Correlation Between STAT3Expression In Aids-related B Lymphoma And Patients Infected With EB Virus

Background and objectives Acquired Immune Deficiency Syndrome is humanbody infected HIV viruse, result in immune function dammage, secondaryopportunistic infections and malignancies, such as Kaposi ’s sarcoma or malignantlymphoma. Lymphoma related to HIV/AIDS is known as ARL. Diffuse large B-celllymphoma with unique clinical features and aggressive progress is one of the mostcommon ARL.The transcription factor STAT3associated with tyrosine phosphorylation signalpathway is expressed in the cytoplasmand known as an oncogene. The STAT3relatedto tumor is receiving more and more attention. STAT3appears to be constantactivation in multiple myeloma, leukemia, head and neck squamous cell carcinoma,and its express intensity associated with tumor growth, metastasis and prognosis.Recent studies have shown that HIV-1integrated into the upstream of the first codingexon sequences of STAT3gene in ARL, then activated STAT3in the nucleus, andpromoted malignant transformation of B cells..The patients with HIV/AIDS showedimmune function deficiency and got more chance to infected with EBV. Studies havefound that EBV associated with a wide variety of human tumors, especiallylymphoma. As a recognized cancer-causing virus, its relationship with the occurrence of abnormal proliferation of lymphocytes are receiving more attention. To investigatethe expression of STAT3and its role in the pathogenesis of ARL-DLBCL, and theinfection status of the EBV, the immunohistochemical staining was used to detect theexpression of STAT3protein in ARL-DLBCL and in situ hybridization was used tocheck EBV infection and the correlation between STAT3expression and EBVinfection in ARL-DLBCL was analyzed.Materials and methods21ARL-DLBCL tissue specimens was collected andserved as experimental group. The control groups include6cases fornonARL-DLBCL (A group),4cases for HIV+-RH (B group) and5cases for HIV--RH(C group) respectively. The immunohistochemistry and in situ hybridizationtechniques was used to detect the expression of STAT3and EBER in four group, andthe results was analyzed with clinical pathological features.Results1. Basic clinical information:21ARL-DLBCL, the male: femaleratio was3.2:1; age range29-66years, median age47.5years; lymph node lesions15cases, extranodal lesions6cases, GCB5cases, nonGCB16cases, clinical stageⅠ-Ⅱ8cases, Ⅲ-Ⅳ13cases. The control group15cases, the male: female ratio was2:1;age range27-72years, median age49.5years.2. STAT3expression andARL-DLBCL immune type have significant difference(P=0.004), the expression innonGCB is higher than in GCB, indicates that STAT3positive in ARL-DLBCLassociated with worse prognosis, with gender,age,diseased region and clinical staginghave no significant difference((P=0.553, P=1.000, P=0.598, P=0.606).3. STAT3immunohistochemistry results: The total STAT3positive rate of21ARL-DLBCLwas76.19%(16/21), the nuclear expression accounted for81.25%(13/16), nuclearstrong positive18.75%(3/16); The total STAT3positive rate of A groupnonARL-DLBCL was66.67%(4/6), the nucleus expression accounted for50%(2/4),nuclear strong positive25%(1/4), compared two tumor groups, the total positiverate and nuclear positive rate was no significant difference (P=0.633, P=0.249);Group B HIV+-RH and Group C HIV--RH, STAT3only expressed in follicular cells,not expressed or scattered outside of the germinal center.4. The results of EBER:20ARL-DLBCL, the total positive rate of EBER was30%(6/20), including4cases of STAT3and EBER coexpression, EBER positive with STAT3nuclei strongpositive;14cases Control group, the total positive rate of EBER was14.29%(2/14),A group is40%(2/5), STAT3nuclei positive1case, the nucleus and cytoplasmcoexpression1case; statistically, Tumor group have no significant difference(P=1.000). Group B and group C EBER were negative.5.STAT3and EBER:Tumor group, STAT3protein and EBER expression rate were significant difference(P=0.006), the expression of STAT3protein was higher than EBER, but theexpression consistency poor(kappa<0.4).Conclusion1. The STAT3expression is relatived to the immunity type ofARL-DLBCL. The STAT3expression in nonGCB is higher than its in GCB; andit is irrelevant with gender, age, diseased region and clinical staging.2.Theexpression of STAT3is higher in ARL-DLBCL and nonARL-DLBCL, andexpressed in nuclear mainly, suggesting that STAT3overexpression is relatived to thetumorigenesis, and there is no obvious relationship between STAT3overexpressionand HIV infection.3. EBER were expressed in ARL-DLBCL, nonARL-DLBCL,suggesting that the infection of EB virus concerned with the occurrence of part ofDLBCL, no obvious relationship with HIV infection.4.The activation of STAT3protein has no relation with EBV infection.