We investigated the factors modulating adjuvant cancer therapies by examining p53 gene mutations and chromosome 17p allelic losses in 15 rectal cancers treated by a preoperative combined therapy consisting of radiation, intraluminal hyperthermia and 5-fluorouracil suppositories.
Two other family members, one with a rectal carcinoma aged 55, the other with two separate benign lesions under the age of 45, were both wild-type for the TP53 mutation.
Thus, our current meta-analysis indicates no evidence for the association between the p53Arg72Pro polymorphism and CRC risk in the Asian population, but significant association in Chinese population, especially for rectal cancer and in men.
Without correction for multiple testing, one polymorphism in GPX2 and three polymorphisms in GPX3 were associated with a significant risk reduction for rectal cancer at α = 0.05, specifically for rectal cancers with TP53 mutations.
There was no correlation between p53, deleted in colorectal cancer gene, or thymidylate synthase immunohistochemical staining or between p53 polymerase chain reaction-single-strand conformation polymorphism and local recurrence or survival in locally advanced low rectal cancers treated with preoperative adjuvant therapies.
Mutations in p53 tumor suppressor gene were examined in 44 Chinese patients with rectal cancer, including 22 cases with advanced schistosomiasis japonica and 22 cases without schistosomiasis.
In this comprehensive study of genetic variability in IL23R across the spectrum of colorectal carcinogenesis, as well as within colon and rectal tumor molecular subtypes, we observed associations between SNPs in IL23R and risk of rectal cancer: the 88413 C>A (rs10889675) and 69450 C>A (rs7542081) polymorphisms were associated with decreased rectal cancer risk overall (p-trend=0.04 and 0.05 respectively), and specifically with rectal tumors bearing a TP53 mutation (88413 CA/AA vs. CC OR: 0.66; 95% CI: 0.46-94; 69450 CA/AA vs. CC OR: 0.60; 95% CI: 0.37-0.98).
Our objective was to establish a correlation between specific KRAS mutations and rectal cancer response to CRT and to investigate if the correlation was related to a different association between KRAS and TP53 mutations.
These results suggest that the TP53Arg72Pro polymorphism CC genotype may contribute to an increased risk of CRC, especially for rectal cancer and among Asians.
Fifty patients with locally advanced rectal cancer were treated with preoperative radiotherapy combined with mitomycin C and capecitabine. p21 and p53 immumohistochemical staining was performed on pretreatment biopsies and the results were compared with tumor regression according to grading systems by Dworak (TRG grades) and by Wheeler (RCRG grades).
Utilizing a novel in silico clonal evolution algorithm, we identified common tumor-initiating events involving APC, KRAS and TP53 genes in RCC, LCC and rectal cancers.
Therefore, this combination therapy can induce an additive or synergistic anti-tumour effect in rectal cancers with wild-type p53 as well as in those with mutated p53 through apoptosis, offering new therapeutic opportunities and a better prognosis.
Little information is available on the clinical significance of cancer-related genes such as KRAS, NRAS, BRAF, PIK3CA and TP53 in nonmetastatic rectal cancer.
The results of the present meta-analysis indicate that P53 status is a predictive factor for response in rectal cancer patient undergoing neoadjuvant radiation-based therapy.