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Mutations of the PIK3CA Gene in Diffuse Large B Cell Lymphoma

Baohua, Yu MD* †; Xiaoyan, Zhou MD, PhD* †; Tiecheng, Zhang MD, PhD* †; Tao, Qin BA* †; Daren, Shi MD* †

doi: 10.1097/PDM.0b013e31815d0588
Original Articles

The PI3K/AKT pathway might be involved in the development of some certain diffuse large B-cell lymphoma (DLBCL) by as-yet unclear mechanisms. PIK3CA mutations in exons 9 and 20 were investigated in 76 primary human DLBCLs, 3 DLBCL cell lines (LY1, LY8, and LY10), and 9 related samples using polymerase chain reaction-based sequence analysis to assess the possible relevance of PIK3CA mutations in DLBCL to the PI3K/AKT pathway activation. AKT phosphorylation (pAKT) of 3 DLBCL cell lines and 76 primary DLBCL samples was also detected by Western blot and immunohistochemistry. All 3 cell lines showed high levels of pAKT, and 72.4% (55/76) of the DLBCLs expressed pAKT at various levels, indicating the activation of AKT. However, no mutation was found in exons 9 or 20 in PIK3CA in any of the 3 cell lines. Only 1 out of 76 primary DLBCLs (1.32%) harbored an exon 9 mutation, and no exon 20 mutation was detected. The case with mutations contained 3 mutation points. One was c.1634A>C resulting in E545A, which was in a previously reported hotspot. The other 2 were novel c.1658G>C and c.1659delT frameshift mutations. We conclude that the PI3K/AKT pathway is activated in DLBCL and that PIK3CA is rarely mutated in DLBCL, indicating there could be some other PI3K-pathway activation mechanisms operative in DLBCL.

*Department of Pathology, Cancer Hospital of Fudan University

Department of Oncology, Shanghai Medical College of Fudan University, Shanghai, People's Republic of China

Supported by a grant from the National Nature Science Funding of China (NSFC) (Code No. 30470737).

Reprints: Zhou Xiaoyan, MD, PhD, Department of Pathology, Cancer Hospital of Fudan University, 270 Dong-an Road, Shanghai 200032, People's Republic of China (e-mail:

© 2008 Lippincott Williams & Wilkins, Inc.