Results 51 to 60 of about 114,065 (338)

p53 expression in chronic lymphocytic leukaemia

open access: yesمجلة كلية الطب, 2005
Background:
Nasir AL-Allawi   +4 more
doaj   +1 more source

Multiset sparse partial least squares path modeling for high dimensional omics data analysis

open access: yesBMC Bioinformatics, 2020
Background Recent technological developments have enabled the measurement of a plethora of biomolecular data from various omics domains, and research is ongoing on statistical methods to leverage these omics data to better model and understand biological
Attila Csala   +2 more
doaj   +1 more source

Characterizing and prognosticating chronic lymphocytic leukemia in the elderly: prospective evaluation on 455 patients treated in the United States. [PDF]

open access: yes, 2017
BACKGROUND: Median age at diagnosis of patients with chronic lymphocytic leukemia (CLL) is \u3e 70 years. However, the majority of clinical trials do not reflect the demographics of CLL patients treated in the community.
Bhushan, Shriya   +12 more
core   +3 more sources

Autoimmunity in chronic lymphocytic leukaemia [PDF]

open access: yesPostgraduate Medical Journal, 1988
Summary Seventy-nine patients with chronic lymphocytic leukaemia were evaluated for the presence of autoimmune diseases and autoantibodies. One patient has polymyositis and two additional patients presented with features suggestive of pernicious anaemia and chronic active hepatitis.
M, Lischner   +3 more
openaire   +2 more sources

C-reactive protein-to-albumin ratio is an independent poor prognostic factor in newly diagnosed chronic lymphocytic leukaemia: A clinical analysis of 322 cases

open access: yesTranslational Oncology, 2021
Chronic lymphocytic leukaemia is one of the most common types of adult leukaemia. Cancer-related systemic inflammation response has been characterized to correlate with therapeutic outcome in patients with cancer.
Han-Ning Tang   +6 more
doaj   +1 more source

KITD816V+ systemic mastocytosis associated with KITD816V+ acute erythroid leukaemia: first case report with molecular evidence for same progenitor cell derivation [PDF]

open access: yes, 2009
Toll-like receptor (TLR)-9 recognizes CpG motifs in microbial DNA. TLR9 signalling stimulates innate antimicrobial immunity and modulates adaptive immune responses including autoimmunity against chromatin, e.g., in systemic lupus erythematosus (SLE ...
H-P Horny   +4 more
core   +1 more source

The PI3Kδ inhibitor roginolisib (IOA‐244) preserves T‐cell function and activity

open access: yesMolecular Oncology, EarlyView.
Identification of novel PI3K inhibitors with limited immune‐related adverse effects is highly sought after. We found that roginolisib and idelalisib inhibit chronic lymphocytic leukemia (CLL) cells and Treg suppressive functions to similar extents, but roginolisib affects cytotoxic T‐cell function and promotion of pro‐inflammatory T helper subsets to a
Elise Solli   +7 more
wiley   +1 more source

Frequency of 17p Deletion in Chronic Lymphocytic Leukemia Patients Presenting to Combined Military Hospital Rawalpindi

open access: yesPakistan Armed Forces Medical Journal
Objective: To assess the frequency and factors related to the presence of 17p deletion among patients diagnosed with chronic lymphocytic leukaemia at the Oncology Department of Combined Military Hospital Rawalpindi Study Design: Cross-sectional study.
Atiq-ur- Rehman   +5 more
doaj   +1 more source

Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia [PDF]

open access: yes, 2015
Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3). FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates a cascade of phosphorylated proteins ...
A Puissant   +49 more
core   +2 more sources

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

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