Ki67 and p53 in gastrointestinal stromal tumors - GIST

Neves, Lúcio Roberto de Oliveira das; Oshima, Celina Tizuko Fujiyama; Neto, Ricardo Artigiani; Yanaguibashi, Gianni; Lourenço, Laércio Gomes; Forones, Nora Manoukian

doi:10.1590/s0004-28032009000200008

Cited by 26 publications

(16 citation statements)

References 40 publications

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“…Our meta-analysis showed that p53 expression appeared more often in recurred or metastasized GIST (malignant group) than in tumors with disease-free follow-up (benign group). Furthermore, p53 expression was significantly associated with the established prognostic criteria (NIH system), and was consistent with most previous GIST studies (6,(11)(12)(13)15,(16)(17)(18)(19). NIH I+H showed more positivity with p53 than NIH VL+L tumors.…”

Section: Discussionsupporting

confidence: 90%

“…A total of 19 publications met the inclusion criteria (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). The studies by Chou et al, Padilla et al, Romeo et al and Kwon et al were excluded due to insufficient information to calculate an OR (25)(26)(27)(28), and the study by Sakurai et al was also excluded since they used telomerase activity as the criteria for measuring the malignant risk of GIST (29).…”

Section: Study Characteristicsmentioning

confidence: 99%

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Predictive value of p53 expression in the risk of malignant gastrointestinal stromal tumors: Evidence from 19 studies

Zong

Chen

Jiang

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The current published data on p53 expression and its predictive value in the risk of malignant gastrointestinal stromal tumors (GIST) has are inconclusive. To derive a more precise estimation of the correlation between p53 and the biological behavior of GIST, a meta-analysis was performed. Studies were identified by searching PubMed and Embase. Inclusion criteria were GIST patients, and the evaluation of p53 expression and risk of malignancy. The odds ratio (OR) for a positive rate of p53 in the benign group vs. that in the malignant group and the ORs for the positive rate of p53 in the National Institutes of Health (NIH) very low risk + low risk group (VL+L) vs. the NIH intermediate risk + high risk (I+H) group were calculated with a 95% confidence interval (CI) for each study as an estimation of the predictive value of p53. A total of 19 studies including 1163 patients were involved in this meta-analysis. The overall OR for the positive rate of p53 in the malignant group vs. the benign group revealed that significantly elevated risks of positive p53 in the malignant group were achieved (OR 0.14, 95% CI: 0.06-0.31, P<0.00001, P heterogeneity =0.86). Moreover, significantly elevated risks of correlation between p53 expression and the NIH I+H group were achieved in the comparison of the NIH VL+L group vs. the NIH I+H group (OR, 0.25; 95% CI, 0.17-0.38; P<0.00001, P heterogeneity =0.04). The results indicate that p53 expression correlates with poor prognosis in GIST and has a close relationship within the NIH I+H group.

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Section: Discussionsupporting

confidence: 90%

Section: Study Characteristicsmentioning

confidence: 99%

Predictive value of p53 expression in the risk of malignant gastrointestinal stromal tumors: Evidence from 19 studies

Zong

Chen

Jiang

et al. 2011

Experimental and Therapeutic Medicine

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“…Sheikh et al (24) evaluated the expression of Ki-67 in colorectal adenomas and observed an invariably stronger expression in areas with higher dysplasia. In a study on p53 and Ki-67 in gastrointestinal stromal tumors, Neves et al (16) found higher values of Ki-67 in patients with tumors of medium and high risk.…”

Section: Discussionmentioning

confidence: 96%

“…In fact, the proliferative activity of cells in the colorectal mucosa and throughout the gastrointestinal tract is constant, but increases under special circumstances, such as in inflammatory and neoplastic conditions (15,16,24,25) . In a study of patients with ulcerative colitis, Shinozaki et al (25) found a higher expression of Ki-67 in areas of dysplastic mucosa compared with areas without dysplasia.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical evaluation of p53 and Ki-67 proteins in colorectal adenomas

Sousa

Rodrigues

Júnior

et al. 2012

Arq. Gastroenterol.

