Results 101 to 110 of about 2,494,673 (310)
Incidence of anemia in patients diagnosed with solid tumors receiving chemotherapy, 2010–2013
Hairong Xu,1 Lanfang Xu,2 John H Page,1 Kim Cannavale,2 Olivia Sattayapiwat,2 Roberto Rodriguez,3 Chun Chao2 1Center for Observational Research, Amgen Inc., Thousand Oaks, CA, USA; 2Department of Research and Evaluation, Kaiser Permanente Southern ...
Xu L +6 more
core
Microsatellite instability and somatic gene variant profile in solid organ tumors
Introduction Absence of mismatch repair (MMR) genes in tumor cells or errors in the replication repair process may lead to DNA-MMR deficiency and microsatellite instability (MSI) formation.
Ibrahim Halil Erdogdu +6 more
core +1 more source
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
wiley +1 more source
Combination Radioimmunotherapy Strategies for Solid Tumors
Combination radioimmunotherapy is an emerging approach for the treatment of solid tumors where radio immunotherapy alone has proven to be reasonably ineffective. Radioimmunotherapy (RIT) using monoclonal antibodies (mAbs) labeled with radionuclides is an
Yong-Jin Lee +4 more
core +1 more source
Role of Bcl-3 in solid tumors [PDF]
Bcl-3 is an established oncogene in hematologic malignancies, such as B-cell chronic lymphocytic leukemias. Nevertheless, recent research has shown that it also participates in progression of diverse solid tumors.
Vilma Maldonado +3 more
core +1 more source
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
Background Oxaliplatin (OXA) has become a key chemotherapeutic agent in the treatment of esophageal squamous cell carcinoma (ESCC). Toll-like receptor 4 (TLR4) is frequently upregulated in OXA-treated tumors, yet its role in regulating OXA sensitivity in
Ziqi Zhu +6 more
doaj +1 more source
CEACAM1 participation in breast cancer progression
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin +3 more
wiley +1 more source
Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
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

