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.
Highlights
Diffuse large B cell lymphoma (DLBCL) is one of the most common types of aggressive B cell nonHodgkin lymphomas [1, 2]
Previous studies have reported that the genetic changes of PIK3CA and phosphatase and tensin homolog (PTEN) occurred in DLBCL, little has been known about the clinicopathological significance of genetic changes of both PIK3CA and PTEN on DNA level in DLBCL
Both amplification of PIK3CA and PTEN loss were shown to have occurred on DNA level with the help of fluorescent in-situ hybridization (FISH) approach in DLBCL
Summary
Diffuse large B cell lymphoma (DLBCL) is one of the most common types of aggressive B cell nonHodgkin lymphomas [1, 2]. Studies showed that constitutive activation of the PI3K/AKT signaling pathway [6, 7] as well as its inhibitor, phosphatase and tensin homolog (PTEN) [8], in GCB-DLBCL plays a central role in promoting survival and chemotherapy-resistance and represents a rational therapeutic target in relapsed or refractory GCBDLBCL. Deregulation of the PI3K/AKT pathway by the www.impactjournals.com/oncotarget inactivation of PTEN, was found in 55 % of GCB-DLBCL cases, but only in 14 % of non-GCB-DLBCL and worsens prognosis [8]. The both of PTEN and PI3K/AKT signaling pathway has emerged as promising therapeutic targets for relapsed DLBCL [9]. Some inhibitors [7, 8] of PI3K subunit has been currently evaluated in an ongoing early phase I study as a single-agent in patients with relapsed/refractory DLBCL
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
