Updates On The Molecular Genetics Of Colorectal Cancer-Books Pdf

Updates on the Molecular Genetics of Colorectal Cancer
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Colorectal Cancer Open Access, Vol 3 No 1 2, ISSN 2471 9943. Table 1 List of genetic changes in CRC patients, Study Author Month. Gene Function Regulation role in Colon Cancer Type of Study. year of publication, Encodes DNA helicase plays Homozygous c 672 673delGGinsC mutation in. Genome mapping study in two, an essential role in homologous MCM9 chr6 119243200 caused a frame shift. Goldberg 12 2015 1 MCM9 consanguineous Ashkenazi, recombination mediated double strand leading to premature truncation associated with.
break repair polyposis and early onset CRC, POT1 Telomere length maintenance Disruptive mutation Whole exome sequencing was. Subunit of polymerase epsilon enzyme Mutation causes polymerase proofreading performed on 1 006 patients. Chubb 6 2016 2 complex associated polyposis with early onset familial CRC. Double strand break repair nuclease 55 years who also had a first. MRE11 Inactivated in mismatch repair deficient cancer degree relative with CRC. involved in homologous recombination, Investigated effects of ATF3. Member of ATF CREB family of basic, ATF3 was overexpressed in human colorectal on apoptosis cell cycle. Jiang 2 2016 3 AFT3 region leucine zipper bZip proteins. cancer cells cell migration and epithelial, regulates transcription by binding DNA. mesenchymal transition EMT, TET consists of a family of Analyzed both the mRNA and.
Nuclear expression of TET2 is absent in a, enzymes that catalyze the oxidation protein level of the TET family. Huang 1 2016 4 TET2 significant portion of CRC tissues in association. of 5 methylcytosine 5mC to members in our colorectal cancer. w metastasis, 5 hydroxymethylcytosine 5hmC specimens. CpG island methylator phenotype, CIMP is due to hypermethylation of. multiple CpG islands that encompass the, CIMP CpG promoter regions of multiple genes This. Poorer prognosis for pts w CIMP CIMP H CRC, Jia 3 2016 5 island methylator may prevent the binding of transcription Systematic review of 36 studies.
than with CIMP CIMP L CRC, phenotype factors to tumor suppressor genes. Consequently the suppressor genes are, silenced which lead to the progression. Association of processed meat w CRC was, strongest among individuals with the rapid. Bioactivate heterocyclic aromatic amines NAT2 phenotype intermediate among those w Meta analysis Studied in. Wang 12 2015 6 N acetyltransferase, formed in cooked meat intermediate NAT2 phenotype and null among Japanese and African Americans. those w slow phenotype Similar interaction was, found for NAT2 and total red meat.
Gene located in intestinal epithelial Down regulation is associated with MMR. Caudal related Evaluation of 191 tumor biopsies, cells that that plays an important deficiency right sided tumors and poor. homeobox from colon cancer patients to, Olsen 2 2016 7 role in intestinal development and differentiation at both the mRNA and protein. transcription factor 2 investigate CDX2 expression in. differentiation by encoding intestine level, CDX2 colon cancer. specific transcription factors, Thoc1 is involved in the development and. Gene that encodes nuclear matrix, THO complex 1 progression of CRC and elevated expression of Evaluation of 185 CRC samples.
Liu 12 2015 8 protein playing vital roles in transcription. Thoc1 Thoc1 is associated with aggressive phenotype for Thoc1 activity. elongation and mRNA export, and poor prognosis in CRC. Enzyme that catalyzes the degradation Both CD147 and MMP 11 were over expressed. MMP 11 of 1 antitrypsin and insulin like growth on both the mRNA and protein level in CRC. factor binding protein 1 IGF BP 1 tissue samples They also found a direct. correlation between CD147 and MMP 11 Evaluated the expression of. Tian 10 2015 9 protein expression in CRC tissues CD147 and CD147 and MMP 11 in 56 tissue. Stimulates the secretion of MMPs from MMP 11 expression also influenced lymph biopsies with known CRC. CD147 tumor cells as well as regulates their node metastasis distant metastasis and TNM. expression and activity stage Increased expression of both genes also. correlated with a shorter survival time, miR 320b expression was down regulated in. MicroRNAs miRNAs are small, both CRC tissues and cells Overexpression. noncoding RNAs that potentially, of miR 320b in CRC cells was statistically. play a critical role in tumorigenesis, correlated with a decrease of cell growth in vitro Evaluated miR 320b activity in.
