Role of auto- and allotransplantation in B-cell chronic lymphocytic leukemia

2004 ◽  
Vol 18 (4) ◽  
pp. 915-926 ◽  
Author(s):  
Emili Montserrat
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Cell Chronic Lymphocytic Leukemia

Somatic ATM Mutations Indicate a Pathogenic Role of ATM in B-Cell Chronic Lymphocytic Leukemia

Blood ◽  
1999 ◽  
Vol 94 (2) ◽  
pp. 748-753 ◽  
Author(s):  
Claudia Schaffner ◽  
Stephan Stilgenbauer ◽  
Gudrun A. Rappold ◽  
Hartmut Döhner ◽  
Peter Lichter
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Point Mutation ◽  
Mutation Analysis ◽  
Germ Line ◽  
Lymphocytic Leukemia ◽  
Pathogenic Role ◽  
Atm Gene ◽  
Cell Chronic Lymphocytic Leukemia

Abstract Deletion in chromosome bands 11q22-q23 is one of the most common chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). It is associated with extensive lymph node involvement and poor survival. The minimal consensus deletion comprises a segment, which contains the ATM gene presenting an interesting candidate gene, as mutations in ATM predispose A-T patients to lymphoid malignancies. To investigate a potential pathogenic role of ATM in B-cell tumorigenesis, we performed mutation analysis of ATM in 29 malignant lymphomas of B-cell origin (B-CLL = 27; mantle cell lymphoma, [MCL] = 2). Twenty-three of these carried an 11q22-q23 deletion. In five B-CLLs and one MCL with deletion of one ATMallele, a point mutation in the remaining allele was detected, which resulted in aberrant transcript splicing, alteration, or truncation of the protein. In addition, mutation analysis identified point mutations in three cases without 11q deletion: two B-CLLs with one altered allele and one MCL with both alleles mutated. In four cases analyzed, theATM alterations were not present in the germ line indicating a somatic origin of the mutations. Our study demonstrates somatic disruption of both alleles of the ATM gene by deletion or point mutation and thus its pathogenic role in sporadic B-cell lineage tumors.

Somatic ATM Mutations Indicate a Pathogenic Role of ATM in B-Cell Chronic Lymphocytic Leukemia

Blood ◽  
1999 ◽  
Vol 94 (2) ◽  
pp. 748-753 ◽  
Author(s):  
Claudia Schaffner ◽  
Stephan Stilgenbauer ◽  
Gudrun A. Rappold ◽  
Hartmut Döhner ◽  
Peter Lichter
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Point Mutation ◽  
Mutation Analysis ◽  
Germ Line ◽  
Lymphocytic Leukemia ◽  
Pathogenic Role ◽  
Atm Gene ◽  
Cell Chronic Lymphocytic Leukemia

Deletion in chromosome bands 11q22-q23 is one of the most common chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). It is associated with extensive lymph node involvement and poor survival. The minimal consensus deletion comprises a segment, which contains the ATM gene presenting an interesting candidate gene, as mutations in ATM predispose A-T patients to lymphoid malignancies. To investigate a potential pathogenic role of ATM in B-cell tumorigenesis, we performed mutation analysis of ATM in 29 malignant lymphomas of B-cell origin (B-CLL = 27; mantle cell lymphoma, [MCL] = 2). Twenty-three of these carried an 11q22-q23 deletion. In five B-CLLs and one MCL with deletion of one ATMallele, a point mutation in the remaining allele was detected, which resulted in aberrant transcript splicing, alteration, or truncation of the protein. In addition, mutation analysis identified point mutations in three cases without 11q deletion: two B-CLLs with one altered allele and one MCL with both alleles mutated. In four cases analyzed, theATM alterations were not present in the germ line indicating a somatic origin of the mutations. Our study demonstrates somatic disruption of both alleles of the ATM gene by deletion or point mutation and thus its pathogenic role in sporadic B-cell lineage tumors.

