Results 51 to 60 of about 1,804 (185)
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
Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu +13 more
wiley +1 more source
Tumor B‐cell infiltration in platinum‐treated advanced muscle‐invasive urothelial carcinoma
Bladder tumors with higher pretreatment memory B‐cell infiltration were linked to longer survival after cisplatin chemotherapy, but not carboplatin. These tumors also showed more organized immune structures (tertiary lymphoid structures) and a shared pro‐inflammatory B‐cell‐rich community, suggesting that memory B cells may help identify patients most ...
Konrad Stawiski +10 more
wiley +1 more source
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim +3 more
wiley +1 more source
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +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
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
Single‐cell DNA methylation (scDNAme) profiling maps epimutational clonal evolution, revealing mechanisms of malignancy and therapeutic resistance across diverse cancer types. By providing a high‐resolution landscape of intratumoral heterogeneity, these technologies empower precise patient stratification, guide the development of enhanced ...
Ik Soo Kim
wiley +1 more source
Interferon type 1 (IFN‐1) production and signaling is associated with the acquisition of therapy resistance, following chronic DNA damage, via Interferon‐related DNA damage resistance signature (IRDS) gene expression. An alternative, DNA damage‐independent role of sustained IFN‐1 mediated resistance was identified and characterized by the emergence of ...
Ashlyn Conant +11 more
wiley +1 more source
CEACAM1 participation in breast cancer progression
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin +3 more
wiley +1 more source

