PIK3CA is implicated as an oncogene in ovarian cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-01

AUTHORS

Laleh Shayesteh, Yiling Lu, Wen-Lin Kuo, Russell Baldocchi, Tony Godfrey, Colin Collins, Daniel Pinkel, Bethan Powell, Gordon B. Mills, Joe W. Gray

ABSTRACT

Ovarian cancer is the leading cause of death from gynecological malignancy and the fourth leading cause of cancer death among American women1, yet little is known about its molecular aetiology. Studies using comparative genomic hybridization (CGH) have revealed several regions of recurrent, abnormal, DNA sequence copy number2, 3, 4 that may encode genes involved in the genesis or progression of the disease. One region at 3q26 found to be increased in copy number in approximately 40% of ovarian2 and other5 cancers contains PIK3CA, which encodes the p110α catalytic subunit of phosphatidylinositol 3-kinase (PI3-kinase). The association between PIK3CA copy number and PI3-kinase activity makes PIK3CA a candidate oncogene because a broad range of cancer-related functions have been associated with PI3-kinase mediated signalling6. These include proliferation7, glucose transport and catabolism8, cell adhesion9, apoptosis10, RAS signalling6 and oncogenic transformation11, 12, 13, 14. In addition, downstream effectors of PI3-kinase, AKT1 and AKT2, have been found to be amplified15, 16 or activated17 in human tumours, including ovarian cancer. We show here that PIK3CA is frequently increased in copy number in ovarian cancers, that the increased copy number is associated with increased PIK3CA transcription, p110α protein expression and PI3-kinase activity and that treatment with the PI3-kinase inhibitor LY294002 decreases proliferation and increases apoptosis. Our observations suggest PIK3CA is an oncogene that has an important role in ovarian cancer. More... »

PAGES

99-102

Journal

TITLE

Nature Genetics

ISSUE

1

VOLUME

21

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/5042

    DOI

    http://dx.doi.org/10.1038/5042

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9916799


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    21 schema:description Ovarian cancer is the leading cause of death from gynecological malignancy and the fourth leading cause of cancer death among American women1, yet little is known about its molecular aetiology. Studies using comparative genomic hybridization (CGH) have revealed several regions of recurrent, abnormal, DNA sequence copy number2, 3, 4 that may encode genes involved in the genesis or progression of the disease. One region at 3q26 found to be increased in copy number in approximately 40% of ovarian2 and other5 cancers contains PIK3CA, which encodes the p110α catalytic subunit of phosphatidylinositol 3-kinase (PI3-kinase). The association between PIK3CA copy number and PI3-kinase activity makes PIK3CA a candidate oncogene because a broad range of cancer-related functions have been associated with PI3-kinase mediated signalling6. These include proliferation7, glucose transport and catabolism8, cell adhesion9, apoptosis10, RAS signalling6 and oncogenic transformation11, 12, 13, 14. In addition, downstream effectors of PI3-kinase, AKT1 and AKT2, have been found to be amplified15, 16 or activated17 in human tumours, including ovarian cancer. We show here that PIK3CA is frequently increased in copy number in ovarian cancers, that the increased copy number is associated with increased PIK3CA transcription, p110α protein expression and PI3-kinase activity and that treatment with the PI3-kinase inhibitor LY294002 decreases proliferation and increases apoptosis. Our observations suggest PIK3CA is an oncogene that has an important role in ovarian cancer.
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