Results 111 to 120 of about 33,049,667 (246)
Translating whole‐genome doubling into precision medicine in cancer
Molecular Oncology, EarlyView.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
Vanderbilt Law School Death Penalty Debate
, 2009 Includes descriptive metadata provided by producer in QuickTime movie file: "Law School - General Events - Vanderbilt Law School Death Penalty Debate - Vanderbilt University > From the Colleges > Law School > General Events > Vanderbilt Law School Death ...
Vanderbilt University. Law School
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Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Molecular Oncology, EarlyView.Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source
, 2015 Title from PDF caption (viewed on March 2, 2018)."SP OHA 9130 (9/15)."This archived document is maintained by the State Library of Oregon as part of the Oregon Documents Depository Program.
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Spatial biology in cancer epigenetics
Molecular Oncology, EarlyView.Spatial epigenomics combines molecular profiling with tissue architecture to reveal how gene regulation is organized within intact tissues. In cancer, these technologies uncover the mechanisms driving tumor heterogeneity and microenvironmental interactions, opening new opportunities for biomarker discovery and precision medicine.
Eva Crespo‐García, Manel Esteller
wiley +1 more source
Molecular Oncology, EarlyView.Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou +4 more
wiley +1 more source
Molecular Oncology, EarlyView.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
Molecular Oncology, EarlyView.High‐risk bladder cancer is typically treated with Bacillus Calmette‐Guérin (BCG), but 30–40% of patients relapse. No FDA‐ or CE‐approved biomarkers currently predict or prognosticate BCG failure. We systematically reviewed the literature and identified 72 eligible studies, revealing several promising biomarkers associated with BCG treatment response ...
Rui Ribeiro‐Pereira +7 more
wiley +1 more source
Molecular Oncology, EarlyView.Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh +11 more
wiley +1 more source
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
Molecular Oncology, EarlyView.How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source