Role of surface IgM and IgD on survival of the cells from B-cell chronic lymphocytic leukemia

Blood ◽  
2002 ◽  
Vol 99 (6) ◽  
pp. 2277-2278 ◽  
Author(s):  
Simona Zupo ◽  
Giovanna Cutrona ◽  
Massimo Mangiola ◽  
Manlio Ferrarini
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Cell Chronic Lymphocytic Leukemia

Role of the STAT1 pathway in apoptosis induced by fludarabine and JAK kinase inhibitors in B-cell chronic lymphocytic leukemia

2005 ◽  
Vol 46 (3) ◽  
pp. 435-442 ◽  
Author(s):  
Luis Martinez-Lostao ◽  
Javier Briones ◽  
Ignasi Forné ◽  
Monica Martinez-Gallo ◽  
Beatriz Ferrer ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Kinase Inhibitors ◽  
Lymphocytic Leukemia ◽  
Jak Kinase ◽  
Cell Chronic Lymphocytic Leukemia

scholarly journals Role of LFA-1 and ICAM-1 in Cancer

2017 ◽  
Author(s):  
Manuel Reina ◽  
Enric Espel
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Tumor Cells ◽  
Human Body ◽  
Detailed Examination ◽  
Lymphocytic Leukemia ◽  
Lymphocyte Function ◽  
Tumor Growth And Metastasis ◽  
Cell Chronic Lymphocytic Leukemia

The lymphocyte function–associated antigen-1 (LFA-1) (also CD11a/CD18 and alphaLbeta2), is just one of many integrins in the human body, but its significance derives from its exclusive presence in leukocytes. In this review, we summarize the studies relating LFA-1 and its major ligand ICAM-1 (CD54) with cancer, through the function of lymphocytes and myeloid cells on tumor cells. We consider how LFA-1 mediates the interaction of leukocytes with tumors and the role of ICAM-1 in tumor dynamics, which can be independent of its interaction with LFA-1. A more detailed examination of LFA’s role within B-cell chronic lymphocytic leukemia is made. Finally, we discuss the role of LFA-1-harboring exosomes in tumor growth and metastasis.

scholarly journals Role of caspases and apoptosis-inducing factor (AIF) in cladribine-induced apoptosis of B cell chronic lymphocytic leukemia

Leukemia ◽  
2002 ◽  
Vol 16 (10) ◽  
pp. 2106-2114 ◽  
Author(s):  
P Pérez-Galán ◽  
I Marzo ◽  
P Giraldo ◽  
D Rubio-Félix ◽  
P Lasierra ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Induced Apoptosis ◽  
Apoptosis Inducing Factor ◽  
Cell Chronic Lymphocytic Leukemia

scholarly journals miR-15b/16-2 deletion promotes B-cell malignancies

2015 ◽  
Vol 112 (37) ◽  
pp. 11636-11641 ◽  
Author(s):  
Francesca Lovat ◽  
Matteo Fassan ◽  
Pierluigi Gasparini ◽  
Lara Rizzotto ◽  
Luciano Cascione ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Knockout Mice ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Flow Cytometric Analysis ◽  
Lymphocytic Leukemia ◽  
White Pulp ◽  
Cell Chronic Lymphocytic Leukemia

The central role of the microRNA (miR) 15a/16-1 cluster in B-cell oncogenesis has been extensively demonstrated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the deletion of the miR-15a/16-1 locus at 13q14. Despite the well-established understanding of the molecular mechanisms occurring during miR-15a/16-1 dysregulation, the oncogenic role of other miR-15/16 family members, such as the miR-15b/16-2 cluster (3q25), is still far from being elucidated. Whereas miR-15a is highly similar to miR-15b, miR-16-1 is identical to miR-16-2; thus, it could be speculated that both clusters control a similar set of target genes and may have overlapping functions. However, the biological role of miR-15b/16-2 is still controversial. We generated miR-15b/16-2 knockout mice to better understand the cluster’s role in vivo. These mice developed B-cell malignancy by age 15–18 mo with a penetrance of 60%. At this stage, mice showed significantly enlarged spleens with abnormal B cell-derived white pulp enlargement. Flow cytometric analysis demonstrated an expanded CD19+ CD5+ population in the spleen of 40% knockout mice, a characteristic of the chronic lymphocytic leukemia-associated phenotype found in humans. Of note, miR-15b/16-2 modulates the CCND2 (Cyclin D2), CCND1 (Cyclin D1), and IGF1R (insulin-like growth factor 1 receptor) genes involved in proliferation and antiapoptotic pathways in mouse B cells. These results are the first, to our knowledge, to suggest an important role of miR-15b/16-2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.

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