuses on molecular and genomic aberrations that predict rapid progression, poor response to therapy, and inferior survival. Ongoing and future efforts examining early intervention strategies in high risk CLL are reviewed. In Section II, Drs. Ian Flinn and Jesus G. Berdeja focus on the discussion of CLL patients when symptomatic disease has developed. This includes an updated review of monotherapy trials with nucleoside analogs and recent trials that have combined these with monoclonal antibodies and/or alternative chemotherapy agents. Appropriate application of more aggressive therapies such as autologous and allogeneic immunotherapy and less aggressive treatments for appropriate CLL patient candidates are discussed. In Section III, Dr. John Byrd focuses on the discussion that occurs with CLL patients whose disease is refractory to fludarabine. The application of genetic risk stratification in choosing therapy for this subset of patients is reviewed. Available data with conventional combination based therapies and monoclonal antibodies are discussed. Finally, alternative promising investigational therapies including new antibodies, kinase inhibitors (CDK, PDK1/AKT, PKC) and alternative targeted therapies (DNA methyltransferase inhibitors, histone deacetylase inhibitors, etc.) are reviewed with an emphasis on the most promising agents for this patient population.
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17

Rozman, Ciril, and Emilio Montserrat. "Chronic Lymphocytic Leukemia." New England Journal of Medicine 333, no. 16 (October 19, 1995): 1052–57. http://dx.doi.org/10.1056/nejm199510193331606.

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18

Flinn, Ian W., and Michael R. Grever. "Chronic lymphocytic leukemia." Cancer Treatment Reviews 22, no. 1 (January 1996): 1–13. http://dx.doi.org/10.1016/s0305-7372(96)90013-4.

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19

FERRARINI, M. "Chronic Lymphocytic Leukemia." Hematology/Oncology Clinics of North America 18, no. 4 (August 2004): xiii—xv. http://dx.doi.org/10.1016/s0889-8588(04)00045-0.

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20

Stahl, Robert L., and Robert Silber. "Chronic Lymphocytic Leukemia." Clinics in Geriatric Medicine 1, no. 4 (November 1985): 857–67. http://dx.doi.org/10.1016/s0749-0690(18)30914-5.

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21

Ghia, Paolo, Andrés J. M. Ferreri, and Federico Caligaris-Cappio. "Chronic lymphocytic leukemia." Critical Reviews in Oncology/Hematology 64, no. 3 (December 2007): 234–46. http://dx.doi.org/10.1016/j.critrevonc.2007.04.008.

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22

Shanshal, Mohammed, and Rami Y. Haddad. "Chronic Lymphocytic Leukemia." Disease-a-Month 58, no. 4 (April 2012): 153–67. http://dx.doi.org/10.1016/j.disamonth.2012.01.009.

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23

Caguioa, Priscilla B., Sualp Tansan, and Ronald P. McCaffrey. "Chronic Lymphocytic Leukemia." American Journal of the Medical Sciences 308, no. 3 (September 1994): 196–200. http://dx.doi.org/10.1097/00000441-199409000-00016.

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24

Dutcher, Janice P. "Chronic Lymphocytic Leukemia." Medical Oncology 22, no. 2 (June 2005): 211–12. http://dx.doi.org/10.1007/bf03253950.

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25

Kalil, Nelson, and Bruce D. Cheson. "Chronic Lymphocytic Leukemia." Oncologist 4, no. 5 (October 1999): 352–69. http://dx.doi.org/10.1634/theoncologist.4-5-352.

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26

Kipps, Thomas J. "Chronic lymphocytic leukemia." Current Opinion in Hematology 4, no. 4 (1997): 268–76. http://dx.doi.org/10.1097/00062752-199704040-00008.

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27

Kipps, Thomas J. "Chronic lymphocytic leukemia." Current Opinion in Hematology 5, no. 4 (1998): 244–53. http://dx.doi.org/10.1097/00062752-199807000-00003.

