Results 131 to 140 of about 16,973,530 (253)
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
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Boston University School of Medicine catalog
Course catalog and informational material for the Boston University School of ...
Boston University School of Medicine
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Boston University School of Medicine catalog [PDF]
Course catalog and informational material for the Boston University School of ...
Boston University School of Medicine
core
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
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu +3 more
wiley +1 more source
Tumour heterogeneity and clonal evolution of metastatic salivary gland cancer were evaluated in two patients with adenoid carcinoma and one patient with myoepithelial carcinoma. Radiology‐guided autopsy enabled multi‐region sampling (total samples n = 149), followed by whole‐genome sequencing and phylogenetic reconstruction (17 tumour samples, 4–7 per ...
Gerben Lassche +10 more
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This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi +6 more
wiley +1 more source
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley +1 more source

