Results 71 to 80 of about 177,226 (290)

In vitro and in silico modelling of ROS1‐positive non‐small cell lung cancer reveals fusion‐dependent tyrosine kinase inhibitor responses

open access: yesMolecular Oncology, EarlyView.
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

Differential control of muscle-specific gene expression specified by src and myc oncogenes in myogenic cells.

open access: yes, 1990
Myogenic cells can be transformed in vitro by the introduction of several exogenous viral oncogenes. Transformed myoblasts are prevented from terminal differentiation into myotubes by the continuous expression of oncogenes such as myc and src, chosen as ...
Falcone G   +3 more
core  

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

Genome wide analysis of oral squamous cell carcinoma.

open access: yes, 2009
[[abstract]]Oncogenes serve as specific and unique targets for drug intervention to treat cancer, as their activation (amplification and activating mutation) is essential for tumor development.
I-Wen Chiu
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

Risk factors for oral cancer

open access: yesRevista Cubana de Estomatología, 2016
Introduction: oral cancer is a disease with high morbidity and mortality, associated with risk factors whose complex interplay is subject to scientific debate.
Pedro Antonio Miguel Cruz   +3 more
doaj  

Oncogenes [PDF]

open access: yes
An oncogene is a mutated form of a normal cellular gene – called a proto-oncogene – that contributes to the development of a cancer. Proto-oncogenes typically regulate cell growth and cell differentiation.
حسینی اصل, سید سعید
core  

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

Oncogenous osteomalacia

open access: yesJournal of Cancer Research and Therapeutics, 2009
Oncogenous osteomalacia is a rare paraneoplastic renal phosphaturic condition, often associated with highly vascular benign mesenchymal tumors. We report a case of a 48-year-old male who presented with debilitating osteomalacia unresponsive to standard therapy.
Ghosh, Soumitra   +3 more
openaire   +2 more sources

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

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