Is exon 5 of the PTEN/MMAC1 gene a prognostic marker in anaplastic glioma?

Rustia, Alessandro; Wierzbicki, Venceslao; Marrocco, Luigi; Tossini, Alessandro; Zamponi, Carlo; Lista, Florigio

doi:10.1007/pl00014589

Cited by 10 publications

(6 citation statements)

References 47 publications

(46 reference statements)

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“…Low expression of PTEN gene product was implicated in the clinicopathological stage and metastasis of various malignancies. We found that PTEN expression was negatively correlated with invasive depth, metastasis, and growth patterns of gastric carcinomas, similar to other kinds of tumors 24–31 . It was suggested that reduced expression of the PTEN protein probably regulated invasion, metastasis and growth patterns of gastric carcinoma.…”

Section: Discussionsupporting

confidence: 68%

Role of PTEN and MMP‐7 expression in growth, invasion, metastasis and angiogenesis of gastric carcinoma

Zheng

Sun

et al. 2003

Pathology International

184

191

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To investigate the role of PTEN and matrix metalloproteinase-7 (MMP-7) expression in tumorigenesis and progression of gastric carcinoma, their expression in 113 gastric carcinomas was studied by immunohistochemistry. Microvessel density (MVD) was counted using the anti-CD34 antibody. The expressions of PTEN and MMP-7, and MVD were compared with the clinicopathological parameters of tumors, and the relationship between PTEN and MMP-7 expression and MVD was analyzed. It was found that PTEN was expressed less frequently in primary gastric carcinoma cells than in adjacent epithelial cells (P < 0.05), whereas this was reversed for MMP-7 (P < 0.05). PTEN expression was negatively correlated with invasion, metastasis, growth pattern, Lauren's classification and histological classification (P < 0.05). Matrix metalloproteinase-7 expression was positively associated with tumor size, Borrmann's classification, invasive depth, metastasis and TNM staging (P < 0.05), but negative with PTEN expression (P < 0.05). A positive correlation of MVD with tumor size, invasive depth, metastasis and TNM staging was found (P < 0.05). Microvessel density depended on decreased PTEN expression and increased MMP-7 expression (P < 0.05). The results of the present study suggested that down-regulated PTEN expression and up-regulated MMP-7 expression were greatly implicated in tumorigenesis and progression of gastric carcinoma. Close correlation between PTEN on MMP-7 expression provided a novel insight into the regulatory effects of PTEN on MMP-7 expression in gastric carcinoma.

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Section: Discussionsupporting

confidence: 68%

Role of PTEN and MMP‐7 expression in growth, invasion, metastasis and angiogenesis of gastric carcinoma

Zheng

Sun

et al. 2003

Pathology International

184

191

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“…Mutations in the PTEN gene are closely related to cancer-predisposing genetic diseases including Cowden's BRRS syndrome (16). PTEN mutations have been found in a variety of tumors including prostate cancer, endometrial cancer, glioma, lung cancer and liver cancer (17).…”

Section: Effects Of the Upregulation Of Pten On Proliferation And Apomentioning

confidence: 99%

Effects of PTEN on the proliferation and apoptosis of colorectal cancer cells via the phosphoinositol-3-kinase/Akt pathway

Sun

Tian

Wang³

2015

Oncology Reports

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Colorectal cancer (CRC) is one of the most common type of malignancy with a poor prognosis, due to a high frequency of metastasis and tumor recurrence. It has been reported that deletion and/or mutation of the PTEN gene can be involved in the pathogenesis of many types of cancers through the activation of the PI3K/Akt signaling pathway. Immunohistochemical staining was conducted to detect PTEN expression in CRC, adenomas and normal tissues. For the measurement of cell proliferation, CCK-8 was used. Apoptotic cells were quantified using FACS. Immunohistochemical staining results demonstrated that the expression of PTEN gradually decreased from normal colorectal mucosa, to colon hyperplastic polyps, adenomas, and ultimately primary colorectal adenocarcinomas. Upregulation of PTEN expression inhibited the proliferation of LoVo and SW480 cells, inducing G1 phase arrest and reducing the number of cells in the S phase. LoVo and SW480 cells with upregulated PTEN were sensitive to apoptosis induced by 5-FU. In addition, upregulation of PTEN inhibited the activity of Akt and activated the FoxO transcription factor. This is the first report of a gradual decrease in expression of PTEN from normal colon epithelial tissue to colon hyperplastic polyps, colorectal adenomas and finally CRC. Upregulation of PTEN inhibited the activity of the Akt pathway and regulated downstream genes involved in the cell cycle. These results suggest that inhibition of CRC cell proliferation and cell cycle arrest by PTEN are closely related to PI3K/Akt/FoxO.

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“…PTEN is also a powerful inhibitor of cell motility which was found to be independent of its catalytic domain [78] and might be linked to the N-terminal tensin and auxilin homology domains. Mutant PTEN might be linked to an aggressive clinical course [68,99]. On the other hand, human and murine tumors with an activated PI3K/PTEN/Akt pathway might be exquisitely sensitive to rapamycin, a macrolid antibiotic that downregulates mTOR and potentially opens a new therapeutic window for these tumors [22,121].…”

Section: Ink4amentioning

confidence: 99%