Pre-Cancer Diagnosis via TP53 Gene Mutations Applied Ensemble Algorithms

According to current study, individuals with cancer who have a gene mutation have a bad prognosis. Young women with breast cancer had a poorer prognosis than older women, although it is unknown if the p53 gene mutation contributed to this. Due in part to the devastation of cancer, the appropriate technology may help cancer sufferers in regaining their lives. Researchers seek for mutations in cancer-causing gene sequences in order to identify the precancerous stage. While genetic testing may be used to forecast some kinds of cancer, there is presently no effective technique for identifying all cancers caused by TP53 gene mutations. It is one of the most often discovered genetic anomalies in human cancer is a malfunction in the action of the protein P53. As a consequence, the Universal Mutation Database is used to identify gene mutations (UMDCell-line2010). The issue is that, although many basic databases (for example, Excel format databases) exist that include datasets of TP53 gene mutations associated with disease (cancer), this huge database is incapable of detecting cancer. Thus, the purpose the objective of this study is to create an approach for data mining that utilizes a neural network to ascertain the pre-cancerous state. To begin, bioinformatics techniques such as BLAST, CLUSTALW, and NCBI were used to determine whether or not there were any malignant mutations; second, the proposed method was carried out in two stages: to begin, bioinformatics techniques such as BLAST, CLUSTALW, and NCBI were used to determine whether or not there were any malignant mutations; and third, the proposed method was carried out in two stages: to begin, bioinformatics techniques such as To begin, bioinformatics tools such as BLAST and CLUSTAL Vote Algorithms were utilized to classify pre-cancer by malignant mutations in the disease's early stages. The writers teach and evaluate their subjects using a variety of situations, including cross validation and percentages. This page contains a review of the algorithms discussed before.

Sensitive Detection of Single-Nucleotide Polymorphisms by Solid Nanopores Integrated With DNA Probed Nanoparticles

Single-nucleotide polymorphisms (SNPs) are the abundant forms of genetic variations, which are closely associated with serious genetic and inherited diseases, even cancers. Here, a novel SNP detection assay has been developed for single-nucleotide discrimination by nanopore sensing platform with DNA probed Au nanoparticles as transport carriers. The SNP of p53 gene mutation in gastric cancer has been successfully detected in the femtomolar concentration by nanopore sensing. The robust biosensing strategy offers a way for solid nanopore sensors integrated with varied nanoparticles to achieve single-nucleotide distinction with high sensitivity and spatial resolution, which promises tremendous potential applications of nanopore sensing for early diagnosis and disease prevention in the near future.

Detection of R282w P53 Gene Mutation on Exon 8 in Gastric Cancer Patients in Southwest Iran

Background: Gastric adenocarcinoma is the most common type of gastric cancer all around the world. The epithelial cells of stomach tissue are influenced by environmental factors and genetic disorders. P53 is the most remarkable gene that controls the growth of cells. Mutation in some nucleotides of the P53 gene increases the genetic instability and is assumed as an important prognostic factor in gastric cancer. More than 90% of mutations occur in the exons 5-8 of p53. Objectives: This study was conducted in Kohgiluyeh and Boyer Ahmad (K&B) province (Southwest Iran) to determine the rate of R282W P53 gene mutation of exon 8 in gastric cancer. Methods: This case-control study was conducted on 90 subjects that were divided into two groups (each including 45 patients and 45 controls). The samples were randomly collected from the tissue bank of the pathology laboratory in Yasuj city and then were transferred to the Cellular and Molecular Research Center. DNA extraction was performed by the DNA extraction kit. Molecular analysis on exon 8 was performed by the PCR-RFLP method and using the MspI restricting enzyme. Data were analyzed by descriptive statistics and bivariate correlation tests. Results: No difference was found between the two groups concerning age, gender, and education level. The prevalence of R282W P53 gene mutation on exon 8 in the cancer group was 17.8% (8/45), while no mutation was found in the control group. Conclusions: According to the results, the R282W P53 gene mutation on exon 8 may play an important role in the development of gastric cancer in Yasuj district, Southwest Iran.

