卵巣明細胞癌で６割変異する遺伝子：サイエンスより

卵巣明細胞癌という癌は下に示すようにあまり予後の良くない癌らしい。（元来卵巣がんそのものの予後も不良なのだが）その明細胞癌の６割弱に変異が認められる遺伝子が見つかった。ARID1Aといってクロマチンのリモデリング関連遺伝子のようだ。6割とはは高頻度である。４２例中２４例で５７％。ボーゲルシュタインのグループである。

Frequent Mutations of Chromatin Remodeling Gene ARID1A in Ovarian Clear Cell Carcinoma

Siân Jones,¹ Tian-Li Wang,² Ie-Ming Shih,³ Tsui-Lien Mao,⁴ Kentaro Nakayama,⁵ Richard Roden,³ Ruth Glas,⁶ Dennis Slamon,⁶ Luis A. Diaz, Jr.,¹ Bert Vogelstein,¹ Kenneth W. Kinzler,^1,* Victor E. Velculescu,^1,* Nickolas Papadopoulos^1,*

Ovarian clear cell carcinoma (OCCC) is an aggressive human cancer that is generally resistant to therapy. To explore the genetic origin of OCCC, we determined the exomic sequences of eight tumors after immunoaffinity purification of cancer cells. Through comparative analyses of normal cells from the same patients, we identified four genes that were mutated in at least two tumors. PIK3CA, which encodes a subunit of phosphatidylinositol-3 kinase, and KRAS, which encodes a well-known oncoprotein, had previously been implicated in OCCC. The other two mutated genes were previously unknown to be involved in OCCC: PPP2R1A encodes a regulatory subunit of serine/threonine phosphatase 2, and ARID1A encodes adenine-thymine (AT)–rich interactive domain–containing protein 1A, which participates in chromatin remodeling. The nature and pattern of the mutations suggest that PPP2R1A functions as an oncogene and ARID1A as a tumor-suppressor gene. In a total of 42 OCCCs, 7% had mutations in PPP2R1A and 57% had mutations in ARID1A. These results suggest that aberrant chromatin remodeling contributes to the pathogenesis of OCCC.

Originally published in Science Express on 8 September 2010
Science 8 October 2010:
Vol. 330. no. 6001, pp. 228 - 231

大阪医療センターHPからのデータ

表層上皮性卵巣がんの組織型別の治療成績(1993-95)

組織型	臨床進行期
	l期		ll期		lll期		lV期
	例数	生存率	例数	生存率	例数	生存率	例数	生存率
漿液性腺がん	427	89.4	153	65.4	1188	32.7	254	18.5
粘液性腺がん	477	90.7	44	78.7	149	38.0	38	12.3
類内膜腺がん	228	87.0	82	69.1	208	37.6	46	24.6
明細胞腺がん	101	83.6	27	63.5	68	27.4	15	0
未分化腺がん	56	81.0	19	49.8	103	29.8	40	0