scholarly journals Molecular Determinants of Scaffold-induced Linear Ubiquitinylation of B Cell Lymphoma/Leukemia 10 (Bcl10) during T Cell Receptor and Oncogenic Caspase Recruitment Domain-containing Protein 11 (CARD11) Signaling

2016 ◽  
Vol 291 (50) ◽  
pp. 25921-25936 ◽  
Author(s):  
Yong-Kang Yang ◽  
Chao Yang ◽  
Waipan Chan ◽  
Zhaoquan Wang ◽  
Katelynn E. Deibel ◽  
...  
1989 ◽  
Vol 1 (1) ◽  
pp. 15-22 ◽  
Author(s):  
James K. Park ◽  
Timothy W. McKeithan ◽  
Michelle M. le Beau ◽  
Mitchell A. Bitter ◽  
Wilbur A. Franklin ◽  
...  

Hematology ◽  
2013 ◽  
Vol 18 (3) ◽  
pp. 138-143 ◽  
Author(s):  
Xianfeng Zha ◽  
Qingsong Yin ◽  
Huo Tan ◽  
Chunyan Wang ◽  
Shaohua Chen ◽  
...  

2016 ◽  
Vol 70 (7) ◽  
pp. 575-578 ◽  
Author(s):  
Ali Ismail ◽  
Jawed A Mallick ◽  
Dahui Qin ◽  
Mohammad O Hussaini

AimTo report the first case of a Richter syndrome where small lymphocytic lymphoma (SLL) progressed to a CD3+ diffuse large B-cell lymphoma (DLBCL).MethodsMacrodissection of small and large cell lymphomatous components was performed. This was followed by flow cytometric analysis along with molecular B-cell immunoglobulin (heavy and light chains) and T-cell receptor (γ and β chains) gene rearrangement studies to investigate a clonal relationship between the components.ResultsThe immunophenotypic profile was similar between small and large cell components of the lymphoma by flow cytometry. Furthermore, shared clonal peaks were observed between both components based on molecular B-cell and T-cell receptor gene rearrangement studies, confirming a clonal relationship.ConclusionsChronic lymphocytic leukaemia/SLL may rarely undergo Richter transformation to a DLBCL demonstrating lineage infidelity. This is a potentially important diagnostic pitfall and such cases should not be confused with a de novo T-cell lymphoma.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Liang Wang ◽  
Meng Xu ◽  
Chunyan Wang ◽  
Lihua Zhu ◽  
Junyan Hu ◽  
...  

Restricted T-cell receptor (TCR) Vα/Vβrepertoire expression and clonal expansion ofαβT cells especially for putative tumor-associated antigens were observed in patients with hematological malignancies. To further characterize theγδT-cell immune status in B-cell non-Hodgkin lymphoma (B-NHL), we investigated the distribution and clonality of TCR Vγ/Vδrepertoire in peripheral blood (PB), bone marrow (BM), and lymph node (LN) from patients with B-NHL. Four newly diagnosed B-NHL cases, including three with diffuse large B-cell lymphoma (DLBCL) and one with small lymphocytic lymphoma (SLL), were enrolled. The restrictive expression of TCR Vγ/Vδsubfamilies with different distribution patterns could be detected in PB, BM, or LN from all of four patients, and partial subfamily T cells showed clonal proliferation. At least one clonally expanded Vδsubfamily member was found in PB from each patient. However, the expression pattern and clonality of TCR Vγ/Vδchanged in different immune organs and showed individual feature in different patients. The clonally expanded Vδ5, Vδ6, and Vδ8 were detected only in PB but neither in BM nor LN while clonally expanded Vδ2 and Vδ3 could be detected in both PB and BM/LN. In conclusion, the results provide a preliminary profile of distribution and clonality of TCRγ/δsubfamilies T cells in PB, BM, and LN from B-NHL; similar clonally expanded Vδsubfamily T cells in PB and BM may be related to the same B-cell lymphoma-associated antigens, while the different reactive clonally expanded Vγ/VδT cells may be due to local immune response.


Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 612-615 ◽  
Author(s):  
JE Groopman ◽  
JL Sullivan ◽  
C Mulder ◽  
D Ginsburg ◽  
SH Orkin ◽  
...  

Abstract Lymphoma occurs at increased frequency in patients with the acquired immunodeficiency syndrome (AIDS). We studied, using serologic and molecular techniques, one such lymphoma for (a) evidence of infection with human T lymphotropic virus, type III (HTLV-III), and Epstein-Barr virus (EBV), (b) monoclonal rearrangement of immunoglobulin and T cell receptor genes, and (c) rearrangement of the c-myc oncogene. Immunoglobulin and T cell receptor gene studies demonstrated that the tumor was of monoclonal B cell origin. Similar to cases of Burkitt's lymphoma unrelated to AIDS, there were DNA sequences in the lymphoma that hybridized to EBV-specific probes and demonstrated evidence of c- myc rearrangement. HTLV-III sequences were not detected in the malignant B cells. The pathogenesis of some B cell neoplasms in patients with the syndrome may involve transformation by EBV and deregulation of oncogene expression without direct infection of the malignant B cells by HTLV-III.


Sign in / Sign up

Export Citation Format

Share Document