title: PTEN tumor suppressor plays less prognostic role than P53 tumor suppressor in diffuse large B-cell lymphoma.
abstract: The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and P53 tumor suppressors are among the most commonly inactivated or mutated genes in human cancers, whose pathways cross-talk and interact in a complementary mode. In order to understand their roles and relationship in diffuse large B-cell lymphoma (DLBCL), we examined their expression and evaluated their prognostic significance in 62 patients with DLBCL treated with standard chemotherapy. Results showed that PTEN protein was lost in 23 (37.1%) cases, and the loss was associated with the activation of PI3K/AKT pathway, but was not associated with patient's clinical outcome. P53 mutation protein was detected in 30 (48.4%) cases and was associated with poor survival. Results of multivariate analysis showed that P53 mutation but not PTEN loss is associated with short survival in patients with DLBCL. PTEN status has no effect on P53 mutation-associated poor survival. We conclude that PTEN may play less prognostic role than P53 and that P53 mutation protein should be considered as a predictive factor of the need for a more aggressive therapy in patients with DLBCL who express P53.
authors.affiliation: Department of Internal Medicine, Henan Provincial Cancer Hospital, Henan Provincial Institute of Cancer, Zhengzhou, Henan Province, China. liuyanyan4827@yahoo.com
authors.forename: Yan-Yan
authors.initials: YY
authors.lastname: Liu
authors.forename: Shu-Na
authors.initials: SN
authors.lastname: Yao
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Zhi-Hua
authors.initials: ZH
authors.lastname: Yao
authors.forename: Jie
authors.initials: J
authors.lastname: Ma
authors.forename: Qing-Xin
authors.initials: QX
authors.lastname: Xia
authors.forename: Kai
authors.initials: K
authors.lastname: Fu
authors.forename: Shu-Jun
authors.initials: SJ
authors.lastname: Yang
mesh_terms: D000328:Adult; D000368:Aged; D058846:Antibodies, Monoclonal, Murine-Derived / Q000008:administration & dosage; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D001402:B-Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D003520:Cyclophosphamide / Q000008:administration & dosage; D004247:DNA / Q000235:genetics; D004317:Doxorubicin / Q000008:administration & dosage; D053492:Elafin / Q000235:genetics / Q000378:metabolism; D005260:Female; D005838:Genotype; D006801:Humans; D007124:Immunoenzyme Techniques; D016403:Lymphoma, Large B-Cell, Diffuse / Q000188:drug therapy / Q000378:metabolism* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D016133:Polymerase Chain Reaction; D011241:Prednisone / Q000008:administration & dosage; D011379:Prognosis; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D000069283:Rituximab; D015996:Survival Rate; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism*; D014750:Vincristine / Q000008:administration & dosage; D055815:Young Adult
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D014408:Biomarkers, Tumor; D053492:Elafin; C506806:PI3 protein, human; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D000069283:Rituximab; D014750:Vincristine; D004317:Doxorubicin; D003520:Cyclophosphamide; D004247:DNA; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human; D011241:Prednisone