2016
DOI: 10.1097/01.xej.0000484374.45600.32
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Expression of α-methyl coenzyme A racemase and p16 in colorectal adenoma and adenocarcinoma

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Cited by 2 publications
(2 citation statements)
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“…These previous studies were in accordance with Kuefer et al [34], Atef and Bedeer [35] and Adil et al [36] who demonstrated high AMACR expression in well to moderately differentiated CRCs and weak expression in poorly/anaplastic CRCs. Their data also suggested that AMACR expression can be a marker of tumor differentiation.…”
Section: Fig 6 Correlations Between Amacr Cyclin D1 and Ki67 Expressi...supporting
confidence: 91%
“…These previous studies were in accordance with Kuefer et al [34], Atef and Bedeer [35] and Adil et al [36] who demonstrated high AMACR expression in well to moderately differentiated CRCs and weak expression in poorly/anaplastic CRCs. Their data also suggested that AMACR expression can be a marker of tumor differentiation.…”
Section: Fig 6 Correlations Between Amacr Cyclin D1 and Ki67 Expressi...supporting
confidence: 91%
“…P16 is a tumor suppressor gene with function in cell cycle regulation [13][14][15][16][17]. A study performed by Atef et al (2016) showed that p16 expression was higher in colorectal adenoma than in colorectal carcinoma (72% versus 22.5%), which has supported the statement that gene inactivation or loss plays a crucial part in the carcinogenesis process [21]. However, in the analysis performed by Al-Ahwal et al (2016), immunoexpression of the gene was slightly higher in colorectal carcinomas, compared to adenomas and normal mucosa, suggesting that the absence of p16 is a sign of the benign course of the adenoma and a key factor in monitoring the progression towards malignancy [13].…”
Section:  Discussionmentioning
confidence: 99%