scholarly journals CSNK1α1 mediates malignant plasma cell survival

Leukemia ◽  
2014 ◽  
Vol 29 (2) ◽  
pp. 474-482 ◽  
Author(s):  
Y Hu ◽  
W Song ◽  
D Cirstea ◽  
D Lu ◽  
N C Munshi ◽  
...  
Keyword(s):  
Cell Survival ◽  
Plasma Cell ◽  
Malignant Plasma Cell

scholarly journals Whole Transcriptome Profiling Identifies CD93 and Other Plasma Cell Survival Factor Genes Associated with Measles-Specific Antibody Response after Vaccination

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0160970 ◽  
Author(s):  
Iana H. Haralambieva ◽  
Michael T. Zimmermann ◽  
Inna G. Ovsyannikova ◽  
Diane E. Grill ◽  
Ann L. Oberg ◽  
...  
Keyword(s):  
Antibody Response ◽  
Cell Survival ◽  
Plasma Cell ◽  
Specific Antibody ◽  
Transcriptome Profiling ◽  
Specific Antibody Response ◽  
Survival Factor ◽  
Whole Transcriptome ◽  
Cell Survival Factor

scholarly journals Metabolic Links between Plasma Cell Survival, Secretion, and Stress

2018 ◽  
Vol 39 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Wing Y. Lam ◽  
Deepta Bhattacharya
Keyword(s):  
Cell Survival ◽  
Plasma Cell

scholarly journals CD28 Regulates Metabolic Fitness for Long-Lived Plasma Cell Survival

Cell Reports ◽  
2020 ◽  
Vol 31 (12) ◽  
pp. 107815 ◽  
Author(s):  
Adam Utley ◽  
Colin Chavel ◽  
Shivana Lightman ◽  
G. Aaron Holling ◽  
James Cooper ◽  
...  
Keyword(s):  
Cell Survival ◽  
Plasma Cell ◽  
Metabolic Fitness

scholarly journals Analysis of DNA Aneuploidy and c-myc Oncoprotein Content of Canine Plasma Cell Tumors Using Flow Cytometry

1993 ◽  
Vol 30 (6) ◽  
pp. 505-511 ◽  
Author(s):  
K. S. Frazier ◽  
M. E. Hines ◽  
A. I. Hurvitz ◽  
P. G. Robinson ◽  
A. J. Herron
Keyword(s):  
Flow Cytometry ◽  
Plasma Cell ◽  
Malignant Tumors ◽  
Malignant Potential ◽  
Benign Tumors ◽  
Malignant Plasma Cell ◽  
Formalin Fixed Paraffin ◽  
Significant Difference ◽  
Formalin Fixed Paraffin Embedded ◽  
Canine Plasma

To derive a method for determining malignant potential of plasma cell tumors, a retrospective analysis of the DNA ploidy and relative p62c-myc oncoprotein content using bivariate flow cytometry was performed on 23 formalin-fixed, paraffin-embedded tissues from 23 dogs. The samples included one tissue each from 17 males and six females 2 to 16 years of age (mean = 7.5 years). Twelve breeds were represented, including three Cocker Spaniels, three Golden Retrievers, and five of mixed breed. Ten of the samples were histologically classified as malignant-plasma cell tumors, and ten specimens were classified as benign. Three samples of plasmacytic inflammation, from two Cocker Spaniels and one Shih Tsu, were included as controls. The ploidy and relative c-myc content data obtained were compared with the histologic grade. A significant difference in ploidy was found between benign and malignant tumors (P ≤ 0.05). Five of nine malignant plasma cell tumors were aneuploid; the remainder were diploid (4/9) or tetraploid (1/9). Only one of the benign plasmacytomas was aneuploid (1/10), whereas six were diploid (6/10), and three were tetraploid (3/10). All of the controls were diploid (3/32). When relative amounts of p62c-myc from malignant and benign tumors were compared by flow cytometry, a greater significant difference was established (P ≤ 0.01) than by using aneuploidy alone. Relative values of p62c-myc content ranged from 219 to 553 units in 8/10 malignant plasma cell tumors and from 86 to 392 units in 3/10 benign plasmacytomas. The remainder of the neoplasms (2/10 malignant and 7/10 benign) lacked measurable values of p62c-myc above background fluorescence concentrations. Two atypical cutaneous plasmacytomas with later metastasis were included in the study. The results indicate that simultaneous analysis of ploidy and relative p62c-myc concentration can be used as an aid in assessment of malignant potential in canine plasma cell tumors.

