CpG Islands
DNA Methylation
Dinucleoside Phosphates
Promoter Regions, Genetic
Azacitidine
Gene Silencing
Epigenesis, Genetic
Indian Ocean Islands
Pacific Islands
DNA (Cytosine-5-)-Methyltransferase
Base Sequence
DNA Modification Methylases
Genome, Human
Sequence Analysis, DNA
Molecular Sequence Data
Gene Expression Regulation, Neoplastic
Methylation
Genes, Tumor Suppressor
Genes, p16
Polymerase Chain Reaction
Prince Edward Island
Mediterranean Islands
Microsatellite Instability
Transcription Initiation Site
Deoxyribonuclease HpaII
Long Interspersed Nucleotide Elements
DNA
Genomic Imprinting
Cyclin-Dependent Kinase Inhibitor p16
Epigenomics
United States Virgin Islands
5-Methylcytosine
Melanesia
Colorectal Neoplasms
Oligonucleotide Array Sequence Analysis
Cyclin-Dependent Kinase Inhibitor p15
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Transcription, Genetic
Micronesia
Oligodeoxyribonucleotides
Glutathione S-Transferase pi
Genes, Neoplasm
Chromatin
Exons
Histones
Geography
Death-Associated Protein Kinases
Proto-Oncogene Proteins B-raf
Channel Islands
Chromosome Mapping
Phenotype
Tumor Suppressor Proteins
Reunion
Falkland Islands
Polynesia
Alu Elements
DNA Primers
RNA, Messenger
Gene Expression Profiling
Gene Expression Regulation
Neoplasm Proteins
Models, Genetic
Core Binding Factor Alpha 3 Subunit
Microsatellite Repeats
Chromosomes, Human, Pair 21
Genome
X Chromosome
Restriction Mapping
Toll-Like Receptor 9
Introns
Mutation
Alleles
Cadherins
Chromatin Immunoprecipitation
Tumor Markers, Biological
Nuclear Proteins
Blotting, Southern
5' Flanking Region
Methyl-CpG-Binding Protein 2
Transcription Factors
Adenine Phosphoribosyltransferase
Repressor Proteins
DNA-Binding Proteins
Adaptor Proteins, Signal Transducing
Detailed methylation analysis of the glutathione S-transferase pi (GSTP1) gene in prostate cancer. (1/4270)
Glutathione-S-Transferases (GSTs) comprise a family of isoenzymes that provide protection to mammalian cells against electrophilic metabolites of carcinogens and reactive oxygen species. Previous studies have shown that the CpG-rich promoter region of the pi-class gene GSTP1 is methylated at single restriction sites in the majority of prostate cancers. In order to understand the nature of abnormal methylation of the GSTP1 gene in prostate cancer we undertook a detailed analysis of methylation at 131 CpG sites spanning the promoter and body of the gene. Our results show that DNA methylation is not confined to specific CpG sites in the promoter region of the GSTP1 gene but is extensive throughout the CpG island in prostate cancer cells. Furthermore we found that both alleles are abnormally methylated in this region. In normal prostate tissue, the entire CpG island was unmethylated, but extensive methylation was found outside the island in the body of the gene. Loss of GSTP1 expression correlated with DNA methylation of the CpG island in both prostate cancer cell lines and cancer tissues whereas methylation outside the CpG island in normal prostate tissue appeared to have no effect on gene expression. (+info)Comparative sequence analysis of human minisatellites showing meiotic repeat instability. (2/4270)
The highly variable human minisatellites MS32 (D1S8), MS31A (D7S21), and CEB1 (D2S90) all show recombination-based repeat instability restricted to the germline. Mutation usually results in polar interallelic conversion or occasionally in crossovers, which, at MS32 at least, extend into DNA flanking the repeat array, defining a localized recombination hotspot and suggesting that cis-acting elements in flanking DNA can influence repeat instability. Therefore, comparative sequence analysis was performed to search for common flanking elements associated with these unstable loci. All three minisatellites are located in GC-rich DNA abundant in dispersed and tandem repetitive elements. There were no significant sequence similarities between different loci upstream of the unstable end of the repeat array. Only one of the three loci showed clear evidence for putative coding sequences near the minisatellite. No consistent patterns of thermal stability or DNA secondary structure were shared by DNA flanking these loci. This work extends previous data on the genomic environment of minisatellites. In addition, this work suggests that recombinational activity is not controlled by primary or secondary characteristics of the DNA sequence flanking the repeat array and is not obviously associated with gene promoters as seen in yeast. (+info)Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia. (3/4270)
The DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) removes alkyl adducts from the O6 position of guanine. MGMT expression is decreased in some tumor tissues, and lack of activity has been observed in some cell lines. Loss of expression is rarely due to deletion, mutation, or rearrangement of the MGMT gene, but methylation of discrete regions of the CpG island of MGMT has been associated with the silencing of the gene in cell lines. We used methylation-specific PCR to study the promoter methylation of the MGMT gene. All normal tissues and expressing cancer cell lines were unmethylated, whereas nonexpressing cancer cell lines were methylated. Among the more than 500 primary human tumors examined, MGMT hypermethylation was present in a subset of specific types of cancer. In gliomas and colorectal carcinomas, aberrant methylation was detected in 40% of the tumors, whereas in non-small cell lung carcinomas, lymphomas, and head and neck carcinomas, this alteration was found in 25% of the tumors. MGMT methylation was found rarely or not at all in other tumor types. We also analyzed MGMT expression by immunohistochemistry in relation to the methylation status in 31 primary tumors. The presence of aberrant hypermethylation was associated with loss of MGMT protein, in contrast to retention of protein in the majority of tumors without aberrant hypermethylation. Our results suggest that epigenetic inactivation of MGMT plays an important role in primary human neoplasia. (+info)Methylation-associated silencing of the tissue inhibitor of metalloproteinase-3 gene suggest a suppressor role in kidney, brain, and other human cancers. (4/4270)
Tissue inhibitor of metalloproteinase-3 (TIMP-3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastasis. Loss of TIMP-3 has been related to the acquisition of tumorigenesis. Herein, we show that TIMP-3 is silenced in association with aberrant promoter-region methylation in cell lines derived from human cancers. TIMP-3 expression was restored after 5-aza-2'deoxycytidine-mediated demethylation of the TIMP-3 proximal promoter region. Genomic bisulfite sequencing revealed that TIMP-3 silencing was related to the overall density of methylation and that discrete regions within the TIMP-3 CpG island may be important for the silencing of this gene. Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and lung, but not in any of 41 normal tissue samples. The most frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normally expresses the highest TIMP-3 levels. This methylation correlated with a lack of detectable TIMP-3 protein in these tumors. Together, these data show that methylation-associated inactivation of TIMP-3 is frequent in many human tumors. (+info)Chlamydia infections and heart disease linked through antigenic mimicry. (5/4270)
Chlamydia infections are epidemiologically linked to human heart disease. A peptide from the murine heart muscle-specific alpha myosin heavy chain that has sequence homology to the 60-kilodalton cysteine-rich outer membrane proteins of Chlamydia pneumoniae, C. psittaci, and C. trachomatis was shown to induce autoimmune inflammatory heart disease in mice. Injection of the homologous Chlamydia peptides into mice also induced perivascular inflammation, fibrotic changes, and blood vessel occlusion in the heart, as well as triggering T and B cell reactivity to the homologous endogenous heart muscle-specific peptide. Chlamydia DNA functioned as an adjuvant in the triggering of peptide-induced inflammatory heart disease. Infection with C. trachomatis led to the production of autoantibodies to heart muscle-specific epitopes. Thus, Chlamydia-mediated heart disease is induced by antigenic mimicry of a heart muscle-specific protein. (+info)Molecular detection of tumor cells in bronchoalveolar lavage fluid from patients with early stage lung cancer. (6/4270)
