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Originally published online as doi:10.2353/ajpath.2009.081000 on April 6, 2009

Published online before print April 6, 2009
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(American Journal of Pathology. 2009;174:1597-1601.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.081000

Short Communications

Frequent Activating Mutations of PIK3CA in Ovarian Clear Cell Carcinoma

Kuan-Ting Kuo*{dagger}, Tsui-Lien Mao{dagger}, Siân Jones{ddagger}, Emanuela Veras*, Ayse Ayhan§, Tian-Li Wang**, Ruth Glas, Dennis Slamon, Victor E. Velculescu{ddagger}||, Robert J. Kuman*** and Ie-Ming Shih***

From the Departments of Pathology,* and Gynecology/Obstetrics,** The Ludwig Center,{ddagger} and the Howard Hughes Medical Institute,|| Kimmel Cancer Center, Johns Hopkins Medical Institutions, Baltimore, Maryland; the Department of Pathology,{dagger} National Taiwan University Hospital, Taipei, Taiwan; the Department of Pathology,§ Seirei Mikatahara Hospital, Hamamatsu, Japan; and the Division of Hematology/Oncology, David Geffen School of Medicine at the University of California, Los Angeles, California

Ovarian clear cell carcinoma (CCC) is one of the most malignant types of ovarian carcinomas, particularly at advanced stages. Unlike the more common type of ovarian cancer, high-grade serous carcinoma, ovarian CCC is often resistant to platinum-based chemotherapy, and therefore an effective treatment for this tumor type at advanced stages is urgently needed. In this study, we analyzed 97 ovarian CCCs for sequence mutations in KRAS, BRAF, PIK3CA, TP53, PTEN, and CTNNB1 as these mutations frequently occur in other major types of ovarian carcinomas. The samples included 18 CCCs for which affinity-purified tumor cells from fresh specimens were available, 69 microdissected tumors from paraffin tissues, and 10 tumor cell lines. Sequence mutations of PIK3CA, TP53, KRAS, PTEN, CTNNB1, and BRAF occurred in 33%, 15%, 7%, 5%, 3%, and 1% of CCC cases, respectively. Sequence analysis of PIK3CA in 28 affinity-purified CCCs and CCC cell lines showed a mutation frequency of 46%. Samples with PIK3CA mutations showed intense phosphorylated AKT immunoreactivity. These findings demonstrate that ovarian CCCs have a high frequency of activating PIK3CA mutations. We therefore suggest that the use of PIK3CA-targeting drugs may offer a more effective therapeutic approach compared with current chemotherapeutic agents for patients with advanced-stage and recurrent CCC.




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