<b>Objectives:</b> TP53 is an important tumor suppressor gene to maintain genomic integrity, and its mutations increase the susceptibility to oral carcinoma.
<i>TP53, KRAS, APC</i>) has limited diagnostic sensitivity (40-60%), however, methylated DNA including <i>SEPT9, SFRP1, SDC2</i> can be applied with higher sensitivity (up to 90%) for CRC.Circulating miRNAs (e.g. miR-21, miR-92, miR-141) provide comparably high sensitivity for CRC as the circulating tumor cell mRNA markers (e.g.EGFR, CK19, CK20, CEA).
<i>In vitro</i> and <i>in vivo</i> studies revealed that this combined strategy can greatly reinforce DNA damage and apoptosis of hypoxic tumor cells, while significantly suppressing tumor growth, improving tumor hypoxia and promoting p53 up-regulation and HIF1α down-regulation.
<sup>PMI</sup>Bcr/Abl-R6 effectively induced apoptosis of HCT116 p53<sup>+/+</sup> cells in vitro in a p53-dependent manner and potently inhibited tumor growth in a nude mouse xenograft model by stabilizing p53 in vivo.
(1) Tp53 mutations in the urine sediment could be a useful indicator of tumor recurrence or tumor residual in patients ( approximately 40%) with primary mutated bladder cancer tissue.
(2) Coincidental p53 allele mutation and PML loss shifts the tumor profile toward sarcoma formation, which is paralleled in human leiomyosarcomas (indicated by immunohistochemistry; IHC).
(2006) also demonstrate that restoration of p53 activity results in tumor regression but add the sobering caveat that tumors may be able to quickly generate resistance by finding other ways to disrupt the p53 pathway.
(99m)Tc-MIBI efflux rates were measured using a gamma camera in three Brca1 (-/-); p53 (-/-) mouse mammary tumors that have different Mdr1a/b expression levels.
(III) The gain of function caused by mutations that transform the oncosuppressor p53 gene into a dominant transforming oncogene and (IV) The phosphorylative regulation of p53 and its relationship with the mitogenic signaling cascade involving protein kinase C and tumor promoters.
(p = 0.010) The expression of p53 protein was found in one (12.5%) of eight MSI-H tumors, five (31.3%) of 16 MSS tumors, and seven of 15 EMAST tumors.(p = 0.247)
1337-1344) describe a mutant p53 knock-in mouse in which normal tissues and some tumors have low levels of mutant p53 protein unless Mdm2 or p16(INK4A) are absent.
17p losses were associated with p53 gene mutations and with a significantly higher number of chromosomal imbalances than tumors with normal chromosome 17 profile.
17p13 loss and p53 mutation were associated with poor prognosis in recurrent tumors and chromosome 10 loss was associated with short PFS and OS in primary tumors.
1847-1857) develop a new mouse model of osteosarcoma in which a GOF mutant p53 allele is expressed specifically in osteoblasts, while the tumor microenvironment remains wild type for p53, allowing for the study of cell-autonomous functions.