Infrequent p53 gene alterations in ulcerative colitis

Mattar, Rejane; Alexandrino, Ana Maria; Laudanna, Antônio Atílio

doi:10.1590/s0100-879x1999000900005

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…In the present study p53 expression was similar to in those studies. However, Mattar et al [16] did not find p53 gene mutation in UC that was histologically negative for dysplasia. Reactive species produced during inflammation and sustained oxidative stress can induce p53 mutation.…”

Section: Discussionmentioning

confidence: 95%

Expression of p53, VEGF, Microvessel Density, and Cyclin-D1 in Noncancerous Tissue of Inflammatory Bowel Disease

et al. 2008

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We aimed to evaluate the carcinogenesis risk in inflammatory bowel disease via p53 mutation and its relation with hyperproliferation (cyclin-D1) and angiogenesis (with vascular endothelial growth factor [VEGF] and microvessel density) and whether these events play important roles in pathogenesis of inflammatory bowel disease. Colonic tissue samples of 26 ulcerative colitis, 6 Crohn's disease, and 8 amoebic colitis patients as well as samples of 10 healthy controls were stained with p53, cyclin-D1, CD34, and VEGF monoclonal antibodies by immunohistochemistry and evaluated semiquantitatively. Expression of p53 was higher in ulcerative colitis than in the healthy control and amoebic colitis groups (4.15 +/- 2.07, 1.4 +/- 1.5, 1.3 +/- 1.5; P < 0.001). The Crohn's disease group had the highest p53 expression (4.6 +/- 1.6). The Crohn's disease, ulcerative colitis, and amoebic colitis groups all had higher VEGF expression than did the healthy controls (respectively, 4.3 +/- 1.2, 2.92 +/- 2.0, 2.3 +/- 1.5, 0.6 +/- 0.97; P < 0.001). Also, microvessel density was statistically higher in all three colitis groups than in healthy controls. Cyclin-D1 expression in all four groups was similar. The study showed that p53 mutation was present in nonneoplastic mucosa of inflammatory bowel disease patients. Detecting strong p53 overexpression with VEGF overexpression may help in differentiating inflammatory bowel disease from other colitis.

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Section: Discussionmentioning

confidence: 95%

Expression of p53, VEGF, Microvessel Density, and Cyclin-D1 in Noncancerous Tissue of Inflammatory Bowel Disease

et al. 2008

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“…The PCR product (5 l) was then incubated with exonuclease I (1 l) and shrimp alkaline phosphatase (1 l) contained in the PCR product presequencing kit (USB, Cleveland, OH) for 15 min at 37°C, and then inactivated for 15 min at 80°C, and finally incubated at 4°C. Exonuclease I and shrimp alkaline phosphatase included in the PCR product presequencing kit were used to effectively remove the excess deoxynucleoside triphosphates and primers from DNA produced by PCR amplification (Matter et al, 1999). For cycle sequencing, the reaction mixture (20 l) consisted of 2 l of BigDye Terminator Version 3 (Applied Biosystems, Uppsala, Sweden), 1.6 pmol of a sequencing primer (Table 2), 3 l of (1ϫ) sequencing buffer (Applied Biosystems), and 4.4 l of the PCR products (10 -40 ng of the PCR-amplified DNA).…”

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confidence: 99%

Six Novel NonsynonymousCYP1A2Gene Polymorphisms: Catalytic Activities of the Naturally Occurring Variant Enzymes

Murayama¹,

Soyama²,

Saito³

et al. 2003

J Pharmacol Exp Ther

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Six novel nonsynonymous nucleotide alterations were found in the cytochrome P450 1A2 gene in a Japanese population, which resulted in the following amino acid substitutions: T83M, E168Q, F186L, S212C, G299A, and T438I. These individuals were heterozygous for the amino acid substitutions. The potential functional alterations caused by the amino acid substitutions were characterized by a cDNA-mediated expression system using Chinese hamster V79 cells. Among the six CYP1A2 variants, F186L showed the most profound and statistically significant reduction in O-deethylation of phenacetin and 7-ethoxyresorufin. Kinetic analyses performed for the ethoxyresorufin O-deethylation revealed that the V max of the F186L variant was approximately 5% of that of the CYP1A2 wild type, despite a 5-fold lower K m value of the variant, the consequence of which was reduced enzymatic activity toward the substrate. Thus, for the first time, phenylalanine at residue 186 is suggested to be a critical amino acid for catalytic activity.

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Analysis of mutations in TP53, APC, K-ras, and DCC genes in the non-dysplastic mucosa of patients with inflammatory bowel disease

Rapozo

Grinmann

Carvalho

et al. 2009

Int J Colorectal Dis

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Infrequent p53 gene alterations in ulcerative colitis

Cited by 4 publications

References 28 publications

Expression of p53, VEGF, Microvessel Density, and Cyclin-D1 in Noncancerous Tissue of Inflammatory Bowel Disease

Expression of p53, VEGF, Microvessel Density, and Cyclin-D1 in Noncancerous Tissue of Inflammatory Bowel Disease

Six Novel NonsynonymousCYP1A2Gene Polymorphisms: Catalytic Activities of the Naturally Occurring Variant Enzymes

Analysis of mutations in TP53, APC, K-ras, and DCC genes in the non-dysplastic mucosa of patients with inflammatory bowel disease

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