PIK3CA amplification and PTEN loss in diffused large B-cell lymphoma

// Wenli Cui 1, * , Mingfu Ma 1, * , Shutao Zheng 2, 3 , Zhiping Ma 1 , Liping Su 1 and Wei Zhang 1 1 Department of Pathology, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, Xinjiang, PR.China 2 Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, Xinjiang, PR.China 3 State Key Lab Incubation Base of Xinjiang Major Diseases Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, Xinjiang, PR.China * These authors have contributed equally to this work Correspondence to: Wenli Cui, email: cwl860@163.com Keywords: diffuse large B-cell lymphoma (DLBCL), PTEN, PIK3CA, FISH, prognosis Received: May 10, 2017     Accepted: July 12, 2017     Published: August 03, 2017 ABSTRACT Although it has been known that PIK3CA was amplified and PTEN was deficient on protein level in DLBCL, the clinicopathological significance of PIK3CA and PTEN genetic change on DNA level hasn’t been established. Here, in our present study, to understand the clinical significance of genetic status of PIK3CA and PTEN in DLBCL, fluorescent in-situ hybridization (FISH) was employed to evaluate the genetic change of PIK3CA and PTEN in clinical sample tissues consist of 205 cases. Incidentally, to understand the clinicopathological significance of genetic change of PIK3CA and PTEN, Cross-table analysis was used to analyze the association between genetic change of PIK3CA and PTEN versus clinicopathological variables available to us, including age, gender, size, location, international prognosis index, performance state, B-symptom, clinical stage, Extra nodal site, concentration of lactate dehydrogenase, therapeutic effects, treatment and overall prognosis. It was found that PIK3CA was amplified and PTEN was deficient on DNA level, the percentage of amplification and loss was 12.7% (26/205) and 12.2% (25/205), respectively. Additionally, no significant association was observed between genetic change of PIK3CA and PTEN versus clinicopathological variables available. Nor was the significant correlation found between loss of PTEN versus PIK3CA amplification. Our results suggest that PTEN deficiency and amplification of PIK3CA on DNA level was an event in the pathogenesis of DLBCL.