CHARACTERIZATION OF SOME BIOLOGICAL FEATURES OF CARCINOGENESIS IN THE DEVELOPING OF GASTRIC CANCER

Purpose of the work: the ability to increase the effectiveness of comprehensive treatment of patients with stomach cancer by individualization based on the definition of carcinogenesis indicators of the malignant process. Materials and methods: 80 patients with stomach cancer were examined, who were identified by MSI on loci VAT 25; VAT 26, the proliferation index of Ki-67 and the p53 gene mutation. The frequency of wild and mutant variants of the p53 gene was studied according to statement of the VAT 25 ta VAT 26 genes stability. In order to assess the prolefethative potential of cells in stomach cancer, the tumor tissue studied the expression of Ki-67, depending on the presence of instability of microsatellites in the loci VAT 25 ta VAT 26. The level of proliferation activity was also assessed depending on the presence of a p53 mutation. Results: The presence of MSI in tumor cells on the locus of VAT 25, there was in most cases a wild version of the gene p53. The absence of MSI according to these loces, the p53 mutation was observed more often. When comparing the differences between them, there were found that in the absence of MSN on VAT 26, the ratio between the absence of a p53 mutation and its presence was reliably different from the ratio of instability. That is why, this can be argued that in stomach cancer mutation of the p53 gene was observed mainly in tumors with the absence of MSN on loci VAT 25 ta 26. Conclusions. And now has been proven, that the data suggest that there are a multifaceted genetic disorder in carcinogenesis. In tumors with preserved function of stability genes, that is why, with the possibility of restoring chromosomal breakdowns, the occurrence and proliferation of malignant cells is associated with the violation of apoptosis at critical points in the process of cell division. In this case, this realize due to the impossibility of mutant form of the p53 gene to synthesize the necessary quarter configuration of the corresponding protein with the latter’s continued inability to stop the process of DNA replication. In this topic has been established that the mutation of the main control gene leads to loss of control over DNA and can contribute to the emergence of a malignant cell, and further loss of cell differentiation is caused by other factors. Furthermore has been revealed that the proliferative activity of swollen cells in stomach cancer has a clear association with the instability of microsatellites on both studied loca of chromosomes.

Protective Effects of Garlic and Cinnamon Oils on Hepatocellular Carcinoma in Albino Rats

Natural oils are traditional medicinal herbs, which have attracted interests for its potential anti-inflammatory and anticancer activities. The present work is aimed at evaluating the protective effect of garlic oil and cinnamon oil on diethylnitrosamine- (DENA-) and 2-acetylaminofluorene- (2-AAF-) induced p53 gene mutation and hepatocarcinogenesis in rats. Forty male albino rats were divided into 4 equal groups: control, hepatocellular carcinoma (HCC), garlic oil-HCC, and cinnamon oil-HCC. The HCC-induced group showed a significant decrease in the body mass and a significant elevation in the liver weight, alpha-fetoprotein (AFP), liver enzymes, hepatic malondialdehyde (MDA), and p53 protein expression levels as well as genetic mutations in intron 5 of p53 gene in the form of Single-Nucleotide Polymorphisms (SNPs) and insertions. In addition, the glutathione (GSH) level and superoxide dismutase (SOD) activities were increased. While HCC rats pretreated with garlic oil or cinnamon oil were significantly reversed, these destructive actions increased GSH and SOD levels. The HCC-induced group showed histopathological features of liver cancer including hypercellularity, nuclear hyperchromasia, mitotic figures, and preneoplastic foci. On the other hand, HCC rats pretreated with garlic oil or cinnamon oil revealed partial reversal of normal liver architecture. The present findings proposed that these natural oils have the ability to improve liver function, significantly reduced the liver toxicity and HCC development. However, further sophisticated studies are recommended before their use as conventional therapeutics for HCC treatment.

Immunohistochemical evaluation of stress-responsive protein sestrin2 and its correlation with p53 mutational status in eyelid sebaceous gland carcinoma

Backgroundp53 is a stress-activated tumour suppressor gene, and its mutation has been associated with solid tumours including non-melanoma skin cancers. Sestrin2 expression is associated with DNA damage and oxidative stress and has been described as a downstream target of p53 network. However, its role in sebaceous gland carcinoma (SGC) remains unexplored.ObjectivesTo determine the role of p53 and its downstream target gene sestrin2 expression and p53 gene mutation status in SGC.MethodsTwenty cases of eyelid SGC tumour and circulating cell-free DNA (ccfDNA) were subjected to mutational analysis of p53 gene. p53 and sesrin2 expression was evaluated by immunohistochemistry. Results were correlated with the clinicopathological features of eyelid SGC.Resultsp53 gene mutations was detected in 25% of the SGC cases. A C>T transition was identified in exon 6 in a single patient in both tumour and ccfDNA. A G>T transversion leading to amino acid change D259Y was seen in four patients. A splice site mutation affected a single case in exon 6. p53 expression was observed in 55% SGC. Loss of sestrin2 in 55% SGC cases correlated with poor tumour differentiation (P=0.0001), upper eyelid involvement (P=0.004), p53 mutation (P=0.039) and with mutant p53 expression (P=0.0001).ConclusionSestrin2 expression was found to be significantly reduced in p53 mutated SGC cases and in cases with strong p53 nuclear immunopositivity, suggesting that loss of sestrin2 may be of biological significance in the development of SGC and as a key downstream component of p53 tumour suppression network in eyelid SGC.