Results 121 to 130 of about 409,349 (266)
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder +10 more
wiley +1 more source
Many patients with urothelial cancer do not benefit from treatment with pembrolizumab, while at risk of severe side effects. Changes in the levels of circulating tumor DNA early during treatment, measured by a simple and affordable assay that can be easily implemented in the clinic, can be used as a prognostic tool to identify these patients.
Youssra Salhi +14 more
wiley +1 more source
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source
Drug resistance limits treatment success in a subset of lung cancers driven by ROS1 gene alterations. Using patient‐derived cells and computer simulations, we studied three key mutations and how they affect five targeted drugs. The mutations reduced drug effectiveness in different ways by altering protein structure and behavior.
Farhan Ul Haq +8 more
wiley +1 more source
The CP-violating phase $$\phi _s$$ ϕ s , the $$B_{s}$$ B s decay width ( $$\varGamma _s$$ Γ s ), and the $$B_{s}$$ B s decay width difference ( $$\varDelta \varGamma _s$$ Δ Γ s ) are sensitive probes to new physics and can constrain the heavy quark ...
Xiaomei Li, Manqi Ruan, Mingrui Zhao
doaj +1 more source
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi +11 more
wiley +1 more source
Detecting circulating tumor cells (CTCs) in blood before surgery may help predict outcomes in patients with head and neck squamous cell carcinoma (HNSCC). Here, we show when combined with tumor size and lymph node involvement from routine imaging, CTC status identifies high‐risk patients with poorer survival—offering a simple, minimally invasive tool ...
Susanne Flach +9 more
wiley +1 more source
LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang +9 more
wiley +1 more source
Translating whole‐genome doubling into precision medicine in cancer
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
wiley +1 more source