BACKGROUND: Conventional cytologic analysis of sputum is an insensitive test for the diagnosis of non-small-cell lung cancer (NSCLC). We have recently demonstrated that polymerase chain reaction (PCR)-based molecular methods are more sensitive than cytologic analysis in diagnosing bladder cancer. In this study, we examined whether molecular assays could identify cancer cells in bronchoalveolar lavage (BAL) fluid. METHODS: Tumor-specific oncogene mutations, CpG-island methylation status, and microsatellite alterations in the DNA of cells in BAL fluid from 50 consecutive patients with resectable (stages I through IIIa) NSCLC were assessed by use of four PCR-based techniques. RESULTS: Of 50 tumors, 28 contained a p53 mutation, and the identical mutation was detected with a plaque hybridization assay in the BAL fluid of 39% (11 of 28) of the corresponding patients. Eight of 19 adenocarcinomas contained a K-ras mutation, and the identical mutation was detected with a mutation ligation assay in the BAL fluid of 50% (four of eight) of the corresponding patients. The p16 gene was methylated in 19 of 50 tumors, and methylated p16 alleles were detected in the BAL fluid of 63% (12 of 19) of the corresponding patients. Microsatellite instability in at least one marker was detected with a panel of 15 markers frequently altered in NSCLC in 23 of 50 tumors; the identical alteration was detected in the BAL fluid of 14% (three of 22) of the corresponding patients. When all four techniques were used, mutations or microsatellite instability was detected in the paired BAL fluid of 23 (53%) of the 43 patients with tumors carrying a genetic alteration. CONCLUSION: Although still limited by sensitivity, molecular diagnostic strategies can detect the presence of neoplastic cells in the proximal airway of patients with surgically resectable NSCLC. (+info)Genomic structure and expression of the mouse growth factor receptor related to tyrosine kinases (Ryk). (7/4270)
We report the genomic organization of the mouse orphan receptor related to tyrosine kinases (Ryk), a structurally unclassified member of the growth factor receptor family. The mouse RYK protein is encoded by 15 exons distributed over a minimum of 81 kilobases. Genomic DNA sequences encoding a variant protein tyrosine kinase ATP-binding motif characteristic of RYK are unexpectedly found in two separate exons. A feature of the gene is an unmethylated CpG island spanning exon 1 and flanking sequences, including a TATA box-containing putative promoter and single transcription start site. Immunohistochemical examination of RYK protein distribution revealed widespread but developmentally regulated expression, which was spatially restricted within particular adult organs. Quantitative reduction of Southern blotting stringency for the detection of Ryk-related sequences provided evidence for a retroprocessed mouse pseudogene and a more distantly related gene paralogue. Extensive cross-species reactivity of a mouse Ryk kinase subdomain probe and the cloning of a Ryk orthologue from Caenorhabditis elegans demonstrate that Ryk and its relatives encode widely conserved members of a novel receptor tyrosine kinase subfamily. (+info)Isolation of DNA fragments associated with methylated CpG islands in human adenocarcinomas of the lung using a methylated DNA binding column and denaturing gradient gel electrophoresis. (8/4270)
We have constructed a library of DNA fragments heavily methylated in human adenocarcinomas of the lung to permit the comprehensive isolation of methylated CpG islands in cancer. Heavily methylated genomic DNA fragments from tumors of nine male patients were enriched using a methylated DNA binding column and used for construction of the library. From this library, DNA fragments having properties of CpG islands were isolated on the basis of their reduced rate of strand dissociation during denaturing gradient gel electrophoresis. Approximately 1,000 clones, corresponding to 0.3% of the library were analyzed, and nine DNA fragments were identified as being associated with CpG islands that were methylated in tumor DNA. One CpG island was methylated specifically in tumor DNA, whereas the remaining eight CpG islands were methylated both in normal and tumor DNA derived from the same patients. Our results suggest that the number of CpG islands methylated specifically in tumors is not large. The library, which contains DNA fragments from methylated CpG islands comprehensively, is expected to be valuable when elucidating epigenetic processes involved in carcinogenesis. (+info)MSI is a common feature of many types of cancer, including colorectal cancer, gastrointestinal cancers, and endometrial cancer. It is estimated that up to 15% of all cancers exhibit MSI, with the highest prevalence found in colon cancer (40-50%).
MSI can be caused by a variety of genetic mutations, including defects in DNA repair genes such as MLH1 and MSH2, which are involved in the repair of microsatellites. Other causes of MSI include defects in the proofreading mechanism of DNA replication and the absence of the protein that corrects errors during DNA replication.
