scholarly journals Systematic identification of personal tumor-specific neoantigens in chronic lymphocytic leukemia

Blood ◽  
2014 ◽  
Vol 124 (3) ◽  
pp. 453-462 ◽  
Author(s):  
Mohini Rajasagi ◽  
Sachet A. Shukla ◽  
Edward F. Fritsch ◽  
Derin B. Keskin ◽  
David DeLuca ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Dna Sequencing ◽  
Lymphocytic Leukemia ◽  
Class I ◽  
Massively Parallel ◽  
Central Tolerance ◽  
Key Points ◽  
Tumor Specificity ◽  
Massively Parallel Dna Sequencing ◽  
Systematic Identification

Key Points Tumor neoantigens are a promising class of immunogens based on exquisite tumor specificity and the lack of central tolerance against them. Massively parallel DNA sequencing with class I prediction enables systematic identification of tumor neoepitopes (including from CLL).

scholarly journals Chronic lymphocytic leukemia cells induce defective LFA-1–directed T-cell motility by altering Rho GTPase signaling that is reversible with lenalidomide

Blood ◽  
2013 ◽  
Vol 121 (14) ◽  
pp. 2704-2714 ◽  
Author(s):  
Alan G. Ramsay ◽  
Rachel Evans ◽  
Shahryar Kiaii ◽  
Lena Svensson ◽  
Nancy Hogg ◽  
...  
Keyword(s):  
T Cell ◽  
Chronic Lymphocytic Leukemia ◽  
Cell Motility ◽  
Rho Gtpase ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Key Points ◽  
Gtpase Activation ◽  
Activation Signaling

Key Points CLL cells induce defects in T-cell LFA-1–mediated migration by altering Rho GTPase activation signaling, downregulating RhoA and Rac1, and upregulating Cdc42. Lenalidomide repairs these T-cell defects by restoring normal Rho GTPase activation signaling.

Novel OTOF gene mutations identified using a massively parallel DNA sequencing technique in DFNB9 deafness

2018 ◽  
Vol 138 (10) ◽  
pp. 865-870 ◽  
Author(s):  
Yanfei Wang ◽  
Yu Lu ◽  
Jing Cheng ◽  
Lei Zhang ◽  
Dongyi Han ◽  
...  
Keyword(s):  
Dna Sequencing ◽  
Gene Mutations ◽  
Massively Parallel ◽  
Sequencing Technique ◽  
Massively Parallel Dna Sequencing

scholarly journals CLL dedifferentiation to clonally related myeloid cells

2020 ◽  
Vol 4 (24) ◽  
pp. 6169-6174
Author(s):  
Qianze Dong ◽  
Yan Xiu ◽  
Aaron Bossler ◽  
Sergei Syrbu ◽  
Hongming Wang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Progenitor Cells ◽  
Myeloid Cells ◽  
Lymphocytic Leukemia ◽  
Key Points ◽  
Myeloid Leukemias ◽  
Acute Myeloid

Key Points Common progenitor cells exist in clonally related concomitant chronic lymphocytic leukemia and acute myeloid leukemias. CLL cells dedifferentiated to clonally related myeloid cells posttransplantation.

scholarly journals Wnt5a induces ROR1 to recruit DOCK2 to activate Rac1/2 in chronic lymphocytic leukemia

Blood ◽  
2018 ◽  
Vol 132 (2) ◽  
pp. 170-178 ◽  
Author(s):  
Md Kamrul Hasan ◽  
Jian Yu ◽  
George F. Widhopf ◽  
Laura Z. Rassenti ◽  
Liguang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Key Points

Key Points Wnt5a enhances activation of Rac1/2 by inducing ROR1 to interact with DOCK2. ROR1-DOCK2 interaction contributes to Wnt5a-enhanced CLL cell proliferation.

scholarly journals Association of polygenic risk score with the risk of chronic lymphocytic leukemia and monoclonal B-cell lymphocytosis

Blood ◽  
2018 ◽  
Vol 131 (23) ◽  
pp. 2541-2551 ◽  
Author(s):  
Geffen Kleinstern ◽  
Nicola J. Camp ◽  
Lynn R. Goldin ◽  
Celine M. Vachon ◽  
Claire M. Vajdic ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Risk Score ◽  
Clinical Impact ◽  
Lymphocytic Leukemia ◽  
Polygenic Risk Score ◽  
Polygenic Risk ◽  
Key Points ◽  
High Discrimination

Key Points PRS, based on the known CLL loci, predicts CLL risk with high discrimination. This PRS predicts risk of monoclonal B-cell lymphocytosis, a precursor to CLL and a condition that has clinical impact beyond risk for CLL.

scholarly journals Novel ACTG1 mutations in patients identified by massively parallel DNA sequencing cause progressive hearing loss

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hiroki Miyajima ◽  
Hideaki Moteki ◽  
Timothy Day ◽  
Shin-ya Nishio ◽  
Takaaki Murata ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Dna Sequencing ◽  
Massively Parallel ◽  
Progressive Hearing Loss ◽  
Massively Parallel Dna Sequencing

scholarly journals ATR inhibition induces synthetic lethality and overcomes chemoresistance in TP53- or ATM-defective chronic lymphocytic leukemia cells

Blood ◽  
2016 ◽  
Vol 127 (5) ◽  
pp. 582-595 ◽  
Author(s):  
Marwan Kwok ◽  
Nicholas Davies ◽  
Angelo Agathanggelou ◽  
Edward Smith ◽  
Ceri Oldreive ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Synthetic Lethality ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Selective Cytotoxicity ◽  
Key Points ◽  
Synthetically Lethal

Key PointsATR inhibition is synthetically lethal to TP53- or ATM-defective CLL cells. ATR targeting induces selective cytotoxicity and chemosensitization in TP53- or ATM-defective CLL cells in vitro and in vivo.

scholarly journals Association between molecular lesions and specific B-cell receptor subsets in chronic lymphocytic leukemia

Blood ◽  
2013 ◽  
Vol 121 (24) ◽  
pp. 4902-4905 ◽  
Author(s):  
Davide Rossi ◽  
Valeria Spina ◽  
Riccardo Bomben ◽  
Silvia Rasi ◽  
Michele Dal-Bo ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Lymphocytic Leukemia ◽  
Key Points ◽  
Genetic Profiles

Key Points BCR subsets 2 and 8 show specific genetic profiles influencing CLL course.

Lenalidomide reduces survival of chronic lymphocytic leukemia cells in primary cocultures by altering the myeloid microenvironment

Blood ◽  
2013 ◽  
Vol 121 (13) ◽  
pp. 2503-2511 ◽  
Author(s):  
Angela Schulz ◽  
Claudia Dürr ◽  
Thorsten Zenz ◽  
Hartmut Döhner ◽  
Stephan Stilgenbauer ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Cell Motility ◽  
Lymphocytic Leukemia ◽  
Leukemia Cells ◽  
Key Points ◽  
And Migration

Key Points Lenalidomide treatment of primary CLL/nurse-like cell cocultures resulted in significantly decreased viability of CLL cells. Lenalidomide increased IL-10 levels, activation of STAT1, expression of ICAM-1, and migration-related genes, and reduced CLL cell motility.

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