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28

Wierda, William G., and Thomas J. Kipps. "Chronic lymphocytic leukemia." Current Opinion in Hematology 6, no. 4 (July 1999): 253. http://dx.doi.org/10.1097/00062752-199907000-00010.

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29

Kipps, Thomas J. "Chronic lymphocytic leukemia." Current Opinion in Hematology 7, no. 4 (July 2000): 223–34. http://dx.doi.org/10.1097/00062752-200007000-00005.

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30

Hallek, Michael, and Natali Pflug. "Chronic lymphocytic leukemia." Annals of Oncology 21 (October 2010): vii154—vii164. http://dx.doi.org/10.1093/annonc/mdq373.

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31

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2001, no. 1205 (December 5, 2001): 100199. http://dx.doi.org/10.1182/ashimagebank-2001-100199.

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32

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2003, no. 0305 (March 5, 2003): 100638. http://dx.doi.org/10.1182/ashimagebank-2003-100638.

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33

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2003, no. 0428 (April 28, 2003): 100690. http://dx.doi.org/10.1182/ashimagebank-2003-100690.

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34

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2003, no. 1124 (November 24, 2003): 100897. http://dx.doi.org/10.1182/ashimagebank-2003-100897.

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35

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2004, no. 0425 (April 25, 2004): 101105. http://dx.doi.org/10.1182/ashimagebank-2004-101105.

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36

Maslak, P. "Chronic Lymphocytic Leukemia." ASH Image Bank 2004, no. 0506 (May 6, 2004): 101114. http://dx.doi.org/10.1182/ashimagebank-2004-101114.

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37

Andritsos, Leslie, and Hanna Khoury. "Chronic lymphocytic leukemia." Current Treatment Options in Oncology 3, no. 3 (June 2002): 225–31. http://dx.doi.org/10.1007/s11864-002-0012-5.

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38

Nabhan, Chadi, and Steven T. Rosen. "Chronic Lymphocytic Leukemia." JAMA 312, no. 21 (December 3, 2014): 2265. http://dx.doi.org/10.1001/jama.2014.14553.

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39

Motta, Marina, William G. Wierda, and Alessandra Ferrajoli. "Chronic lymphocytic leukemia." Cancer 115, no. 17 (September 1, 2009): 3830–41. http://dx.doi.org/10.1002/cncr.24479.

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40

Kipps, Thomas J. "Chronic lymphocytic leukemia." Best Practice & Research Clinical Haematology 20, no. 3 (September 2007): 361–62. http://dx.doi.org/10.1016/j.beha.2007.05.001.

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41

Esber, Natacha, and Thomas Schulz. "Leukemic Meningitis in Chronic Lymphocytic Leukemia." Kansas Journal of Medicine 2, no. 4 (September 1, 2009): 96–98. http://dx.doi.org/10.17161/kjm.v2i4.11303.

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42

Maslak, G. S., G. P. Chernenko, S. V. Abramov, I. Yu Pismenetska, I. V. Davydenko, L. M. Lushnya, and Makarets M. F. "Glycobiom Lymphocytes Surface Study of Patients with B-Cell Chronic Lymphocytic Leukemia." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, no. 6 (December 25, 2021): 134–40. http://dx.doi.org/10.26693/jmbs06.06.134.

