ArticleInternational journal of experimental pathology2006
Alterations of p53, BCL-2, and hMSH2 protein expression in the normal brain tissues, gliosis, and gliomas.
Article in International journal of experimental pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 28 citations in OpenAlex.
- NF-κB inhibitor with Temozolomide results in significant apoptosis in glioblastoma via the NF-κB(p65) and actin cytoskeleton regulatory pathways.Scientific reports · 2020Article
- Long intergenic non-protein coding RNA 00475 silencing acts as a tumor suppressor in glioma under hypoxic condition by impairing microRNA-449b-5p-dependent AGAP2 up-regulation.Therapeutic advances in medical oncology · 2020Article
- MicroRNA based theranostics for brain cancer: basic principles.Journal of experimental & clinical cancer research : CR · 2019Review
- Nuclear factor-kappa B1 inhibits early apoptosis of glioma cells by promoting the expression of Bcl-2.OncoTargets and therapy · 2017Article
- Predictive Role of p53 Protein as a Single Marker or Associated with ki67 Antigen in Oral Leukoplakia: A Retrospective Longitudinal Study.The open dentistry journal · 2015Article
- MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway.Cancer science · 2014Article
- Article
- Ectopic expression of human MutS homologue 2 on renal carcinoma cells is induced by oxidative stress with interleukin-18 promotion via p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways.The Journal of biological chemistry · 2012Article
- Predictive Role of p53 Protein as a Single Marker or Associated to Ki67 Antigen in Oral Carcinogenesis.The open dentistry journal · 2008Article
- The role of the human DNA mismatch repair gene hMSH2 in DNA repair, cell cycle control and apoptosis: implications for pathogenesis, progression and therapy of cancer.Journal of molecular histology · 2006Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumorigenesis involves alterations in the tumor suppressor genes (p53), protooncogenes (BCL-2), and housekeeping genes (human MutS homologue-2 (hMSH2). We hypothesized that development of gliomas is associated with alterations of p53, BCL-2, and hMSH2 protein expression. To test our hypothesis and to examine these issues, we immunostained 60 specimens entailing normal brain tissues, gliosis, and gliomas (Grade I, II, III, IV) for p53, BCL-2, and hMSH2 protein expression. As compared with the normal brain and gliosis, examination of the average weighted scores in gliomas (Grade I, II, III, IV, respectively) showed significant up-regulation of: (i) p53 protein (0.0 +/- 0.0; 0.0 +/- 0.0; 0.9 +/- 0.5; 1.6 +/- 0.8; 1.7 +/- 0.5; and 4.1 +/- 0.8, P < 0.0001) (ii) hMSH2 (1.3 +/- 0.3; 1.5 +/- 0.7; 1.9 +/- 1.1; 2.2 +/- 0.5; 4.1 +/- 1.5; and 4.7 +/- 1.1, P < 0.0006), and (iii) BCL-2 (0.8 +/- 0.5; 1.9 +/- 0.5; 1.9 +/- 0.6; 2.0 +/- 0.6; 4.4 +/- 1.2; and 4.6 +/- 0.8, P < 0.001). The expression values (p53, BCL-2, and hMSH2) were statistically significantly higher (P < 0.05) in astrocytomas (Grade III) than in other gliomas. There was an insignificant negative correlation between p53 and BCL-2 (r = -0.07, P > 0.05) and between p53 and hMSH2 (r = -0.08, P > 0.05) protein expression. Alterations of the p53, BCL-2, and hMSH2 proteins occur during the development of these tumors.
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