The researchers discovered that cells that were at risk of developing cancer but lost both p53 and CDKN2A were weaker and less able to compete with nearby cells, which stopped cancer from spreading.
To directly examine the interplay between mutant p53 or Mdm2 and wild type p53 in gene occupancy and expression, an integrated RNA-seq and ChIP-seq analysis was performed in vivo using isogenically ...
This interaction reactivates a p53-dependent transcriptional program, suggesting a potential new therapeutic strategy for treating HPV-induced cancers. Ganguli et al. show that CDKN2A loss in ...
Investigation of the association of CTRB2 exon 6 deletion with time to progression and overall survival in pancreatic ductal adenocarcinoma. This is an ASCO Meeting Abstract from the 2025 ASCO ...
The primary node molecules in the cell signaling network in cancer tissues are maladjusted and mutated in comparison to normal tissues, which promotes the occurrence and progression of cancer.
In case of CDKN1A (1:50, MA5-14949, Live Technologies), CDKN2A (1:200, ab108349, Abcam), and p53 (1:100, LS-B7723, LSBio, Shirley, USA) antigens were demasked with 10 mM citrate buffer (16 h, 65°C).
Spatially resolved protein profiling in pancreatic adenosquamous carcinoma. Age, number of genomic alterations (GA) per tumor, and alteration frequency of select commonly altered genes based on TP53 ...
The TP53 gene is a gene that is mutated in many cancers. It is the most common gene mutation found in cancer cells. A tumor-suppressor gene, TP53 codes for a protein that inhibits the development and ...