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-Context -The appearance of adenomas and their progression to adenocarcinomas is the result of an accumulation of genetic changes in cells of the intestinal mucosa inherited or acquired during life. Several proteins have been studied in relation to the development and progression of colorectal cancer, including tumor protein p53 (p53) and antigen identified by monoclonal antibody . Objective -To evaluate the expression of p53 and Ki-67 in colorectal adenomas and correlate the observed levels with clinical and pathologic findings. Method -The sample consisted of 50 adenomatous polyps from patients undergoing colonoscopy. After performing polypectomy, polyps were preserved in a formalin solution with 10% (vol./vol.) phosphate buffer, submitted for routine preparation of sections and slides and stained with hematoxylin and eosin. For each adenoma we then performed immunohistochemistry to detect specific p53 and Ki-67 proteins using a streptavidin-biotin-peroxidase enzyme immunoassay.Results -p53 was detected in 18% of the adenomas. The average Ki-67 protein index (i.Ki-67) was 0.49. A statistically significant difference was observed in p53 (P = 0.0003) and Ki-67 (P = 0.02) expression between adenomas with low-and high-grade dysplasia, particularly for p53. The expression of Ki-67 was greater in rectal adenomas than in colic adenomas (P = 0.02). No relationship was found between the expression of the two proteins in the sample. Conclusion -The p53 protein is expressed in a proportion of adenomas, while the Ki-67 protein was expressed in all adenomas. The expression of p53 was higher in adenomas with high-grade dysplasia. The expression of Ki-67 was higher in rectal adenomas and in adenomas with high-grade dysplasia. HEADINGS -Colorectal neoplasm. Tumor suppressor protein p53. Ki67-antigen. Immunohistochemistry.

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“…27,28 It is a classical concern of pathologists to report a parameter related with tumour proliferation index and Ki67-MIB1 as a nuclear proliferation associated antigen expressed in cell cycle (G1,S,G2 and M) but not in the resting phase, G0, which provides information about the portion of active cells in the cell cycle. 37,38 Ki-67 expression by immunohistochemistry can be a prognostic marker allowing the prediction of post-operative survival in different types of cancer. High expression of Ki-67 (cut-off above 10) is associated with worse survival in adenocarcinomas.…”

Section: Discussionmentioning

confidence: 99%

Lung adenocarcinoma: Sustained subtyping with immunohistochemistry and EGFR, HER2 and KRAS mutational status

Sousa

Rodrigues

Silva

et al. 2015

Revista Portuguesa de Pneumologia (English Edition)

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Pulmonary adenocarcinomas are still in the process of achieving morphological, immunohistochemical and genetic standardization. The ATS/ERS/IASLC proposed classification for lung adenocarcinomas supports the value of the identification of histological patterns, specifically in biopsies.Thirty pulmonary adenocarcinomas were subjected to immunohistochemical study (CK7, CK5, 6, 18, CK20, TTF1, CD56, HER2, EGFR and Ki-67), FISH and PCR followed by sequencing and fragment analysis for EGFR, HER2 and KRAS.Solid pattern showed lower TTF1 and higher Ki-67 expression. TTF1 expression was higher in non-mucinous lepidic and micropapillary patterns when compared to acinar and solid and acinar, solid and mucinous respectively. Higher Ki67 expression was present in lepidic and solid patterns compared to mucinous. EGFR membranous staining had increasing expression from non-mucinous lepidic/BA pattern to solid pattern and micropapillary until acinar pattern. EGFR mutations, mainly in exon 19, were more frequent in females, together with non-smoking status, while KRAS exon 2 mutations were statistically more frequent in males, especially in solid pattern. FISH EGFR copy was correlated gross, with mutations. HER2 copy number was raised in female tumours without mutations, in all cases. Although EGFR and KRAS mutations are generally considered mutually exclusive, in rare cases they can coexist as it happened in one of this series, and was represented in acinar pattern with rates of 42.9% and 17.9%, respectively. EGFR mutations were more frequent in lepidic/BA and acinar patterns. Some cases showed different EGFR mutations.The differences identified between the adenocarcinoma patterns reinforce the need to carefully identify the patterns present, with implications in diagnosis and in pathogenic understanding. EGFR and KRAS mutational status can be determined in biopsies representing bronchial

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Ki67 and p53 in gastrointestinal stromal tumors - GIST

Cited by 26 publications

References 40 publications

Predictive value of p53 expression in the risk of malignant gastrointestinal stromal tumors: Evidence from 19 studies

Predictive value of p53 expression in the risk of malignant gastrointestinal stromal tumors: Evidence from 19 studies

Immunohistochemical evaluation of p53 and Ki-67 proteins in colorectal adenomas

Lung adenocarcinoma: Sustained subtyping with immunohistochemistry and EGFR, HER2 and KRAS mutational status

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