Correlation of laterally spreading type and JC virus with methylator phenotype status in colorectal adenoma

Nosho, Katsuhiko; Yamamoto, Hiroyuki; Takahashi, Taiga; Mikami, Masashi; Hizaki, Keiichi; Maehata, Tadateru; Taniguchi, Hiroaki; Yamaoka, Satoshi; Adachi, Yasushi; Itoh, Fumio; Imai, Kohzoh; Shinomura, Yasuhisa

doi:10.1016/j.humpath.2007.10.005

Cited by 13 publications

(12 citation statements)

References 35 publications

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“…[31][32][33][34][35]37 We recently reported an association among miR-31 expression, BRAF mutation and poor prognosis involving a large CRC sample (N 5 721); we also reported that high miR-31 expression is frequently detected in the proximal colon (cecum and ascending and transverse colon) compared to that in the distal colon (the descending and sigmoid colon) and rectum. 38 Because the presence of BRAF mutation is tightly associated with CIMP status, 20,[44][45][46] we examined the association between miR-31 expression and CIMP status in serrated lesions. With regard to CRCs, Slattery et al reported that miR-31 was the one of the upregulated miRNAs in patients with CIMP-high status; however, they did not examine BRAF mutations.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions

Ito

Mitsuhashi

Igarashi

et al. 2014

Intl Journal of Cancer

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The CpG island methylator phenotype (CIMP) is a distinct form of epigenomic instability. Many CIMP-high colorectal cancers (CRCs) with BRAF mutation are considered to arise from serrated pathway. We recently reported that microRNA-31 (miR-31) is associated with BRAF mutation in colorectal tumors. Emerging new approaches have revealed gradual changes in BRAF mutation and CIMP-high throughout the colorectum in CRCs. Here, we attempted to identify a possible association between miR-31 and epigenetic features in serrated pathway, and hypothesized that miR-31 supports the "colorectal continuum" concept. We evaluated miR-31 expression, BRAF mutation and epigenetic features including CIMP status in 381 serrated lesions and 222 non-serrated adenomas and examined associations between them and tumor location (rectum; sigmoid, descending, transverse and ascending colon and cecum). A significant association was observed between high miR-31 expression and CIMPhigh status in serrated lesions with BRAF mutation (p 5 0.0001). In contrast, miR-31 was slightly but insignificantly associated with CIMP status in the cases with wild-type BRAF. miR-31 expression in sessile serrated adenomas (SSAs) with cytological dysplasia was higher than that in SSAs, whereas, no significant difference was observed between traditional serrated adenomas (TSAs) and TSAs with high-grade dysplasia. The frequency of miR-31, BRAF mutation CIMP-high and MLH1 methylation increased gradually from the rectum to cecum in serrated lesions. In conclusion, miR-31 expression was associated with CIMP-high status in serrated lesions with BRAF mutation. Our data also suggested that miR-31 plays an important role in SSA evolution and may be a molecule supporting the colorectal continuum.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions

Ito

Mitsuhashi

Igarashi

et al. 2014

Intl Journal of Cancer

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“…JCPyV-associated malignancy -The transforming potential of JCPyV is well documented in different cell biological situations, which provide biological plausibility and raise the question about the role of JCPyV in human malignancies. A number of human malignancies have been associated with JCPyV including oligodendroglioma, astrocytoma medulloblastoma, ependymoma, and glioblastoma (189,(248)(249)(250)(251) and non-Hodgkin lymphoma (252,253), as well as colorectal carcinoma, and gastric and anal cancer (254)(255)(256)(257)(258)(259)(260).…”

Section: Jcpyv Diseasementioning

confidence: 99%

The human JC polyomavirus (JCPyV): virological background and clinical implications

Hirsch

Kardas

Kranz

et al. 2013

APMIS

149

169

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JC polyomavirus (JCPyV) was the first of now 12 PyVs detected in humans, when in 1964, PyV particles were revealed by electron microscopy in progressive multifocal leukoencephalopathy (PML) tissues. JCPyV infection is common in 35–70% of the general population, and the virus thereafter persists in the renourinary tract. One third of healthy adults asymptomatically shed JCPyV at approximately 50 000 copies/mL urine. PML is rare having an incidence of <0.3 per 100 000 person years in the general population. This increased to 2.4 per 1000 person years in HIV‐AIDS patients without combination antiretroviral therapy (cART). Recently, PML emerged in multiple sclerosis patients treated with natalizumab to 2.13 cases per 1000 patients. Natalizumab blocks α4‐integrin‐dependent lymphocyte homing to the brain suggesting that not the overall cellular immunodeficiency but local failure of brain immune surveillance is a pivotal factor for PML. Recovering JCPyV‐specific immune control, e.g., by starting cART or discontinuing natalizumab, significantly improves PML survival, but is challenged by the immune reconstitution inflammatory syndrome. Important steps of PML pathogenesis are undefined, and antiviral therapies are lacking. New clues might come from molecular and functional profiling of JCPyV and PML pathology and comparison with other replicative pathologies such as granule cell neuronopathy and (meningo‐)encephalitis, and non‐replicative JCPyV pathology possibly contributing to some malignancies. Given the increasing number of immunologically vulnerable patients, a critical reappraisal of JCPyV infection, replication and disease seems warranted.

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“…About 35%-94% of CRC tissues and 5-50% of colorectal adenomas were found to host JCV T-antigen, which is often concentrated in the nucleus (Enam et al, 2002; P. Y. Lin et al, 2008;Goel et al, 2006;Link et al, 2009;Nosho et al, 2008Nosho et al, , 2009Ogino et al, 2009;Selgrad et al, 2008;Jung et al, 2008). The expression of JCV T-antigen was significantly higher in colorectal adenomas from liver transplant recipients compared to adenomas in normal controls, pointing to a possible etiologic role for immunosuppression (Selgrad et al, 2008).…”

Section: Cancer In Humanmentioning

confidence: 99%

“…This deletional event probably provides the second hit at the tumour suppressor genes, and eventually leads to clonal expansion. The role of DNA hypermethylation has recently been explored in both colorectal carcinoma and adenoma, nevertheless the results were contradictory (Nosho et al, 2008Goel et al, 2006).…”

Section: Mechanism/ Mechanistic Studiesmentioning

confidence: 99%

The Role of Infectious Agents in Colorectal Carcinogenesis

Hamid¹,

Mustafa²

2012

Colorectal Cancer Biology - From Genes to Tumor

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Correlation of laterally spreading type and JC virus with methylator phenotype status in colorectal adenoma

Cited by 13 publications

References 35 publications

MicroRNA‐31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions

MicroRNA‐31 expression in relation to BRAF mutation, CpG island methylation and colorectal continuum in serrated lesions

The human JC polyomavirus (JCPyV): virological background and clinical implications

The Role of Infectious Agents in Colorectal Carcinogenesis

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