Wang 10 2015 10 miR 320b Mounting evidence indicates that one. and in vivo while c MYC was identified as a CRC tissues of 48 patients. specific miRNA miR 320b is down, target gene of miR 320b in CRC Furthermore. regulated in numerous human cancers, it was found that up regulation of c Myc can. including colorectal cancer CRC, attenuate the effects induced by miR 320b. miRNA 206 levels are significantly lower in CRC, microRNAs miRNAs are small non tissue compared to control tissue. coding RNAs that play important role in patients with low miR 206 expression had Evaluated miR 206 activity in. a variety of biological processes and significantly poorer overall survival CRC tissues and compared it to. Sun 2015 11 miR 206, aberrant expression of miRNA is always over expression of miR 206 can inhibit CRC cell adjacent healthy tissues in 80.
associated with tumor progression and migration and invasion miR 206 functions as a patient. invasion tumor suppressor by inhibiting CRC migration. and invasion, 2 This article is available in http colorectal cancer imedpub com archive php. Colorectal Cancer Open Access, Vol 3 No 1 2, ISSN 2471 9943. Whole genome expression, profiling to evaluate the role. of epigenetic processes on, MAL PRIMA1 DNA hypermethylation and decreased mRNA the progression of CRC They. Kalmar 10 2015 12, PTGDR SFRP1 expression in colorectal adenoma and cancer evaluated 49 colorectal adenoma.
and 49 CRC samples and, compared their gene expression. to 49 healthy samples, Examined MUC5AC activity in. 218 serrated colorectal polyps, MUC5AC hypomethylation occurs early in. including 42 goblet cell rich, the serrated pathway and it is specific for. hyperplastic polyps GCHP, Gastric mucin gene linked to the serrated polyps with MSI CIMP H or the BRAF.
Renaud 3 2016 13 MUC5AC 68 microvesicular hyperplastic. serrated pathway in CRC formation mutation These findings indicate that MUC5AC. polyps MVHP 100 sessile, hypomethylation may be a marker specific for. serrated adenomas SSA, malignant precursors of the serrated pathway. and eight traditional serrated, adenomas TSA, TCF21 was down regulated via promoter. Plays an important role in organ Compared the expression. hypermethylation in CRC tissues There was, Dai 1 2016 14 TCF21 development by promoting the transition of TCF21 in 151 CRC tissue. also a direct correlation between TCF21, of mesenchymal to epithelial cells MET samples to 30 normal samples.
methylation and lymph node invasion, Transient Receptor. Family of ion channels that consist of Significant decrease in the expression of. Potential TRP Investigated the expression of, multiple subsets of genes including TRPV3 TRPV4 TRPV5 TRPM4 and TRPC6. Sozucan 9 2015 15 gene family TRPV3 TRPM TRPV and TRPC in CRC. TRPM melastatin TRPV vanilloid genes in CRC tissues compared to healthy. TRPV4 TRPV5 tissue samples in 93 patients, and TPRC canonical tissue. TRPM4 and TRPC6, Secretory glycoprotein that plays. Increased activity of ANGPTL4 in CRC tissue Examined the molecular. many essential roles in tumorigenesis, Li 11 2015 16 ANGPTL4 compared to normal tissue and an even higher mechanism of ANGPTL4 in 54.
including migration invasion and, level correlated with liver metastasis colon cancer tissue samples. Genome wide analysis of 3494, Multiple SNPs at 6p12 1 nearest the ELOVL5. Phipps 1 2016 SNPs at 6p12 1 patients with metastatic CRC. gene which correlated with a poorer prognosis, across six prospective cohorts. rR evaluation of a genome wide, Locus 14q23 1 SNP SNP at 14q23 1 rs17094983 correlated with an. Lemire 11 2015 17 association study GWAS of, rs17094983 Single nucleotide polymorphisms SNPs increased risk of CRC.
16 517 patients, are the most common type of genetic. variation and they play an important role CASC8 gene SNP of rs7837328 and rs6983267. in the development and progression of are risk factors for CRC among both Caucasian. SNPs single Meta analysis of 34 articles which, many diseases including cancer and Asian whereas rs7014346 and rs10505477. nucleotide included 90 studies to evaluate, are risk factors only in Caucasian. Yao 11 2015 18 polymorphisms for the correlation between SNPs of. SMAD7 gene rs4939827 and rs4464148 are, CASC8 gene and the CASC8 and SMAD7 genes. risk factors for CRC among Caucasian whereas, SMAD7 gene and CRC.