The significance of MSI in cancer is that it can be used as a biomarker for predicting the response of cancer cells to immunotherapy, such as checkpoint inhibitors. Cancer cells that exhibit MSI are more likely to respond to these therapies and have a better prognosis compared to those that do not exhibit MSI. Additionally, MSI can be used as a predictive biomarker for the presence of Lynch syndrome, an inherited condition that increases the risk of developing colorectal cancer and other cancers.
Overall, the study of microsatellite instability is an important area of cancer research, as it can provide valuable insights into the mechanisms of cancer development and progression, and may lead to the development of new diagnostic and therapeutic strategies for cancer treatment.
The causes of colorectal neoplasms are not fully understood, but factors such as age, genetics, diet, and lifestyle have been implicated. Symptoms of colorectal cancer can include changes in bowel habits, blood in the stool, abdominal pain, and weight loss. Screening for colorectal cancer is recommended for adults over the age of 50, as it can help detect early-stage tumors and improve survival rates.
There are several subtypes of colorectal neoplasms, including adenomas (which are precancerous polyps), carcinomas (which are malignant tumors), and lymphomas (which are cancers of the immune system). Treatment options for colorectal cancer depend on the stage and location of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Research into the causes and treatment of colorectal neoplasms is ongoing, and there has been significant progress in recent years. Advances in screening and treatment have improved survival rates for patients with colorectal cancer, and there is hope that continued research will lead to even more effective treatments in the future.
There are several types of stomach neoplasms, including:
1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.
The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.
There are several types of colonic neoplasms, including:
1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.
Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.
Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.
CpG island hypermethylation
CpG site
C7orf50
Eva K. Lee
Regulation of transcription in cancer
Marianne Frommer
Methylated DNA immunoprecipitation
Promoter (genetics)
DNA damage theory of aging
Glioma
CG suppression
Nita Ahuja
SMIM15
5-Methylcytosine
Molecular pathological epidemiology
KDM2A
DNA methyltransferase
Epigenetics of human development
Rob Klose
Demethylase
Adrian Bird
Shuji Ogino
P3 protein
DNMT1
60S ribosomal protein L24
COX7A2L
FKBP3
GRIN2D
GC-content
BAT1
TENM3
Augurin
MiR-137
Short interspersed nuclear element
DNA-PKcs
Sex-chromosome dosage compensation
P16
Prostate cancer
Index of biochemistry articles
Neuronatin
Glossary of Gaelic games terms
Hong Kong
PADI2
Office for Safeguarding National Security of the CPG in the HKSAR
1991 Spanish local elections
The Care Bears Adventure in Wonderland
Methylation
Cortactin
Embryonal fyn-associated substrate
Cancer
Norepinephrine transporter
Infrastructure of Changi Airport
Lynda Resnick
Myotonin-protein kinase
TMEFF2
Transgenerational epigenetic inheritance
PECR
Confounding by repetitive elements and CpG islands does not explain the association between hypomethylation and genomic...
MORF and MOZ acetyltransferases target unmethylated CpG islands through the winged helix domain - PubMed
Rare CpG island methylator phenotype in ulcerative colitis-associated neoplasias.
CpG Islands CpG Islands Track Settings
Methylation profiles of p16, RASSF1C, and hMLH1 promoter CpG islands in brain tumors | AVESİS
KDM2B links the Polycomb Repressive Complex 1 (PRC1) to recognition of CpG islands. - Oxford Neuroscience
FY 2009 Awards
Transgenerational inheritance of acquired epigenetic signatures at CpG islands in mice. | Cell;186(4): 715-731.e19, 2023 02 16...
Mouse mm10 chr12:52,713,333-62,634,435 UCSC Genome Browser v452
Human hg19 chr19:8,532,428-8,532,428 UCSC Genome Browser v448
Frontiers | Fusobacterium and Colorectal Cancer
UHRF1 ubiquitin like with PHD and ring finger domains 1 [Homo sapiens (human)] - Gene - NCBI
Make Enriched Heatmaps
Publication Detail
Mitochondrial DNA copy number can influence mortality and cardiovascular disease via methylation of nuclear DNA CpGs - PubMed
Biomarkers Search
Publications | Tanay Group
Pig genome functional annotation enhances the biological interpretation of complex traits and human disease | Nature...
