Results 71 to 80 of about 82,841 (227)
Break-Induced Replication Is a Source of Mutation Clusters Underlying Kataegis
Clusters of simultaneous multiple mutations can be a source of rapid change during carcinogenesis and evolution. Such mutation clusters have been recently shown to originate from DNA damage within long single-stranded DNA (ssDNA) formed at resected ...
Cynthia J. Sakofsky +6 more
doaj +1 more source
Aldehyde dehydrogenase 1A1 (ALDH1A1) is a cancer stem cell marker in several malignancies. We established a novel epithelial cell line from rectal adenocarcinoma with unique overexpression of this enzyme. Genetic attenuation of ALDH1A1 led to increased invasive capacity and metastatic potential, the inhibition of proliferation activity, and ultimately ...
Martina Poturnajova +25 more
wiley +1 more source
Targeted modulation of IGFL2‐AS1 reveals its translational potential in cervical adenocarcinoma
Cervical adenocarcinoma patients face worse outcomes than squamous cell carcinoma counterparts despite similar treatment. The identification of IGFL2‐AS1's differential expression provides a molecular basis for distinguishing these histotypes, paving the way for personalized therapies and improved survival in vulnerable populations globally.
Ricardo Cesar Cintra +6 more
wiley +1 more source
Adding to the CASeload: unwarranted p53 signaling induced by Cas9
We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines.
Veronica Rendo +2 more
doaj +1 more source
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson +9 more
wiley +1 more source
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
KHS‐Cnd peptide is able to impair biofilm formation and disaggregate mature biofilms in Acinetobacter baumannii clinical isolates. Differences in extracellular metabolites reflect changes in biofilm metabolism due to KHS‐Cnd treatment. Among the differentially represented extracellular metabolites upon KHS‐Cnd treatment, the significantly altered ...
Fernando Porcelli +9 more
wiley +1 more source
There has been extraordinary progress in understanding the roles of lentiviral accessory proteins in antagonizing host antiviral defense proteins. However, the precise primary function of the accessory gene Vpr remains elusive.
Oliver I. Fregoso, Michael Emerman
doaj +1 more source
Mycobacterium tuberculosis O 6-methylguanine-DNA methyltransferase (MtOGT) contributes to protect the bacterial GC-rich genome against the pro-mutagenic potential of O6-methylated guanine in DNA. Several strains of M. tuberculosis found worldwide encode a point-mutated O6-methylguanine-DNA methyltransferase (OGT) variant (MtOGT-R37L), which displays an
Miggiano R +10 more
openaire +5 more sources
NF90–NF45 functions as a negative regulator of methyltransferase‐like 3/14 (METTL3/14)‐mediated N6‐methyladenosine (m6A) modification on primary microRNAs (pri‐miRNAs). NF90–NF45 binds to anti‐oncogenic pri‐miRNAs and inhibits their m6A modification, thereby suppressing the biogenesis of anti‐oncogenic miRNAs.
Takuma Higuchi +6 more
wiley +1 more source

