PIK3CA as an oncogene in cervical cancer

Ying, Yen; Wei, Sung‐Jen; Lin, Yu Chen; Lung, Jia Chyi; Chang, Ting Chang; Whang‐Peng, Jacqueline; Liu, Jacqueline M.; Yang, Deng Mei; Yang, Wei‐Pang; Shen, Chen

doi:10.1038/sj.onc.1203597

Cited by 378 publications

(241 citation statements)

References 25 publications

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“…Increased copy number of the PIK3CA gene has also been identified in cervical cancer and ovarian cancer, and in the latter case has been shown to be associated with increased expression (Shayesteh et al, 1999;Ma et al, 2000).…”

Section: Discussionmentioning

confidence: 96%

Prognostic value of genomic alterations in head and neck squamous cell carcinoma detected by comparative genomic hybridisation

et al. 2003

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A total of 45 primary head and neck squamous cell carcinomas were analysed by comparative genomic hybridisation to identify regions of chromosomal deletion and gain. Multiple regions of copy number aberration were identified including gains affecting chromosomes 3q, 8q, 5p, 7q, 12p and 11q and deletion of material from chromosomes 3p, 11q, 4p, 5q, 8p, 10q, 13q and 21. KaplanMeier survival analysis revealed significant correlations between gain of 3q25 -27 and deletion of 22q with reduced disease-specific survival. In addition, gain of 17q and 20q, deletion of 19p and 22q and amplification of 11q13 were significantly associated with reduced disease-free survival. A Cox proportional hazards regression model identified deletion of 22q as an independent prognostic marker. The data presented here provide further evidence that the creation of a genetically based tumour classification system will soon be possible, complementing current histopathological characterisation.

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Section: Discussionmentioning

confidence: 96%

Prognostic value of genomic alterations in head and neck squamous cell carcinoma detected by comparative genomic hybridisation

et al. 2003

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“…We chose to carry out our experiments in C33A cells since it is known that this cell line harbors amplification of the pik3ca (p110 alpha) gene [12], that it has robust p110 activity, and because it expresses very low levels of endogenous PIK3IP1 mRNA and protein. Overexpression of PIK3IP1 in C33A cells did not lead to alterations in p85 or p110 protein abundance as compared to controls (Supplemental Figures 4A&B).…”

Section: Pik3ip1 Does Not Prevent the Interaction Of P85 And P110mentioning

confidence: 99%

PI3K is negatively regulated by PIK3IP1, a novel p110 interacting protein

Zhu¹,

He²,

Johnson³

et al. 2007

Biochemical and Biophysical Research Communications

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Signaling initiated by Class Ia phosphatidylinositol-3-kinases (PI3Ks) is essential for cell proliferation and survival. We discovered a novel protein we call PI3K Interacting Protein 1 (PIK3IP1) that shares homology with the p85 regulatory PI3K subunit. Using a variety of in vitro and cell based assays, we demonstrate that PIK3IP1 directly binds to the p110 catalytic subunit and modulates PI3K activity. Our studies suggest that PIK3IP1 is a new type of PI3K regulator.

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“…The two most frequent copy number gains were scored for RLGS fragments 3D17 (21/41, 51%) and 3D21 (17/41, 41%), both mapping to 3q26.32. Interestingly, these sequences were located in a region that includes PIK3CA, a known proto-oncogene, not only in HNSCC (Estilo et al, 2003) but also in cervical (Ma et al, 2000), ovarian, breast (Campbell et al, 2004) and lung squamous cell carcinomas (Racz et al, 1999). Numerous patient samples demonstrated consecutive DNA copy number gain in several markers in this region, suggesting that the whole 3q26.1-3q29 region was amplified as a single amplicon (e.g.…”

Section: Subclassification Of Amplicons On Chromosome 3q263-q29mentioning

confidence: 99%

DNA copy number gains in head and neck squamous cell carcinoma

et al. 2005

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Gene amplification, a common mechanism for oncogene activation in cancer, has been used as a tag for the identification of novel oncogenes. DNA amplification is frequently observed in head and neck squamous cell carcinoma (HNSCC) and potential oncogenes have already been reported. We applied restriction landmark genome scanning (RLGS) to study gene amplifications and low-level copy number changes in HNSCC in order to locate previously uncharacterized regions with copy number gains in primary tumor samples. A total of 63 enhanced RLGS fragments, indicative of DNA copy number changes, including gains of single alleles, were scored. Enhanced sequences were identified from 33 different chromosomal regions including those previously reported (e.g. 3q26.3 and 11q13.3) as well as novel regions (e.g. 3q29, 8q13.1, 8q22.3, 9q32, 10q24.32, 14q32.32, 17q25.1 and 20q13.33). Furthermore, our data suggest that amplicons 11q13.3 and 3q26.3-q29 may be divided into possibly two and three independent amplicons, respectively, an observation supported by published microarray expression data.

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PIK3CA as an oncogene in cervical cancer

Cited by 378 publications

References 25 publications

Prognostic value of genomic alterations in head and neck squamous cell carcinoma detected by comparative genomic hybridisation

Prognostic value of genomic alterations in head and neck squamous cell carcinoma detected by comparative genomic hybridisation

PI3K is negatively regulated by PIK3IP1, a novel p110 interacting protein

DNA copy number gains in head and neck squamous cell carcinoma

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