AFF2 gene: MedlinePlus Genetics
Human hg19 chr6:32,582,640-32,582,660 UCSC Genome Browser v448
Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure | SpringerLink
Peter J. Park, PhD - DF/HCC
Epigenomics - Funded Research
Human hg38 chr2:25,160,915-25,168,903 UCSC Genome Browser v448
MPD: Genomic feature: Cpgi363
Name It / Claim It: Epigenetics Now Just Another Evolutionary Mechanism | Uncommon Descent
RFA-DA-09-015: The Mouse Gene Development Initiative (R01)
Methylation16
- Here, we demonstrate that DNA methylation of promoter-associated CpG islands (CGIs) can be transmitted from parents to their offspring in mice . (bvsalud.org)
- Also we downsampled 100000 CpG sites for methylation data. (bioconductor.org)
- First, a methylation score, the sum of individual hypermethylated tumor suppressor associated CpG sites, was calculated and associated with dietary intake of micronutrients involved in one-carbon metabolism and antioxidant activity, and food groups abundant in these nutrients. (nih.gov)
- Second, gene specific analyses using linear modeling with empirical Bayesian variance estimation were conducted to identify if methylation at individual CpG sites was associated with diet. (nih.gov)
- 1. Silencing of Peroxiredoxin 2 and aberrant methylation of 33 CpG islands in putative promoter regions in human malignant melanomas. (nih.gov)
- 8. Genome-wide profiling of CpG methylation identifies novel targets of aberrant hypermethylation in myeloid leukemia. (nih.gov)
- 9. Larger numbers of silenced genes in cancer cell lines with increased de novo methylation of scattered CpG sites. (nih.gov)
- 15. Regulation of human endogenous retrovirus-K expression in melanomas by CpG methylation. (nih.gov)
- 18. Isolation and enrichment of human genomic CpG islands by methylation-sensitive mirror orientation selection. (nih.gov)
- To complicate matters, scientists have long believed that methylation could only silence genes at sites in the genome where CG sequences are highly concentrated, regions known as "CpG islands. (goodnewsnetwork.org)
- Since nearly a third of human genes lack CpG islands, the researchers assumed methylation wouldn't switch these genes off. (goodnewsnetwork.org)
- Actually DNA methylation is the covalent addition of a methyl group to the 5 position of cytosine within CpG dinucleotides and is a fundamental process that not only modulates gene expression, but is also key to regulating chromosomal stability. (nih.gov)
- Local CpG density may determine their complementary binding patterns and therefore that the methylation landscape is encoded in the DNA sequence. (biomedcentral.com)
- We found that the expression of Ard1b in mouse spermatogenic cells and tissues correlated with the CpG island methylation pattern of the gene. (nih.gov)
- Our data suggest that the regulatory mechanism of the transcription of Ard1b/ARD1B is evolutionarily conserved and involves CpG island methylation. (nih.gov)
- Therefore, we determined the percent methylation for CpG islands from DNA extracted from mononuclear blood cells of 24 male spray-painters exposed to 1,6-hexamethylene diisocyanate (HDI) monomer and HDI isocyanurate. (cdc.gov)
Housekeeping genes1
- CpG islands are associated with genes, particularly housekeeping genes, in vertebrates. (ucsc.edu)
Methylator3
- Rare CpG island methylator phenotype in ulcerative colitis-associated neoplasias. (nih.gov)
- 6. Identification of genes targeted by CpG island methylator phenotype in neuroblastomas, and their possible integrative involvement in poor prognosis. (nih.gov)
- 16. The CpG island methylator phenotype: what's in a name? (nih.gov)
Hypermethylation4
- Trinucleotide repeat amplification and hypermethylation of a CpG island in FRAXE mental retardation. (medlineplus.gov)
- CpG islands hypermethylation in the promoter regions of genes- as pejorative prognostic markers in adrenocortical cancer (ACC). (endocrine-abstracts.org)
