PTEN

Effect of TIEG1 on apoptosis and expression of Bcl-2/Bax and Pten in leukemic cell lines

K. Yao, Xing, H. C., Wu, B., Li, Y., Liao, A. J., Yang, W., and Liu, Z. G., Effect of TIEG1 on apoptosis and expression of Bcl-2/Bax and Pten in leukemic cell lines, vol. 14, pp. 1968-1974, 2015.

We examined the effect of transforming growth factor-b inducible early gene-1 (TIEG1) on the apoptosis of leukemic cell lines and expression of B-cell lymphoma 2 (Bcl-2) and phosphatase and tensin homolog (Pten). Four leukemic cell lines (HL-60, U937, Raji, and K562) were treated with 0, 1, 5, 10, and 20 ng/mL TIEG1, respectively. The cell growth inhibitory ratio was assessed using the MTT assay. An inhibitory curve was drawn, and half-maximal inhibitory concentration was calculated.

Genetic polymorphisms of CCND1 and PTEN in progression of esophageal squamous carcinoma

Y. Jang, Lu, S. A., Chen, Z. P., Ma, J., Xu, C. Q., Zhang, C. Z., and Wang, J. J., Genetic polymorphisms of CCND1 and PTEN in progression of esophageal squamous carcinoma, vol. 12, pp. 6685-6691, 2013.

Cyclin D1 (CCND1) plays a significant role in G1-S transition of cell cycle, and phosphatase and a tensin homologue (PTEN) negatively regulate cell cycle through phosphatidylinositol 3-kinase (PI3K)/AKT signaling. CCND1 and PTEN genetic polymorphisms might induce susceptibility to the occurrence of esophageal squamous cell carcinoma (ESCC). Three hundred and four ESCC patients and 413 healthy controls from Anyang, China, were enrolled in this study.

Mutational analysis of genes p14ARF, p15INK4b, p16INK4a, and PTEN in human nervous system tumors

L. O. Almeida, Custódio, A. C., Araújo, J. J., Rey, J. A., Almeida, J. R. W., Santos, M. J., Clara, C. A., and Casartelli, C., Mutational analysis of genes p14ARF, p15INK4b, p16INK4a, and PTEN in human nervous system tumors, vol. 7, pp. 451-459, 2008.

The cancer is one of the most common and severe problems in clinical medicine, and nervous system tumors represent about 2% of the types of cancer. The central role of the nervous system in the maintenance of vital activities and the functional consequences of the loss of neurons can explain how severe brain cancers are. The cell cycle is a highly complex process, with a wide number of regulatory proteins involved, and such proteins can suffer alterations that transform normal cells into malignant ones.

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