Results 111 to 120 of about 481,131 (293)
Loss of the tumor suppressor, Tp53, enhances the androgen receptor-mediated oncogenic transformation and tumor development in the mouse prostate. [PDF]
Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most frequently observed alterations in advanced prostate cancer. However, the biological role of these dual genetic alterations
Aldahl, Joseph +14 more
core
This study shows that copy number variations (CNVs) can be reliably detected in formalin‐fixed paraffin‐embedded (FFPE) solid cancer samples using ultra‐low‐pass whole‐genome sequencing, provided that key (pre)‐analytical parameters are optimized.
Hanne Goris +10 more
wiley +1 more source
The non-coding RNA landscape of plasma cell dyscrasias [PDF]
Despite substantial advancements have been done in the understanding of the pathogenesis of plasma cell (PC) disorders, these malignancies remain hard-to-treat.
Azab, Kareem A +3 more
core +1 more source
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee +8 more
wiley +1 more source
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat +8 more
wiley +1 more source
Targeting p38α in cancer: challenges, opportunities, and emerging strategies
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley +1 more source
Aberrant promoter methylation in p53 and ATM genes was not associated with sporadic breast carcinogenesis in Bulgarian patients [PDF]
Epigenetic silencing of gene expression has become an intensively studied topic regarding breast cancer during the last years. Previous investigations have shown that hypermethylation in gene promoters is an alternative to mutations cancer-related ...
MARIA E. KRASTEVA +6 more
doaj
Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta +10 more
wiley +1 more source
Functional inactivation of tumor suppressor genes drives cancer initiation, progression, and treatment responses. Most tumor suppressor genes are inactivated through 1 of 2 well-characterized mechanisms: DNA-level mutations, such as point mutations or ...
Subhransu S. Sahoo +18 more
doaj +1 more source
Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley +1 more source