rs12953717 is a risk factor in both Caucasians, and Asians. CRC 55 years who also had a first degree relative with CRC ATF3 may also play a role in metastasis as increased expression. 15 16 of these patients were noted to have rare germline in colorectal cancer cells is linked with invasion Over expression. mutations in known CRC genes compared to healthy controls of ATF3 increases the expression cluster of differentiation 44. However POT1 POLE2 and MRE11 were newly identified in this CD44 and also decreases retinoblastoma Rb expression both. study POT1 works in maintaining telomere length and three of which are CRC stem cell markers 18 ATF3 also decreased the. disruptive mutations were noted in the CRC group 15 POLE2 expression of epithelial mesenchymal transition EMT inducing. is a component of the polymerase epsilon enzyme complex A transcription factors which are essential for cancer metastasis. 18 These findings suggest multiple roles for ATF3 in the CRC. mutation in POLE2 leads to polymerase proofreading associated. progression likely through regulating apoptosis and invasion. polyposis 15 MRE11 is a nuclease involved in double strand. break repair and it is active in mismatch repair deficient cancer TET2 mutation. 15 The findings in this study support DNA replication and repair. defects as a basis for inherited CRC Ten eleven translocation TET consists of a family of enzymes. that catalyze the oxidation of 5 methylcytosine 5mC to. ATF3 mutation 5 hydroxymethylcytosine 5hmC 19 TET1 suppresses tumor. progression by inhibiting the WNT pathway 20 In CRC a. Activating transcription factor 3 AFT3 a member of ATF CREB decrease in TET1 messenger RNA mRNA has previously been. family of basic region leucine zipper bZip proteins regulates observed leading to decreased or absent levels of 5hmC 19. transcription by binding DNA 16 This gene is up regulated in However a recent study by Huang et al also revealed a loss of. response to cellular stress such as hypoxia anoxia carcinogens nuclear expression of TET2 in CRC cells 19 In fact loss of TET2. and DNA damage 17 A study by Jiang et al revealed that ATF3 is was linked to a more aggressive phenotype with metastasis 19. overexpressed in human colorectal cancer cells 18 In CRC cells The role of TET2 in CRC is unclear but it has been proposed as. ATF3 down regulates the expression of the B cell lymphoma 2 a tumor suppressor through post translational modification. Bcl 2 a gene that inhibits apoptosis 18 On the other hand 19 TET2 regulates gene expression by binding with DNA in the. ATF3 up regulates the activity of Bak a protein of the BCL 2 nucleus 20 Thus TET1 and TET2 suppress the progression of. family that induces apoptosis 18 CRC through separate mechanisms. 3 This article is available in http colorectal cancer imedpub com archive php. Colorectal Cancer Open Access, Vol 3 No 1 2, ISSN 2471 9943. CpG island methylator phenotype CIMP with a more aggressive phenotype thus leading to decreased. survival Their results suggest that Thoc1 may be used as a. CpG island methylator phenotype CIMP is due to prognostic marker for CRC. hypermethylation of multiple CpG islands that encompass the. promoter regions of multiple genes 21 This may prevent CD147 and MMP 11. binding of transcription factors to tumor suppressor genes 22. Matrix metalloproteinases MMPs are group of enzymes that. Consequently the suppressor genes are silenced which lead to. play an essential role in tumor invasion and metastasis via. the progression of CRC 23 A systematic review of thirty six. degradation of the extracellular matrix ECM during tissue. studies by Jia et al revealed a poorer prognosis in CRC patients. growth and turnover MMP expression is usually down regulated. with high CIMP H or positive CIMP than those with low CIMP L. in healthy tissue but levels are increased in pathological states. or negative CIMP 24, including inflammation and tumorigenesis 36. N acetyltransferase 2 NAT2 genotype Unlike other MMPs MMP 11 also called stromelysin 3 does not. Prior studies have established a correlation between red and play a direct role in ECM remodeling It catalyzes the degradation. processed meat consumption and CRC possibly due to exposure of 1 antitrypsin and insulin like growth factor binding protein 1. to heterocyclic amines HAAs 25 27 HAAs are chemicals that IGF BP 1 37 38 CD147 plays a role in tissue remodeling via. are produced when meats are cooked at high temperatures 27 stimulation of extracellular matrix metalloproteinase inducer. N acetyltransferase2 NAT2 is a gene that activates HAAs vi. the Molecular Genetics of Colorectal Cancer Colorec Cancer 2017 3 1 Introduction Colorectal cancer CRC is one of the most prevalent malignancies in the USA With an estimated incidence of 134 490 new cases and 49 190 deaths in 2016 it is the third most common cause of cancer as well as cancer mortality in both men and women with

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