scholarly journals CD28 Promotes Plasma Cell Survival, Sustained Antibody Responses, and BLIMP-1 Upregulation through Its Distal PYAP Proline Motif

2015 ◽  
Vol 194 (10) ◽  
pp. 4717-4728 ◽  
Author(s):  
Cheryl H. Rozanski ◽  
Adam Utley ◽  
Louise M. Carlson ◽  
Matthew R. Farren ◽  
Megan Murray ◽  
...  
Keyword(s):  
Cell Survival ◽  
Plasma Cell ◽  
Antibody Responses

scholarly journals Malignant plasma cell lines express a functional CD28 molecule

Leukemia ◽  
1998 ◽  
Vol 12 (4) ◽  
pp. 610-618 ◽  
Author(s):  
X-G Zhang ◽  
D Olive ◽  
J Devos ◽  
C Rebouissou ◽  
M Ghiotto-Ragueneau ◽  
...  
Keyword(s):  
Cell Lines ◽  
Plasma Cell ◽  
Cd28 Molecule ◽  
Malignant Plasma Cell

A Novel Mechanism of Ig and Myc Translocations in AID-Deficient Mice.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 990-990 ◽  
Author(s):  
Alexander L. Kovalchuk ◽  
Elizabeth Mushinski ◽  
Brad Burkholder ◽  
Chen-Feng Qi ◽  
Zhaoyang Li ◽  
...  
Keyword(s):  
Plasma Cell ◽  
Cytidine Deaminase ◽  
Rapid Development ◽  
Cell Phenotype ◽  
Primary Tumors ◽  
Malignant Plasma Cell ◽  
Significant Difference ◽  
Activation Induced Cytidine Deaminase ◽  
Switch Regions

Abstract Consistent with the role of activation induced cytidine deaminase (AID) as a major “catalyst” of aberrant translocations between the Ig switch regions and c-myc, AID-sufficient Bcl-xL transgenic mice rapidly develop transplantable plasmacytomas with classical T(12;15) translocations. Unexpectedly, we found that Bcl-xL transgenic BALB/cAn mice deficient for AID (designated pBxAicda−/− mice) also developed plasma cell tumors but with a lower frequency (24% vs. 62%) and with a longer mean latency (108 d vs. 36 d) than AID-sufficient controls. Six out of nine of primary tumors were shown by interphase FISH to contain a T(12;15) translocation and one other had a T(6;15). pBxAicda−/− tumors did not transplant well because they were presumably in early stages of neoplastic development or had not progressed to full malignancy including association with ascites. Nevertheless, two tumors (4885 and 4961) were successfully transplanted and established as stable cell lines. They exhibited mature plasma cell phenotype (CD45−, CD138+, PC-1+, CD19−, CD23−) and secreted IgM. Gene expression profiling showed no significant difference from control plasma cell tumors of AID-sufficient mice. Detailed molecular and cytogenetic analysis of 4885 uncovered an unusual unbalanced T(12;15) translocation with IgH Cμ and Pvt-1 in a head to tail orientation at the breakpoint, resulting in elevated c-myc expression as detected by qPCR. In contrast, 4961, a T(12;15) negative cell line, had elevated N-myc expression as a result of paracentric inversion of Chr. 12. These rearrangements had no direct association with RAG activity. We conclude that rapid development of malignant plasma cell tumors with reciprocal T(12;15) does require AID, and that in AID deficiency a novel less efficient mechanism can be utilized to bring c-myc and Ig genes into juxtaposition.

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