18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high.

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Abstract Text:

Shuji Ogino,Takako Kawasaki,Gregory J Kirkner,Mutsuko Ohnishi,Charles S Fuchs,

BACKGROUND: The CpG island methylator phenotype (CIMP) with widespread promoter methylation is a distinct epigenetic phenotype in colorectal cancer, associated with microsatellite instability-high (MSI-high) and BRAF mutations. 18q loss of heterozygosity (LOH) commonly present in colorectal cancer with chromosomal instability (CIN) is associated with global hypomethylation in tumor cell. A recent study has shown an inverse correlation between CIN and CIMP (determined by MINTs, p16, p14 and MLH1 methylation) in colorectal cancer. However, no study has examined 18q LOH in relation to CIMP-high, CIMP-low (less extensive promoter methylation) and CIMP-0 (CIMP-negative), determined by quantitative DNA methylation analysis. METHODS: Utilizing MethyLight technology (real-time PCR), we quantified DNA methylation in 8 CIMP-specific promoters {CACNA1G, CDKN2A (p16), CRABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1} in 758 non-MSI-high colorectal cancers obtained from two large prospective cohorts. Using four 18q microsatellite markers (D18S55, D18S56, D18S67 and D18S487) and stringent criteria for 18q LOH, we selected 374 tumors (236 LOH-positive tumors with > or = 2 markers showing LOH; and 138 LOH-negative tumors with > or = 3 informative markers and no LOH). RESULTS: CIMP-0 (0/8 methylated promoters) was significantly more common in 18q LOH-positive tumors (59% = 139/236, p = 0.002) than 18q LOH-negative tumors (44% = 61/138), while CIMP-low/high (1/8-8/8 methylated promoters) was significantly more common (56%) in 18q LOH-negative tumors than 18q LOH-positive tumors (41%). These relations persisted after stratification by sex, location, or the status of MSI, p53 expression (by immunohistochemistry), or KRAS/BRAF mutation. CONCLUSION: 18q LOH is correlated positively with CIMP-0 and inversely with CIMP-low and CIMP-high. Our findings provide supporting evidence for relationship between CIMP-0 and 18q LOH as well as a molecular difference between CIMP-0 and CIMP-low in colorectal cancer.

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Publishing Authors By Initials

S Ogino,T Kawasaki,GJ Kirkner,M Ohnishi,CS Fuchs,

For similar biological factors: biological markers: tumor markers, biological research abstracts see: biological factors: biological markers: tumor markers, biological research

PUBMED ID PMID:

MEDLINE DATE:

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: BMC cancer

VOLUME: 7

Page Numbers: 72

Journal Abbreviation: BMC Cancer

ISSN: 1471-2407

DAY: 2

MONTH: 05

YEAR: 2007

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100967800

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Keywords Mesh Terms:

KEYWORDS: Tumor Markers, Biological

MESH TERMS: genetics

Chemical & Substance for Abstract: 18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high. Information

Substance Name: Tumor Markers, Biological

Registry Number: 0

Grant and Affiliation Information for 18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high.

AFFILIATION: Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA. shuji_ogino@dfci.harvard.edu

Country: England

AGENCY: United States NCI

GRANT: P01 CA87969

ACRONYM: CA

MEDLINETA: BMC Cancer

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative CIMP-0 and inversely with CIMP-low and CIMP-high Related Publications

• 18q loss of heterozygosity in microsatellite stable colorectal cancer is correlated with CpG island methylator phenotype-negative (CIMP-0) and inversely with CIMP-low and CIMP-high.
• Acute myelopathy. Retrospective clinical, laboratory, MRI and outcome analysis of 49 cases.
• Adjuvant and neoadjuvant approaches in gastric cancer.
• Adverse events of blood-pressure-lowering drugs: evidence of high incidence in a clinical setting.
• Association of dietary patterns with cancer recurrence and survival in patients with stage III colon cancer.
• Calcium-pterin suppresses mitogen-induced tryptophan degradation and neopterin production in peripheral blood mononuclear cells.
• Canonical notch signaling functions as a commitment switch in the epidermal lineage.
• Cardiac tamponade: a life-threatening complication of Still's disease.
• Catenins: keeping cells from getting their signals crossed.
• Circulating insulin-like growth factor axis and the risk of pancreatic cancer in four prospective cohorts.
• Circulating insulin-like growth factor binding protein-1 and the risk of pancreatic cancer.
• Contribution of the frontal eye field to gaze shifts in the head-unrestrained monkey: effects of microstimulation.
• CpG island methylation, response to combination chemotherapy, and patient survival in advanced microsatellite stable colorectal carcinoma.
• Evaluation of markers for CpG island methylator phenotype (CIMP) in colorectal cancer by a large population-based sample.
• Fatty acid synthase overexpression in colorectal cancer is associated with microsatellite instability, independent of CpG island methylator phenotype.
• Focal adhesion kinase modulates tension signaling to control actin and focal adhesion dynamics.
• GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior.
• Hormone replacement therapy and survival after colorectal cancer diagnosis.
• Identification of novel genes in genomic islands that contribute to Salmonella typhimurium replication in macrophages.
• Long-term aspirin use and mortality in women.
• Loss of a quiescent niche but not follicle stem cells in the absence of bone morphogenetic protein signaling.
• Loss of nuclear p27 (CDKN1B/KIP1) in colorectal cancer is correlated with microsatellite instability and CIMP.
• Neurogenesis in the adult brain: is there an association with mental disorders?
• Oncogenic BRAF regulates beta-Trcp expression and NF-kappaB activity in human melanoma cells.
• Phase I study of gefitinib, irinotecan, 5-fluorouracil and leucovorin in patients with metastatic colorectal cancer.
• Plasma folate, vitamin B6, vitamin B12, and homocysteine and pancreatic cancer risk in four large cohorts.
• Ruthenium-catalyzed mild C-H oxyfunctionalization of cyclic steroidal ethers.
• Suicide attempt aborted by an implantable defibrillator.
• Tcf3 governs stem cell features and represses cell fate determination in skin.
• The relationship between basal level of anxiety and the affective response to inflammation.