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The purpose of the study was to investigate the intensity of exposure of peripheral blood lymphocyte surface glycans in patients with B-cell chronic lymphocytic leukemia by measuring the density of lectin- or antigen-positive epitopes under antitumor therapy in order to evaluate it for a more reasonable selection of qualitative and quantitative composition of therapy. Materials and methods. The objects of the study were blood lymphocytes of patients with chronic lymphocytic leukemia (n=15) aged 58-66 years before and after a course of standard chemotherapy according to the COP scheme. The control group consisted of healthy volunteers (n=15) aged 55 to 65 years. Isolation of lymphocytes was performed by a modified method of A. Boyum. Polyclonal antibodies to α1-acid glycoprotein and fibronectin were used. Exposure to Tn antigen and CD43 on blood lymphocytes was determined with secondary antibodies to mouse immunoglobulins conjugated to FITC (Millipore, USA). To study the exposure of glycans on the surface of lymphocytes, we used a set of seven lectins labeled with FITC. Data recording was performed on a Beckman Flower EPICS flow cytometer. Processing of the results was done using the program FCS3 Express. Results and discussion. Compared with the group of hematologically healthy donors on the surface of lymphocytes in patients with chronic lymphocytic leukemia, a 20-fold increase in the density of exposure to ConA epitopes, 10 times – UEAI- and SNA-positive epitopes were shown; MAA II epitope, Tn, and CD43 antigen densities were increased 100-fold (p <0.01). Exposure densities of MAA II-, Tn-, and CD43-positive epitopes on the plasma membrane of lymphocytes in patients with chronic lymphocytic leukemia receiving alkylation therapy decreased 10-fold relative to treatment data, but remained 10-fold higher than in the group of healthy hematologists. Conclusion. On the plasma membranes of lymphocytes in patients with chronic lymphocytic leukemia, the density of exposure of mannose and neuraminic acid residues was significantly increased. COP therapy reduced the density of these epitopes to control values. A significant increase in the density of carcinogenesis markers – Tn- and CD43-antigens on the plasma membranes of lymphocytes in patients with chronic lymphocytic leukemia has been shown. COP therapy provided only a partial decrease in their density, which indicates the insufficient effectiveness of COP therapy, its inability to completely stop the oncological process in patients with chronic lymphocytic leukemia
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43

Gore, Jill M. "Chronic myeloid leukemia and chronic lymphocytic leukemia." Journal of the American Academy of Physician Assistants 27, no. 2 (February 2014): 45–46. http://dx.doi.org/10.1097/01.jaa.0000442706.18470.9a.

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44

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

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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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45

Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.

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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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46

Piskunova, I. S., T. N. Moiseeva, L. S. Al-Radi, L. V. Plastinina, and S. R. Goryacheva. "Difficulties of anemia diagnosis in patients with B-cell chronic lymphocytic leukemia." Oncohematology 16, no. 2 (June 7, 2021): 40–47. http://dx.doi.org/10.17650/1818-8346-2021-16-2-40-47.

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Cytopenia commonly occurs in case of chronic lymphocytic leukemia. It can either precede the diagnosis of chronic lymphocytic leukemia or appear at any time during the disease. Autoimmune hemolytic anemia, immune thrombocytopenia, and partial red cell aplasia are most often found among cytopenias in chronic lymphocytic leukemia. At the same time, the development of cytopenia may be associated with the displacement of normal hematopoiesis cells by tumor lymphocytes. It is very important to accurately diagnose and identify the cause of cytopenia in chronic lymphocytic leukemia, since the prognosis and therapy differ significantly.
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47

Washburn, Leslie. "CME Chronic lymphocytic leukemia Chronic lymphocytic leukemia: The most common leukemia in adults." Journal of the American Academy of Physician Assistants 24, no. 5 (May 2011): 54–58. http://dx.doi.org/10.1097/01720610-201105000-00009.

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48

Faria, José Roberto de, José Salvador Rodrigues de Oliveira, Rosa Malena Delbone de Faria, Maria Regina Regis Silva, Samuel Goihman, Miohoko Yamamoto, and José Kerbauy. "Prognosis related to staging systems for chronic lymphocytic leukemia." Sao Paulo Medical Journal 118, no. 4 (July 6, 2000): 83–88. http://dx.doi.org/10.1590/s1516-31802000000400002.