- Abstract: DESCRIPTION (provided by applicant): Hypermethylation of promoter CpG islands is an important mechanism to silence the expression of many tumor suppressors, DNA repair, and other genes in cancer. (nih.gov)
- To quantify the demethylation and reactivation of hypermethylation-silenced genes (MSGs) such as RARbeta, p16, MGMT, and hMLH1 by EGCG, characterize the pattern of CpG demethylation, and determine the sustainability of the reactivated gene expression. (nih.gov)
CGIs1
- CpG islands (CGIs) are associated with most mammalian gene promoters. (ox.ac.uk)
Dinucleotides1
- The CpG count is the number of CG dinucleotides in the island. (ucsc.edu)
Chromatin1
- A variety of regulatory proteins including DNA methyltransferases, methyl-CpG binding proteins, histone- modifying enzymes, chromatin remodeling factors, and their multimolecular complexes are involved in the overall epigenetic process. (nih.gov)
Cytosine1
- Normally a C (cytosine) base followed immediately by a G (guanine) base (a CpG) is rare in vertebrate DNA because the Cs in such an arrangement tend to be methylated. (ucsc.edu)
Epigenetic1
- Transgenerational inheritance of acquired epigenetic signatures at CpG islands in mice. (bvsalud.org)
Promoter regions1
- CpG islands are typically common near transcription start sites and may be associated with promoter regions. (ucsc.edu)
Genome2
Humans1
- In humans there are about 45,000 CpG islands, mostly found at the 5' ends of genes. (nih.gov)
Human2
Regions1
- The unmasked version of the track displays potential CpG islands that exist in repeat regions and would otherwise not be visible in the repeat masked version. (ucsc.edu)
Data1
- CpG islands and its associated tables can be explored interactively using the REST API , the Table Browser or the Data Integrator . (ucsc.edu)
Source1
- The source for the cpg_lh program can be obtained from src/utils/cpgIslandExt/ . (ucsc.edu)
Base1
- CpG islands were predicted by searching the sequence one base at a time, scoring each dinucleotide (+17 for CG and -1 for others) and identifying maximally scoring segments. (ucsc.edu)
Methylator phenotype5
- Rare CpG island methylator phenotype in ulcerative colitis-associated neoplasias. (nih.gov)
- CpG island methylator phenotype in plasma is associated with hepatocellular carcinoma prognosis. (cdc.gov)
- CpG island methylator phenotype identifies high risk patients among microsatellite stable BRAF mutated colorectal cancers. (cdc.gov)
- Predictive value of CpG island methylator phenotype for tumor recurrence in hepatitis B virus-associated hepatocellular carcinoma following liver transplantation. (cdc.gov)
- CpG island methylator phenotype predicts progression of malignant melanoma. (cdc.gov)
Methylation5
- To determine the methylation profile of multiple tumor-related genes during multistep hepatocarcinogenesis, we investigated the methylation status of CpG islands of 9 genes, using methylation-specific polymerase chain reaction for 60 paired hepatocellular carcinoma (HCC) and non-HCC liver tissue samples, 22 dysplastic nodule (DN), 30 liver cirrhosis (LC), 34 chronic hepatitis (CH) and 20 normal liver samples. (nih.gov)
- First, a methylation score, the sum of individual hypermethylated tumor suppressor associated CpG sites, was calculated and associated with dietary intake of micronutrients involved in one-carbon metabolism and antioxidant activity, and food groups abundant in these nutrients. (nih.gov)
- Second, gene specific analyses using linear modeling with empirical Bayesian variance estimation were conducted to identify if methylation at individual CpG sites was associated with diet. (nih.gov)
- Methylation changes were prominent in a 500 bp non-CpG island-like region of the Ha- ras promoter and less prominent in a 525 bp CpG island-like region. (cdc.gov)
- Methylation of the CpG sites only on the sense strand of the APC gene is specific for hepatocellular carcinoma. (cdc.gov)
Aberrant CpG1
- Aberrant CpG island hypermethylation in dysplastic nodules and early HCC of hepatitis B virus-related human multistep hepatocarcinogenesis. (cdc.gov)