Results 111 to 120 of about 1,488,945 (267)

Translating whole‐genome doubling into precision medicine in cancer

open access: yesMolecular 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

INS/GPS Tightly Coupled Algorithm based on Unscented Transform

open access: yes, 2005
In this paper, the tightly coupled INS/GPS integration system based on unscented transform is presented for improving the performance of nonlinear kalman filter.
김광진, 박영범, 박찬국
core  

Single‐cell DNA methylation profiling: Technologies, computation, and applications in precision oncology

open access: yesMolecular Oncology, EarlyView.
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

Targeting transcription factors associated with hemoglobinopathies: Lessons from successful interventions and implications for cancer

open access: yesMolecular Oncology, EarlyView.
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

Spatial biology in cancer epigenetics

open access: yesMolecular 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

Climate Simulation Using Tightly Coupled Program And Database

open access: yes, 2007
We report our experience of tightly coupling a global change simulation of the terrestrial carbon cycle with an object--oriented database. By tightly coupled, we mean an interleaving of computational and data access statements within the same module so ...
David R. Mikesell   +2 more
core  

ADP‐ribosylation: An emerging regulator of the epigenome

open access: yesMolecular Oncology, EarlyView.
ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho   +2 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

APOBEC3 activity and DNA polymerase‐ε deficiency are associated with distinct IDH1 R132 hotspot mutations

open access: yesMolecular Oncology, EarlyView.
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler   +3 more
wiley   +1 more source

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