Selected Topics in Chronic Lymphocytic Leukemia Pathogenesis

Bianchi, Sergio; Dighiero, G; Pritsch, Otto

doi:10.5772/38328

Cited by 3 publications

(4 citation statements)

References 118 publications

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“…CLL is the most common human leukemia, representing 30% of all cases (31), which are characterized as accumulation of B cells due to an imbalance between activation of cell proliferation and inhibition of apoptosis (3,4). Most CLL B cells are characterized by high expression of the p27 protein, which blocks the cell cycle progression (32).…”

Section: Discussionmentioning

confidence: 99%

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Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity

Gong

Shi

et al. 2015

Oncology Reports

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Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, and mainly originates from an accumulation of abnormal B cells caused by the dysregulation of cell proliferation and apoptosis. The aberration of proliferation-related gene in CLL cells induces cell arrest at G0/G1 phase, or a small section shows rapid cell growth, which further complicates the pathogenesis of CLL. The constitutively photomorphogenic 1 (COP1), as an E3 ubiquitin ligase, is involved in many biological processes in mammalian cells, but its role in chronic lymphocytic leukemia (CLL) progression remains unclear. In the present study, we analyzed the expression of COP1 in peripheral blood mononuclear cells (PBMCs) from 23 CLL patients and 3 healthy donors. The observed upregulated expression of COP1 in CLL patients was positively correlated with CLL clinical stage and ZAP-70 expression, but not del(13q14) and del(17q-). Overexpression of COP1 significantly promoted cell colony formation and proliferation, especially contributing to the accumulation of cells in S-phase by inhibition of FoxO1 and p21. Moreover, overexpression of COP1 accelerated tumorigenicity of HG3 cells and promoted xenograft growth. Therefore, the present study revealed that COP1 plays an important role in CLL cell proliferation and tumorigenicity, and may be a useful indicator of the chronic lymphocytic leukemia processes.

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Section: Discussionmentioning

confidence: 99%

“…However, the incidence of this disease is gradually increasing also in China (2). It is characterized by an accumulation of abnormal B cells, resulting from the dysregulation of proliferation and apoptosis (3,4). Despite attempts to develop new treatment strategies, CLL is currently incurable (5,6).…”

Section: Introductionmentioning

confidence: 99%

Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity

Gong

Shi

et al. 2015

Oncology Reports

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“…This deletion, also detected in Monoclonal B cell Lymphocytosis (MBL), found at a much lower frequency in multiple myeloma (MM), diffuse large B-cell lymphoma (DLBCL), mature T-cell lymphomas, and in various solid tumors. 3 CXCR4 (chemokine C-X-C motif receptor 4), also known as CD184, is a chemokine G protein coupled receptor, expressed in various cell species, including normal B lymphocytes. CXCR4 is overexpressed in a multiple number of malignancies including CLL, Acute Myeloid Leukemia (AML), MM, lymphomas, and solid tumors.…”

Section: Introductionmentioning

confidence: 99%

CXCR4 as a prognostic marker in Egyptian chronic lymphocytic leukemia patients

El-Sherif

Eldin

Aly

et al. 2021

EJI

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Chronic lymphocytic leukemia (CLL) has variable clinical presentations, and molecular and biological prognostic markers. The C-X-C chemokine receptor 4 (CXCR4) and its ligand stromal cell-derived factor-1 (SDF-1) play an important role in trafficking of lymphocytes and monocytes. The aim was to study lymphocyte expression of CXCR4 and its prognostic value in CLL. A case control study was carried out on 30 newly diagnosed CLL cases and 30 healthy controls. Fludarabine, cyclophosphamide, and rituximab (FCR) was the standard treatment. Flowcytometric measurement of CXCR4 expression on lymphocytes was done. CXCR4 was significantly higher in patients than controls (81.67 ± 17.95 vs. 11.78 ± 2.78; P< 0.001). CXCR4 was significantly higher (P<0.001) in high risk CLL (93.63 ± 6.78) vs. intermediate risk (82.50 ± 7.13) and low risk (75.84 ± 12.23). CXCR4 was significantly higher (P<0.001) in non-responders (91.63 ± 6.98) vs. partial responders (83.11 ± 5.55) and complete responders (70.11 ± 4.44). CXCR4 was significantly lower in survivors vs. non-survivors (80.89 ± 5.09 vs. 85.43 ± 5.51; P< 0.001. CXCR4 had significant positive correlation with WBCs (r=0.45, P=0.01) and lymphocytes (r=0.40, P=0.01) measured at diagnosis. In conclusions, expression of CXCR4 in newly diagnosed CLL is significantly high. CXCR4 increased expression is associated with poor prognosis and resistance to the therapy.so it can be used as prognostic tool.

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“…However, the incidence of this disease is gradually increasing in China (2). CLL is characterized by an accumulation of abnormal B cells, resulting from the dysregulation of proliferation and apoptosis rates (3,4). Despite the advance in pathobiologic research and the development of effective treatment regimens, CLL is still largely an incurable disease (5).…”

Section: Introductionmentioning

confidence: 99%

Plumbagin reduces chronic lymphocytic leukemia cell survival by downregulation of Bcl-2 but upregulation of the Bax protein level

Gong

Shi

et al. 2016

Oncology Reports

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Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, and mainly originates from an accumulation of abnormal B cells caused by the dysregulation of cell proliferation and apoptosis rates. The aberration of apoptosis-related genes in CLL cells results in defective apoptosis of CLL cells in response to traditional therapeutic medicine. Plumbagin (5-hydroxy-2-methyl-1, 4-naphthoquinone), a natural compound from Plumbago zeylinica, has been shown to exhibit pro-apoptotic activities in tumor cells. In the present study, we report that plumbagin effectively inhibited CLL cell viability with a lower dose compared to fludarabine, and inhibited cell proliferation in a dose-dependent manner. In addition, plumbagin promoted accumulation of MEC-1 cells in the S phase, and blocked cell cycle transition of HG3 cells from G0/G1 to S phase. Molecularly, plumbagin markedly induced CLL cell apoptosis through reduction of Bcl-2, but through an increase in the Bax protein level. These results suggest that plumbagin may be considered as a potential anticancer agent for CLL therapy.

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Selected Topics in Chronic Lymphocytic Leukemia Pathogenesis

Cited by 3 publications

References 118 publications

Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity

Expression and regulation of COP1 in chronic lymphocytic leukemia cells for promotion of cell proliferation and tumorigenicity

CXCR4 as a prognostic marker in Egyptian chronic lymphocytic leukemia patients

Plumbagin reduces chronic lymphocytic leukemia cell survival by downregulation of Bcl-2 but upregulation of the Bax protein level

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