Award Winner in the Young Investigator Category, 2017 Society for Biomaterials Annual Meeting and Exposition, Minneapolis, MN, April 05-08, 2017: Lymph node stiffness-mimicking hydrogels regulate human B-cell lymphoma growth and cell surface receptor expr

2017 ◽  
Vol 105 (7) ◽  
pp. 1833-1844 ◽  
Author(s):  
F.N.U. Apoorva ◽  
Ye F. Tian ◽  
Timothy M. Pierpont ◽  
David M. Bassen ◽  
Leandro Cerchietti ◽  
...  
Keyword(s):  
Lymph Node ◽  
Cell Surface ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Cell Surface Receptor ◽  
Award Winner ◽  
Young Investigator ◽  
Surface Receptor ◽  
Human B Cell

scholarly journals The Role of Hvem and its Interaction with Btla and Cd160 in b-Cell Lymphoma Progression

2019 ◽  
Author(s):  
Carla Yago-Diez de Juan
Keyword(s):  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Intermediate Stage ◽  
Cell Surface Receptor ◽  
Loss Of Function ◽  
B Cell Lymphomas ◽  
Tumour Implantation ◽  
Surface Receptor ◽  
The One

SUMMARYDespite the fact that the cell surface receptor HVEM (TNFRSF14) appears to be implicated in the development and progression of B-cell lymphomas, its specific role in these tumours is still unclear. On the one hand, HVEM over-expression is related to worse prognosis in some types of B-cell lymphoma and other solid tumours. On the other hand, most mutations of HVEM in B-cell lymphomas are thought to promote tumour growth through the loss of function. Here, we used a CRISPR-Cas9 system to study the effect of HVEM loss on gene expression in a murine model of A20 B-cell lymphoma (belonging to the diffuse large B-cell lymphoma group). We show that loss of HVEM does not affect the doubling rate of A20 tumour cells in culture, but leads to a decrease in BTLA expression. HVEM-deficient A20 cells do not present a different pattern of metastatic dissemination to lymphoid organs compared with unmodified A20 cells. However, we observed a significant expansion of endogenous B-cells as a result of A20 tumour implantation in the thymus. Although we found no differences in the dissemination or progression of HVEM-deficient A20 cells, our results reveal that loss of HVEM alters the leukocyte recruitment capacity of A20 cells in hepatic tumour nodules at the intermediate stage of tumour development, which may be of relevance as a mechanism of immune evasion.

Clustering of extensive somatic mutations in the variable region of an immunoglobulin heavy chain gene from a human B cell lymphoma

Cell ◽  
1986 ◽  
Vol 44 (1) ◽  
pp. 97-106 ◽  
Author(s):  
Michael L. Cleary ◽  
Timothy C. Meeker ◽  
Shoshana Levy ◽  
Elizabeth Lee ◽  
Martha Trela ◽  
...  
Keyword(s):  
B Cell ◽  
Heavy Chain ◽  
Somatic Mutations ◽  
Cell Lymphoma ◽  
Variable Region ◽  
B Cell Lymphoma ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Immunoglobulin Heavy Chain Gene ◽  
Human B Cell

scholarly journals Tumor staging in a Beagle dog with concomitant large B-cell lymphoma and T-cell acute lymphoblastic leukemia

2021 ◽  
pp. 104063872110110
Author(s):  
Alessandro Ferrari ◽  
Marzia Cozzi ◽  
Luca Aresu ◽  
Valeria Martini
Keyword(s):  
Bone Marrow ◽  
Lymph Node ◽  
T Cell ◽  
B Cell ◽  
Cell Lymphoma ◽  
Tumor Staging ◽  
Lymphoblastic Leukemia ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Cell Acute Lymphoblastic Leukemia

An 8-y-old spayed female Beagle dog was presented with peripheral lymphadenomegaly. Lymph node cytology and flow cytometry led to the diagnosis of large B-cell lymphoma (LBCL). We detected minimal percentages of LBCL cells in peripheral blood and bone marrow samples. However, a monomorphic population of neoplastic cells different from those found in the lymph node was found in the bone marrow. T-cell acute lymphoblastic leukemia was suspected based on flow cytometric immunophenotyping. PCR for antigen receptor rearrangement (PARR) revealed clonal rearrangement of both B-cell and T-cell receptors, and the presence of both neoplastic clones in the lymph node, peripheral blood, and bone marrow. The dog was treated with multi-agent chemotherapy but died 46 d following diagnosis. Tumor staging and patient classification are needed to accurately establish a prognosis and select the most appropriate therapeutic protocol.

scholarly journals Plastin-3 is a diagnostic and prognostic marker for pancreatic adenocarcinoma and distinguishes from diffuse large B-cell lymphoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fei Xiong ◽  
Guan-Hua Wu ◽  
Bing Wang ◽  
Yong-Jun Chen
Keyword(s):  
Lymph Node ◽  
B Cell ◽  
Cell Lymphoma ◽  
Quantitative Polymerase Chain Reaction ◽  
B Cell Lymphoma ◽  
Actin Binding ◽  
Rank Test ◽  
Large B Cell Lymphoma ◽  
Tissue Specimens ◽  
Large B Cell

Abstract Background Altered Plastin-3 (PLS3; an actin-binding protein) expression was associated with human carcinogenesis, including pancreatic ductal adenocarcinoma (PDA). This study first assessed differentially expressed genes (DEGs) and then bioinformatically and experimentally confirmed PLS3 to be able to predict PDA prognosis and distinguish PDA from diffuse large B-cell lymphoma. Methods This study screened multiple online databases and revealed DEGs among PDA, normal pancreas, diffuse large B-cell lymphoma (DLBCL), and normal lymph node tissues and then focused on PLS3. These DEGs were analyzed for Gene Ontology (GO) terms, Kaplan–Meier curves, and the log-rank test to characterize their association with PDA prognosis. The receiver operating characteristic curve (ROC) was plotted, and Spearman’s tests were performed. Differential PLS3 expression in different tissue specimens (n = 30) was evaluated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Results There were a great number of DEGs between PDA and lymph node, between PDA and DLBCL, and between PDA and normal pancreatic tissues. Five DEGs (NET1, KCNK1, MAL2, PLS1, and PLS3) were associated with poor overall survival of PDA patients, but only PLS3 was further verified by the R2 and ICGC datasets. The ROC analysis showed a high PLS3 AUC (area under the curve) value for PDA diagnosis, while PLS3 was able to distinguish PDA from DLBCL. The results of Spearman's analysis showed that PLS3 expression was associated with levels of KRT7, SPP1, and SPARC. Differential PLS3 expression in different tissue specimens was further validated by RT-qPCR. Conclusions Altered PLS3 expression was useful in diagnosis and prognosis of PDA as well as to distinguish PDA from DLBCL.

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