Results 51 to 60 of about 1,604,147 (168)
Molecular Oncology, EarlyView.Cotargeting EGFR and STAT3 with Erlotinib and TTI‐101 impairs both 2D and 3D growth of ETV1‐overexpressing prostate cancer cells by disrupting a self‐sustaining ETV1–EGFR positive feedback loop that promotes EGFR and STAT3 expression and phosphorylation (activation).
Elsa Gomes Paiva +5 more
wiley +1 more source
Molecular Oncology, EarlyView.Human cytomegalovirus infection is common in normal prostate epithelium, prostate tumor tissue, and prostate cancer cell lines. CMV promotes cell survival, proliferation, and androgen receptor signaling. Anti‐CMV pharmaceutical compounds in clinical use inhibited cell expansion in prostate cancer models in vitro and in vivo, motivating investigation ...
Johanna Classon +13 more
wiley +1 more source
Molecular Oncology, EarlyView.In luminal (ER+) breast carcinoma (BC), miRNA profiling identified miR‐195‐5p as a key regulator of proliferation that targets CHEK1, CDC25A, and CCNE1. High CHEK1 expression correlates with worse relapse‐free survival after chemotherapy, especially in patients with luminal A subtype.
Veronika Boušková +14 more
wiley +1 more source
Molecular Oncology, EarlyView.In thyroid cancer patients, high‐dose (≥7.4 GBq) radioactive iodine therapy (RAIT) was associated with a higher prevalence of clonal hematopoiesis (variant allele frequency >2%) in individuals aged ≥50 years (OR = 2.44). In silico analyses showed that truncating PPM1D mutations conferred a selective advantage under these conditions.
Jaeryuk Kim +11 more
wiley +1 more source
Chimeric diphtheria toxin–CCL8 cytotoxic peptide for breast cancer management
Molecular Oncology, EarlyView.DTCCL8 is a recombinant fusion toxin that targets cancer cells expressing chemokine receptors. By combining diphtheria toxin with CCL8, DTCCL8 binds to multiple receptors on tumor cells and induces selective cytotoxicity. This strategy enables receptor‐mediated targeting of cancer and may support the development of chemokine‐guided therapeutics ...
Bernardo Chavez +5 more
wiley +1 more source
ITGAV and SMAD4 influence the progression and clinical outcome of pancreatic ductal adenocarcinoma
Molecular Oncology, EarlyView.In SMAD4‐positive pancreatic ductal adenocarcinoma (PDAC), integrin subunit alpha V (ITGAV) activates latent TGF‐β, which binds to the TGF‐β receptor and phosphorylates SMAD2/3. The activated SMAD2/3 forms a complex with SMAD4, and together they translocate to the nucleus, modulating gene expression to promote proliferation, migration, and invasion. In
Daniel K. C. Lee +9 more
wiley +1 more source
Molecular Oncology, EarlyView.This study presents a novel AI‐based diagnostic approach—comprehensive serum glycopeptide spectra analysis (CSGSA)—that integrates tumor markers and enriched glycopeptides from serum. Using a neural network model, this method accurately distinguishes liver and pancreatic cancers from healthy individuals.
Motoyuki Kohjima +6 more
wiley +1 more source
Exploring the role of cyclin D1 in the pathogenesis of multiple myeloma beyond cell cycle regulation
Molecular Oncology, EarlyView.Cyclin D1 overexpression altered the cell adhesion pathway, while cyclin D2 upregulation had less impact on pathway enrichment analysis. Multiple myeloma (MM) patients with cyclin D1 overexpression showed reduced CD56 expression and increased circulating tumor cells (CTC) levels, suggesting that cyclin D1 may contribute to MM cell dissemination ...
Ignacio J. Cardona‐Benavides +13 more
wiley +1 more source
Molecular Oncology, EarlyView.Small extracellular vesicles are a promising source of diagnostic molecules. We conducted a comprehensive study, including transcriptome profiling and RT‐qPCR validation on large cohorts of samples. Diagnostic panels enabling sensitive detection of colorectal cancer and precancerous lesions were established. Some molecules were differentially expressed
Petra Vychytilova‐Faltejskova +26 more
wiley +1 more source
β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1
Molecular Oncology, EarlyView.Low levels of β‐TrCP (Panel A) allow the accumulation of BRCA1 and CtIP, which facilitate the repair of cisplatin‐induced DNA damage via homologous recombination (HR) and promote tumor cell survival. In contrast, high β‐TrCP expression (Panel B) leads to BRCA1 and CtIP degradation, impairing HR repair, resulting in persistent DNA damage and apoptosis ...
Rocío Jiménez‐Guerrero +8 more
wiley +1 more source