Results 81 to 90 of about 77,245 (318)
Emerging role of ARHGAP29 in melanoma cell phenotype switching
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster +3 more
wiley +1 more source
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici +8 more
wiley +1 more source
SSA-ME Detection of cancer driver genes using mutual exclusivity by small subnetwork analysis [PDF]
Because of its clonal evolution a tumor rarely contains multiple genomic alterations in the same pathway as disrupting the pathway by one gene often is sufficient to confer the complete fitness advantage.
De Maeyer, Dries +3 more
core +2 more sources
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source
Background The APOBEC3 (apolipoprotein B mRNA editing enzyme catalytic polypeptide 3) family of cytidine deaminases is responsible for two mutational signatures (SBS2 and SBS13) found in cancer genomes.
G. Maria Jakobsdottir +4 more
doaj +1 more source
Genomic Alteration Burden in Advanced Prostate Cancer and Therapeutic Implications. [PDF]
The increasing number of patients with sequenced prostate cancer genomes enables us to study not only individual oncogenic mutations, but also capture the global burden of genomic alterations.
Bose, Rohit, Ryan, Matthew J
core +1 more source
This study integrates transcriptomic profiling of matched tumor and healthy tissues from 32 colorectal cancer patients with functional validation in patient‐derived organoids, revealing dysregulated metabolic programs driven by overexpressed xCT (SLC7A11) and SLC3A2, identifying an oncogenic cystine/glutamate transporter signature linked to ...
Marco Strecker +16 more
wiley +1 more source
Revealing evolutionary constraints on proteins through sequence analysis
Statistical analysis of alignments of large numbers of protein sequences has revealed "sectors" of collectively coevolving amino acids in several protein families.
Bitbol, Anne-Florence +2 more
core +3 more sources
Pan-urologic cancer genomic subtypes that transcend tissue of origin [PDF]
Urologic cancers include cancers of the bladder, kidney, prostate, and testes, with common molecular features spanning different types. Here, we show that 1954 urologic cancers can be classified into nine major genomic subtypes, on the basis of ...
Bossé, Dominick +9 more
core +2 more sources
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang +8 more
wiley +1 more source

