Activation but Not Inactivation of theMTS1Gene Is Associated with Primary Colorectal Carcinomas

Ohhara, Moritaka; Esumi, Mariko; Kurosu, Yasuhiko

doi:10.1006/bbrc.1996.1430

Cited by 22 publications

(16 citation statements)

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“…We found that, in a previous immunohistochemical study on 71 archival specimens of CRC, p16 expression-positive tumor cells were seen in roughly 50% specimens, and these p16 expressive specimens were coincident with those with a poorer differentiation grade [46] . Other investigators have also proposed that activation but not inactivation of p16 gene was associated with primary CRC [47] . We will continue our effects to explore the correspondent relation of p16 methylation and p16 expression in the identical CRC specimen, so as to determine how the seemly paradoxical events might unite in one tumor.…”

Section: Discussionmentioning

confidence: 97%

p16 gene methylation in colorectal cancers associated with Duke’s staging

Yi¹,

Wang²,

Hui³

et al. 2001

WJG

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AIM To explore the association of methylation of the CpG island in the promotor of the P16 tumor suppressor gene with the clinicopath ological characteristics of the colorectal cancers.METHODS Methylation-specific PCR (MSP) was used to detect P16 methylation of 62 sporadic colorectal cancer specimens.RESULTS P16 methylation was detected in 42% of the tumors. Dukes' staging was associated with P16 methylation status. p16 methylation occurred more frequently in Dukes' C and D patients (75.9%) than in Dukes' A and B patients (12.1%).CONCLUSION P16 methylation plays a role in the carcinogenes is of a subset of colorectal cancer, and it might be linked to poor prognosis.

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Section: Discussionmentioning

confidence: 97%

p16 gene methylation in colorectal cancers associated with Duke’s staging

Yi¹,

Wang²,

Hui³

et al. 2001

WJG

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“…28 The inactivation of these genes by loss, mutation, or hypermethylation are key events in a variety of tumors, including melanomas, gastrinomas, colorectal carcinoma, and non-small cell carcinomas of the lung. [29][30][31][32] On the short arm of chromosome 11 we were also able to pinpoint a relatively small region that was lost in three pleuropulmonary blastomas in our series, which consisted of 11p14 only. While this region does not appear to contain currently known tumor suppressor genes, it is interesting to note that two genes, WT1 and PAX6, that are highly relevant to pediatric tumorigenesis and development are located on 11p13, which is deleted in two patients.…”

Section: Discussionmentioning

confidence: 97%

Gain of chromosome 8q is a frequent finding in pleuropulmonary blastoma

et al. 2007

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Pleuropulmonary blastomas are rare malignant intrathoracic tumors of early childhood. They appear as a pulmonary-and/or pleural-based mass and their pathogenesis and relationship to other pediatric solid tumors is not well understood. In this study, paraffin-embedded material of five cases of pleuropulmonary blastoma was analyzed for genetic alterations by comparative genomic hybridization and five genetic loci by fluorescence in situ hybridization. Comparative genomic hybridization identified aberrations in all pleuropulmonary blastomas, including four amplifications in three tumors at chromosomes 5q33-34, 11q22.2-ter, 15q25-ter, and 19q11-13.2. The most frequent DNA gains involved 8q11-22.2 (four cases) and 20q (two cases), whereas the most common losses included 9p21-24 (two cases) and 11p14 (three cases). Chromosome 8 gains were confirmed by fluorescent in situ hybridization, resulting in the detection of up to five copies of chromosome 8 centromeres per nucleus. In the two surviving patients, chromosome 8 gains were the only genetic abnormality, suggesting that this might be an early event in pleuropulmonary blastoma carcinogenesis. The identification of new genetic alterations as well as the confirmation of previously reported ones (especially 8q gains) in pleuropulmonary blastoma should help to improve our understanding of both the molecular mechanisms underlying the tumorigenesis of pleuropulmonary blastoma and the relationship of pleuropulmonary blastoma with other pediatric tumors.

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“…INK4A and p21 WAF1 , are present in a variety of human malignancies (Merlo et al, 1995;Ohhara et al, 1996).…”

Section: Kip2mentioning

confidence: 99%

Comparative detection and quantitation of human CDK inhibitor mRNA expression of p15^INK4B, p16^INK4A, p16β, p18^INK4C, p19^INK4D, p21^WAF1, p27^KIP1 and p57^KIP2 by RT‐PCR using a polycompetitive internal standard

Schwaller

Pabst

Bickel³

et al. 1997

Br J Haematol

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For comparative and quantitative analysis of human cyclin‐dependent kinase inhibitor gene expression (CKI; p15INK4B, p16INK4A, p16β, p18INK4C, p19INK4D, p21WAF1, p27KIP1 and p57KIP2) we set up an RT‐PCR assay with a construct termed pCKIquant producing polycompetitive RNA as an internal standard. We demonstrated the reproducibility, accuracy and high sensitivity of the assay in the in vitro model of myeloid leukaemic HL‐60 cells. We also showed that the pCKIquant CKI assay is an excellent tool for the assessment of CKI mRNA expression in clinical samples, e.g. single cryostat sections of lymphoma biopsies.

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Activation but Not Inactivation of theMTS1Gene Is Associated with Primary Colorectal Carcinomas

Cited by 22 publications

References 0 publications

p16 gene methylation in colorectal cancers associated with Duke’s staging

p16 gene methylation in colorectal cancers associated with Duke’s staging

Gain of chromosome 8q is a frequent finding in pleuropulmonary blastoma

Comparative detection and quantitation of human CDK inhibitor mRNA expression of p15^INK4B, p16^INK4A, p16β, p18^INK4C, p19^INK4D, p21^WAF1, p27^KIP1 and p57^KIP2 by RT‐PCR using a polycompetitive internal standard

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Activation but Not Inactivation of theMTS1Gene Is Associated with Primary Colorectal Carcinomas

Cited by 22 publications

References 0 publications

p16 gene methylation in colorectal cancers associated with Duke’s staging

p16 gene methylation in colorectal cancers associated with Duke’s staging

Gain of chromosome 8q is a frequent finding in pleuropulmonary blastoma

Comparative detection and quantitation of human CDK inhibitor mRNA expression of p15INK4B, p16INK4A, p16β, p18INK4C, p19INK4D, p21WAF1, p27KIP1 and p57KIP2 by RT‐PCR using a polycompetitive internal standard

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Comparative detection and quantitation of human CDK inhibitor mRNA expression of p15^INK4B, p16^INK4A, p16β, p18^INK4C, p19^INK4D, p21^WAF1, p27^KIP1 and p57^KIP2 by RT‐PCR using a polycompetitive internal standard