Overexpression of phosphatidylinositol 3-kinase in human lung cancer

Lin, X.; Böhle, A.; Dohrmann, P.; Leuschner, Ivo; Schulz, Andreas; Kremer, Bernd; Fändrich, F.

doi:10.1007/s004230100203

Cited by 72 publications

(59 citation statements)

References 48 publications

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“…In our study, consistent with PIK3CA mRNA overexpression in ESCC, in just half of ESCCs (50.0%) of immunoreactive PIK3CA was observed. The rate of immunoreactive PIK3CA in ESCC corresponded to that in lung squamous cell carcinoma (44). In a similar manner to that in tumor tissues, PIK3CA expression was observed in the cytoplasm of ESCC cell lines by immunofluorescence analysis.…”

supporting

confidence: 67%

Overexpression of PIK3CA is associated with lymph node metastasis in esophageal squamous cell carcinoma

Akagi

Miyashita²,

Makino³

et al. 2009

Int J Oncol

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Abstract. The genomic region containing PIK3CA was found to be amplified in esophageal squamous cell carcinoma (ESCC) tissue. PIK3CA at 3q26, which encodes the p110· catalytic subunit of phosphatidylinositol (PI) 3-kinase, is a unique intracellular signal transducer characterized by its lipid substrate specificity. In order to characterize PIK3CA in ESCC, we investigated hot-spot mutations in exons 1, 9 and 20, the copy number gain, the expression levels of mRNA and protein. Analysis in exon 9 of the PIK3CA gene revealed mutation in 7.7% (4 of 52) of ESCC samples. No mutation was detected in either exon 1 or exon 20. Copy number amplifications of PIK3CA were found in 12 of the 45 patients (26.7%). PIK3CA mRNAs were examined in 37 ESCC patients as determined by quantitative RT-PCR and the mean mRNA level of PIK3CA in ESCC tissues was 2.61-fold higher compared with that in corresponding non-tumorous esophageal epithelia (P<0.001). Immunohistochemically, positive immunoreaction for PIK3CA was detectable in 33 of 66 (50.0%) ESCC cases, while it was not detectable in the remaining 33 cases. Furthermore, comparing the cases with negative staining with those with positive staining for PIK3CA, the presence of node metastasis was significantly correlated with those with positive staining (P<0.05). This study is the first report providing comprehensive analysis of PIK3CA expression in ESCC. These results indicate that PIK3CA may play a crucial role in the development of ESCC and serve as an indicator for lymph node metastasis.

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supporting

confidence: 67%

Overexpression of PIK3CA is associated with lymph node metastasis in esophageal squamous cell carcinoma

Akagi

Miyashita²,

Makino³

et al. 2009

Int J Oncol

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“…12 The PI3K/Akt pathway has been shown to be the predominant growth-factor-activated pathway in LNCaP human prostate carcinoma cells. 13 PI3K activity has been linked to a variety of human tumors including breast cancer, 14 lung cancer, 15 melanomas, 16 and leukemia 17 among others. Further evidence has shown that Akt (protein kinase B, PKB), a downstream kinase of PI3K, is also involved in malignant transformation.…”

Section: Aberrant Pi3k Activity and Oncogenic Transformationmentioning

confidence: 99%

Involvement of PI3K/Akt pathway in cell cycle progression, apoptosis, and neoplastic transformation: a target for cancer chemotherapy

et al. 2003

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“…The PI3K is the predominant growth factor-activated pathway in LNCaP human prostate carcinoma cells. 283,284 Other reports directly implicate PI3K activity in a variety of human tumors including breast cancer, 285 lung cancer, 286 melanomas 287 and leukemia 288 among others. Activated Akt can affect the expression and regulation of the responses of hormone receptors and hence leads to ineffectiveness of hormone ablation therapies.…”

Section: Roles Of the Pi3k/pten/akt/mtor Pathway In Leukemiamentioning

confidence: 99%

Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia

et al. 2008

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Mutations and chromosomal translocations occur in leukemic cells that result in elevated expression or constitutive activation of various growth factor receptors and downstream kinases. The Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways are often activated by mutations in upstream genes. The Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways are regulated by upstream Ras that is frequently mutated in human cancer. Recently, it has been observed that the FLT-3 and Jak kinases and the phosphatase and tensin homologue deleted on chromosome 10 ( PTEN) phosphatase are also frequently mutated or their expression is altered in certain hematopoietic neoplasms. Many of the events elicited by the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways have direct effects on survival pathways. Aberrant regulation of the survival pathways can contribute to uncontrolled cell growth and lead to leukemia. In this review, we describe the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT signaling cascades and summarize recent data regarding the regulation and mutation status of these pathways and their involvement in leukemia

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Overexpression of phosphatidylinositol 3-kinase in human lung cancer

Abstract: PI3K appears to be associated with the process of tumor-cell transformation and proliferation. One of its major downstream effector molecules, AKT2, which contributes to apoptotic cell death, was not upregulated by PI3K overexpression in primary lung carcinomas.

Cited by 72 publications

References 48 publications

Overexpression of PIK3CA is associated with lymph node metastasis in esophageal squamous cell carcinoma

Overexpression of PIK3CA is associated with lymph node metastasis in esophageal squamous cell carcinoma

Involvement of PI3K/Akt pathway in cell cycle progression, apoptosis, and neoplastic transformation: a target for cancer chemotherapy

Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia

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