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CONTEXT: Chronic lymphocytic leukemia (CLL) is a clonal lymphoproliferative disorder, characterized by B lymphocytic proliferation. CLL is the most frequent adult leukemia in Western countries, accounting for 25 to 30% of all white leukemic patients. OBJECTIVE: To evaluate clinical and staging characteristics in prognosis of chronic lymphocytic leukemia. DESIGN: Evaluation of clinical-staging data. SETTING: Universidade Federal de São Paulo - Escola Paulista de Medicina / Universidade de Alfenas. SAMPLE: 73 patients diagnosed from 1977 to 1994. MAIN MEASUREMENTS: Sex, ethnic origin, age, lymphadenopathy, splenomegaly, hepatomegaly, three or more areas of lymphoid enlargement, hemoglobin (g/dl), lymphocytes/mm³, Platelets/mm³ RESULTS: Mean survival of patients was 76 months, median age was 65 years, ranging from 33 to 87. Forty-four patients (60.3%) were male and 29 (39.7%) female. CONCLUSION: The Binet system determined a better prognosis than Rai.
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49

Dreger, Peter. "Allotransplantation for chronic lymphocytic leukemia." Hematology 2009, no. 1 (January 1, 2009): 602–9. http://dx.doi.org/10.1182/asheducation-2009.1.602.

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AbstractEfforts to develop curative treatment strategies for chronic lymphocytic leukemia (CLL) in recent years have focused on allogeneic stem cell transplantation (alloSCT). The crucial anti-leukemic principle of alloSCT in CLL appears to be the immune-mediated anti-host activities conferred with the graft (graft-versus-leukemia effects, GVL). Evidence for GVL in CLL is provided by studies analyzing the kinetics of minimal residual disease on response to immune modulation after transplantation, suggesting that GVL can result in complete and durable suppression of the leukemic clone. AlloSCT from matched related or unrelated donors can overcome the treatment resistance of poor-risk CLL, ie, purine analogue refractory disease and CLL with del 17p-. Even with reduced-intensity conditioning, alloSCT in CLL is associated with significant mortality and morbidity due to graft-versus-host disease, which has to be weighed against the risk of the disease when defining the indication for transplantation. Therefore, it can be regarded as a reasonable treatment option only for eligible patients who fulfill accepted criteria for poor-risk disease. If alloSCT is considered, it should be performed before CLL has advanced to a status of complete refractoriness to assure an optimum chance for a successful outcome. Prospective trials are underway to prove whether allo-SCT can indeed change the natural history of poor-risk CLL.
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50

Silverman, David A., and Dennis J. Chapron. "Lymphopenic Effect of Carbamazepine in a Patient with Chronic Lymphocytic Leukemia." Annals of Pharmacotherapy 29, no. 9 (September 1995): 865–67. http://dx.doi.org/10.1177/106002809502900906.

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Objective: To report a dramatic and reproducible suppressive effect of carbamazepine on circulating lymphocytes in an elderly woman with chronic lymphocytic leukemia. Case Summary: An elderly woman taking phenytoin for a stroke-associated seizure disorder had lymphocyte count of 28 800 × 106 cells/L. Speculating an unusual lymphadenopathic effect of the phenytoin therapy, carbamazepine therapy was substituted. After 15 weeks of carbamazepine treatment, the lymphocyte count declined to 3200 × 106 cells/L. Because of severe diarrhea, carbamazepine therapy was stopped and phenytoin therapy was reinstituted. At the end of 4 months of phenytoin treatment, the lymphocyte count had increased to 23 200 × 106 cells/L. Phenytoin therapy was discontinued and carbamazepine therapy was begun. The lymphocyte count decreased to 10 700 × 106 cells/L. Severe diarrhea recurred and phenytoin treatment was reinstituted. Over 12 days the lymphocyte count increased to 28 900 × 106 cells/L. Phenytoin therapy was stopped and valproic acid therapy was started. The lymphocyte count continued to increase during valproic acid therapy, reaching a peak of 114 300 × 106 cells/L. Discussion: In this patient with chronic lymphocytic leukemia, carbamazepine therapy had a significant and reproducible lymphopenic effect that was readily reversible upon discontinuation of the drug. Unfortunately, this effect was associated with severe diarrhea, preventing further attempts at exploiting this potentially beneficial action. Conclusions: Carbamazepine had a reproducible suppressive effect on lymphocyte counts in an elderly patient with chronic lymphocytic leukemia. This unique observation raises the possibility that carbamazepine therapy may have a useful effect in patients with chronic lymphocytic leukemia.
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