It is shown that retinoblastoma is associated with LINE-1 promoter hypomethylation, increased LINE-1 transcript expression, ORF1p accumulation, and preferential activation of selected LINE-1 loci, which is associated with altered expression of oncogenic signalling pathways and host factors involved in transposable element repression.
Retrotransposons comprise most of the human dark genome and are frequently upregulated during cancer progression. Long interspersed nuclear element-1 (LINE-1), the only autonomously active human retrotransposon, is aberrantly reactivated in pancreatic ductal adenocarcinoma (PDAC), yet how LINE-1 regulates metastatic...
Ching Ngar Wong, Fabricio R. Neira, Cristina Pedorella et al.· Cancer Research· 0 citations
Results indicate that SOX7 functions as a tumor suppressor in MM, and its inactivation promotes cell cycle progression, and the anti-myeloma effects of panobinostat in MM.1S cells may be partially mediated through SOX7 induction.
Arda Ceylan, Xiao-Zhou Hu, Tevfik Hatipoğlu et al.· International Journal of Mol...· 0 citations
It is demonstrated for the first time that LOY is significantly enriched in advanced-stage disease and the aggressive basal molecular subtype, establishing LOY as a causal genetic driver of PDAC progression, acting through epigenetic remodeling to promote EMT, basal subtype identity, metastasis, and therapy resistance.
M. Dorsch, Felix E. G. Beaudry, A. Baginska et al.· Cancer Research· 0 citations
Background/Objectives: Colorectal cancer (CRC) is among the most diagnosed malignancies and is a leading cause of cancer-related deaths globally. Beyond canonical CRC driver mutations, additional molecular alterations such as dysregulated gene expression and epigenetic reprogramming shape the disease behavior and may r...
Abdullah A. Alqasem, Waad Al-Burayk, Muneira Habjar et al.· Genes· 0 citations
A central molecular network through which KMT2Dmut operates in follicular lymphoma subsets is delineated and provided a mechanistic rationale for therapeutic targeting of KMT2D.
One hallmark of pediatric tumors is their low mutational burden, which contrasts with adult tumors, where cancer-causing mutations often accumulate over decades of DNA replication and environmental exposure. This raises the question of how such mutations arise in young patients. We have proposed that developmental mu...
Helen S. Mueller, Kaisha Garvin, Sophia Rha et al.· Cancer Research· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.