PIK3CA mutation incidence was significantly lower in lung adenocarcinoma than in lung squamous cell carcinoma; among eight patients with a PIK3CA mutation, three patients also harbored an EGFR somatic mutation.

There was significant difference in survival between the lung cancer patients with PIK3CA normal copy number and the patients with PIK3CA amplification

PIK3CA has an important role in human lung carcinogenesis, possibly by promoting malignant transformation.

RNA interference-mediated knockdown of PIK3CA inhibited colony formation of cell lines with PIK3CA mutations or gains but was not effective in PIK3CA wild-type cells. PIK3CA mutations or gains are present in a subset of lung cancers

inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers

This study for the first time uncovered PIK3CA alterations in small cell lung cancer

tumors expressing the p110alpha helical domain mutant showed a increase in tumor cell intravasation into the blood and tumor cell extravasation into the lung compared with tumors expressing wild-type p110alpha or the kinase domain mutant.

mutations in PIK3CA is associated with squamous cell carcinomas of the lung.

cIAP2 upregulated by E6 via EGFR/PI3K/AKT cascades may contribute to cisplatin resistance, revealing that the EGFR or PI3K inhibitor combined with cisplatin may improve the chemotherapeutic efficacy in HPV-infected lung cancer.

PIK3CA mutations are associated with drug resistance in non-small cell lung cancer.

Down-regulation of JAK1 by RNA interference inhibits growth of the lung cancer cell line A549 and interferes with the PI3K/mTOR pathway

Data indicate that PIK3CA mutations occur in lung adenocarcinomas, usually concurrently with EGFR, KRAS, and anaplastic lymphoma kinase (ALK).

High p110alpha is associated with non-small cell lung cancer.

The relationship between expression and genetic alterations of the components of the PI3K/AKT pathway in non-small cell lung cancer, was investigated.

The PIK3CA mutation rate was lower in adenocarcinomas compared to other forms of lung cancers

results suggest that PIK3CA gene mutations may play a key role in tumourigenesis and aggressiveness of bronchopulmonary neuroendocrine tumours

PIK3CA amplification was detected in thirty-seven percent of lung squamous tumors and five percent of lung adenocarcinomas.

Targeting the phosphoinositide 3-kinase p110-alpha isoform impairs cell proliferation, survival, and tumor growth in small cell lung cancer.

Data show that a photodynamic therapy (PDT) dose-dependent upregulation of CRP gene, as well as of PTX3 and ficolin 1 genes in lung tumor A549 cells, and indicate critical role played by PI3K/Akt/AP-1 pathway.

PIK3CA mutations are associated with lung cancer.

PIK3CA-mutant lung cancers are dependent on this driver oncogene, whereas in other patient cases, the mutation may modulate the effect of another oncogenic process.

PIK3CA mutations are not associated with tyrosine kinase inhibitors treatment efficacy in non-small cell lung cancer.

Data indicate that responses were noted in patients with HER2-amplified breast cancer resistant to trastuzumab, HER2-mutant non-small-cell lung cancer, and tumor types without identified mutations in the HER-PI3K-mTOR pathway.

Low expression of miR-1 and high expression of PIK3CA are closely related to the invasion, progression and metastasis of non-small-cell lung cancer.There is a negative correlation between the expression of miR-1 and PIK3CA in non-small-cell lung cancer.

PIK3CA mutations are associated with non--small-cell lung cancer.

mutations may confer resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in lung adenocarcinoma patients with mutated EGFR

Increased SOX2 gene copy number is associated with FGFR1 and PIK3CA gene gain in non-small cell lung cancer and predicts improved survival in early stage disease

The expression of PIK3CA and survivin had a significant correlation with pathological grade and lymph node metastasis in the primary adenosquamous lung carcinoma patients.

PIK3CA amplifications and mutations in Non-small cell lung cancer have been reported in 37% and 9%, respectively. Both are poor prognostic factors in Squamous Cell Carcinoma.

The aim of the present study was to obtain the first data for the phosphatidylinositol-4,5-bisphosphate 3-kinase (PIK3CA) mutation frequency among nonsmall-cell lung cancer (NSCLC) patients in Turkey.

A concurrent PIK3CA mutation is a poor prognostic factor in patients with advanced EGFR-mutant or KRAS-mutant lung adenocarcinomas.

PIK3CA mutations are associated with metastatic lung adenocarcinomas.

Data indicate that EPHA3 is involved in regulating the multidrug resistance (MDR) of small cell lung cancer (SCLC) via PI3K/BMX/STAT3 signaling and may be a therapeutic target in SCLC.

A dual PI3K and mTOR inhibitor, BEZ235 with the HDAC inhibitor Trichostatin A (TSA) significantly increased anti-tumor activities compared with BEZ235 and TSA alone, suggesting a combination treatment for non-small-cell lung cancer (NSCLC).

Data show that the incidence of phosphatidylinositol 3-kinase catalytic 110-KD alpha (PIK3CA) mutation is low in small cell lung cancer (SCLC) and the pseudogene-positive alteration of A1634C is prone to occur in exon 9 of PIK3CA mutations in cancers.

PIK3CA mutation may not be associated with primary resistance to EGFR TKI among lung adenocarcinoma patients

Report outcome of PIK3CA/mTOR/MEK co-targeted inhibition strategy in the treatment of non-small cell lung carcinomas.

the most frequent genomic abnormality in patients with primary pulmonary neuroendocrine carcinoma in China

RAS signaling through PI3K is necessary for normal lymphatic vasculature development and for RAS-induced transformation in vitro and in vivo, especially in lung cancer, where it is essential for tumor initiation and necessary for tumor maintenance. [review]

The RAS-PI3K interaction is an important signaling node and potential therapeutic target in EGFR-mutant lung cancer.

Talc-sensitive cells have higher mRNA and protein expression of PI3K catalytic subunit alpha. Both PI3Kalpha and -beta mediate talc-induced cell death and IL-6 secretion in lung carcinoma cells.

PIK3CA mutation is associated with lung cancer risk.

miR10a increases the cisplatin resistance of lung adenocarcinoma circulating tumor cells via targeting PIK3CA in the PI3K/Akt pathway.

Clinical Significance of PIK3CA Gene in Non-Small-Cell lung cancer: A Systematic Review and Meta-Analysis.

mutationally activated PIK3CA(H1047R) cooperates with BRAF(V600E) to promote lung cancer progression.