Relationship between inactivation of p16 gene and gastric carcinoma

Zhao, Gaoping; Li, Tiechen; Shi, Lianghui; Xia, Yabin; Lu, Linming; Huang, Wenbin; Sun, Hongwei; Zhang, Yisheng

doi:10.3748/wjg.v9.i5.905

Cited by 19 publications

(18 citation statements)

References 27 publications

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“…In this study, 89% of cases had loss of expression of p16 (positivity lower than 10%) which is similar to literature data of 40%-90% loss 3,6,7 . Seventy eight percent of the cases showed positivity lower than 1%.…”

Section: Results Results Results Resultssupporting

confidence: 80%

“…Concerning to Lauren histological type, against expectations the diffuse type was predominant, 1,[26][27][28] no statistical difference between Lauren histological type and p16 expression in the two thresholds studied was found as previously reported, 12 although no agreement on this issue have been reached 7,27 . Although it is known that tumours with p16 loss tend to have a higher metastatic potential immunohistochemistry to p16 in lymph nodes was not carried out in this study, since overall p16 expression is much lower in metastatic lymph nodes than in primary lesion 6 .…”

Section: Results Results Results Resultsmentioning

confidence: 34%

“…Recent papers have demonstrated relation between p16 inactivation and development of stomach cancer. Forty to ninety per cent of gastric adenocarcinomas show inactivation of p16, [6][7][8][9][10][11] appearing to have relation with cellular differentiation 7,10,12 . Expression of p16 is decreased in node metastasis 6 .…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

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Expressão do P16 e do PDGFR-Beta no adenocarcinoma gástrico

Pinto

Lima

Kulkzynski

et al. 2009

Rev. Col. Bras. Cir.

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Section: Results Results Results Resultssupporting

confidence: 80%

Section: Results Results Results Resultsmentioning

confidence: 34%

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

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Expressão do P16 e do PDGFR-Beta no adenocarcinoma gástrico

Pinto

Lima

Kulkzynski

et al. 2009

Rev. Col. Bras. Cir.

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“…60 On the other, this signal could represent a cytoplasmic retention, and consequently a functional inactivation, similar to that observed in other tumor suppressor genes, including p16 INK4A . 61 At the mechanistic level, degradation by SKP2 was observed in vivo and demonstrated in vitro by siRNA methodology (Fig. 5), to be the most important downregulating mechanism of both KIPs in NSCLCs.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of the KIP family members p27^KIP1 and p57^KIP2 by SKP2 and the role of methylation in p57^KIP2 inactivation in nonsmall cell lung cancer

Pateras

Apostolopoulou

Koutsami

et al. 2006

Intl Journal of Cancer

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Knowing the status of molecules involved in cell cycle control in cancer is vital for therapeutic approaches aiming at their restoration. The p27 KIP1 and p57 KIP2 cyclin-dependent kinase inhibitors are nodal factors controlling normal cell cycle. Their expression in normal lung raises the question whether they have a mutual exclusive or redundant role in nonsmall cell lung cancer (NSCLC). A comparative comprehensive analysis was performed in a series of 70 NSCLCs. The majority of cases showed significantly reduced expression of both members compared to normal counterparts. Low KIP protein levels correlated with increased proliferation, which seems to be histological subtype preponderant. At mechanistic level, degradation by SKP2 was demonstrated, in vivo and in vitro, by siRNA-methodology, to be the most important downregulating mechanism of both KIPs in NSCLC. Decreased p57 ), suggested that inhibition of the SKP2-degradation mechanism restores p27 KIP1 and p57 KIP2 expression. Double siRNA treatments demonstrated that each KIP is independently capable of restraining cell growth. An additional demethylation step is required for complete reconstitution of p57 KIP2 expression in NSCLC. ' 2006 Wiley-Liss, Inc.

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“…For Bcl-2 and Cyclin D, both are cytoplasmic stainings, and were considered positive if 3 or 4 for intensity and distribution (6,7,18,29) . For Ki-67, the cells were characterized as positive even if stained weakly.…”

Section: Ink4amentioning

confidence: 99%