Results 131 to 140 of about 3,692,549 (295)

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

Molecular Oncology, EarlyView.
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, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

Cancer‐associated mutations in endometriosis reframe a benign disease through molecular oncology

Molecular Oncology, EarlyView.
This review aims to comprehensively analyse cancer‐associated somatic mutations (CAMs) present in endometriotic lesions, emphasizing their biological roles, spatial distribution and implications for translational applications in medicine. By contextualizing a benign state within a genomic framework, this analysis seeks to establish its value as a ...
Clarissa Mujacic, Maria Concetta Vitale, Rita Siino, Emilia Di Giovanni, Carla Ferrante Bannera, Enrico Di Marco, Andrea Gottardo, Tancredi Didier Bazan Russo, Nadia Barraco, Alessandro Perez, Valerio Gristina, Antonio Galvano, Giuseppe Badalamenti, Antonio Russo, Viviana Bazan, Lorena Incorvaia   +15 more
wiley   +1 more source

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

The Consequence of the Presence of Ribonucleotide for ds-DNA’s Electronic Properties: Preliminary Theoretical Studies

Cells
The genome is continuously exposed to different harmful factors whose activity causes different types of lesions. On the other hand, during the DNA replication process, a ribonucleoside (rN) can be inserted more frequently than the occurrence of DNA ...
Boleslaw T. Karwowski
doaj   +1 more source

DNA damage

, 2008
Even under the best of circumstances, DNA is constantly subjected to chemical modifications. Several types of DNA damage such as SSB (single strand break), DSB (double strand break), CPDs (cyclobutane pyrimidine dimers), 6-4PPs (6-4 photoproducts) and their Dewar valence isomers have been identified that result from alkylating agents, hydrolytic ...
Kumari, Sunita, Rastogi, Rajesh P., Singh, Kanchan L., Singh, Shailendra P., Sinha, Rajeshwar P.   +4 more
openaire   +2 more sources

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

Molecular 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

Cellular Processing Pathways Contribute to the Activation of Etoposide- Induced DNA Damage Responses

, 2009
Cytotoxic action (tumor cell killing) and carcinogenic side effect ( therapy-related secondary leukemia) of etoposide are closely related to its ability in stabilizing topoisomerase II cleavable complex (TOP2cc), a unique form of protein- linked DNA ...
FAN, JIA-RONG;PENG, AN-LIN;LO, SHU-CHI;HUANG, TING-HSIANG;LI, TSAI-KUN, 范嘉榕;彭安林;羅淑祺;黃鼎翔;李財坤   +1 more
core   +1 more source

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

Molecular 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, Puspa Das, Xing Zhang, Xiaodong Cheng   +3 more
wiley   +1 more source

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, Barbara Karakyriakou, Patricia C. Muskus, Alyssa M. Roberts, Justin Rendleman, Alexa Warren, Hanxu Lu, Kimberly A. Birmingham, Malone K. Friedman, Abigail E. Goen, Huijuan Yang, Owen M. Wilkins, Fred W. Kolling, Eugene Demidenko, Julie M. Jorns, Brock C. Christensen, Todd W. Miller   +16 more
wiley   +1 more source

Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization

Current Issues in Molecular Biology
Replication stress (RS) is a hallmark of cancer, largely driven by oncogene activation. Due to high levels of RS, cancer cells depend heavily on the RS response mechanisms to avoid DNA damage. This dependency creates a therapeutic opportunity that can be
Spyridon N. Vasilopoulos, Ioanna Tremi, Ioly Kotta-Loizou, Angeliki Gkikoudi, Ourania E. Tsitsilonis, Sophia Havaki, Alexandros G. Georgakilas   +6 more
doaj   +1 more source