[Expression of TOPK/PBK in children with malignant lymphoma or reactive lymphoid hyperplasia].

OBJECTIVE: To study the difference in expression of TOPK/PBK in lymph nodes between children with malignant lymphoma and those with reactive lymphoid hyperplasia. METHODS: Eighty children with malignant lymphoma and twenty children with reactive lymphoid hyperplasia were enrolled as subjects. Immunohistochemistry was used to determine the expression of TOPK/PBK in all the subjects. The expression of TOPK/PBK was compared between the two groups. RESULTS: The TOPK/PBK-positivity rate was significantly higher in children with malignant lymphoma than in those with reactive lymphoid hyperplasia (P<0.05). There was no significant difference in the TOPK/PBK-positivity rate between the children with Hodgkin's lymphoma and non-Hodgkin's lymphoma (NHL). There were significant differences in the TOPK/PBK-positivity rate among children with different pathological types of NHL (P<0.05): the children with lymphoblastic lymphoma showed the highest TOPK/PBK-positivity rate and those with mature B-cell lymphoma and mature T/NK-cell lymphoma had a similar TOPK/PBK-positivity rate. CONCLUSIONS: The expression of TOPK/PBK is up-regulated in the lymph nodes of children with malignant lymphoma. The expression level of TOPK/PBK may be related to the pathological type of NHL.

Expression of activation-induced cytidine deaminase in malignant lymphomas infiltrating the bone marrow.

Somatic hypermutation of immunoglobulin genes and class switch recombination are pivotal processes in the germinal center (GC) reaction and have been implicated in the development of malignant B-cell lymphoma. Both processes require the enzyme activation-induced cytidine deaminase (AID). Expression of AID is largely restricted to GC B cells and B cells that undergo class switch recombination outside the GC. AID is also expressed in many B-cell lymphomas. This study investigates the expression of AID of malignant lymphomas infiltrating the bone marrow. Bone marrow trephines (n=130) with infiltration of Hodgkin lymphoma and non-Hodgkin lymphoma of B cell and T-cell type and trephines with reactive lymphoid follicles (n=16) were analyzed immunohistochemically for AID protein. AID is expressed in bone marrow infiltrates of malignant lymphomas. AID was generally detected in lymphomas of GC origin. Tumor cells of hairy cell leukemia are mostly AID. There is apparently no different expression of AID found in bone marrow infiltrates of malignant lymphomas compared with a control group with nodal malignant lymphoma infiltrates (n=105). These results suggest that the expression pattern of AID in lymphoma infiltrates in the bone marrow reflects that of extramedullary lymphoma infiltrates.

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

The tumor suppressor PTEN is frequently inactivated in human cancers. A major downstream effector of PTEN is Akt, which is hyperactivated via PTEN inactivation. It is not known, however, whether diminished Akt activity is sufficient to inhibit tumorigenesis initiated by Pten deficiency. Here we showed that the deficiency of Akt1 is sufficient to dramatically inhibit tumor development in Pten+/- mice. Akt1 deficiency had a profound effect on endometrium and prostate neoplasia, two types of human cancer, in which PTEN is frequently mutated, and also affected thyroid and adrenal medulla tumors and intestinal polyps. Even haplodeficiency of Akt1 was sufficient to markedly attenuate the development of high-grade prostate intraepithelial neoplasia (PIN) and endometrial carcinoma. These results have significant implications for cancer therapy.

CD10 expression in follicular lymphoma and large cell lymphoma is different from that of reactive lymph node follicles.

BACKGROUND AND OBJECTIVES: CD10 is a proteolytic enzyme expressed on the surface of germinal center cells and lymphomas derived from these cells. There is a well-known association between CD10 expression and lymphomas of follicular center cell origin. However, the reported frequency of CD10 positivity in follicular lymphomas is widely variable, and no studies have addressed the importance of assessing the intensity of CD10 expression in the diagnosis of these tumors. In this study, we utilized flow cytometry to determine differences in CD10 expression in lymphomas and follicular hyperplasias. METHODS: Cell suspensions from 61 follicular lymphomas, 43 diffuse large B-cell lymphomas, and 44 lymph nodes with follicular hyperplasia were analyzed simultaneously with phycoerythrin-labeled anti-CD20 and fluorescein isothiocyanate-labeled anti-CD10. RESULTS: CD10 expression was mainly observed on B cells and was detected in 89% of follicular lymphomas, 56% of diffuse large B-cell lymphomas, and 55% of lymph nodes showing follicular hyperplasia. In follicular hyperplasia, two subpopulations of B cells displaying dim and bright CD20 expression were recognized. CD10 expression was restricted to the bright CD20-positive cells, which accounted for an average of 16% of B cells. In CD10-positive follicular and diffuse large B-cell lymphoma cases, a significantly higher proportion of B cells (73%) coexpressed CD10. Furthermore, the intensity of CD10 expression in follicular lymphoma and diffuse large B-cell lymphoma was much higher than that of follicular hyperplasia. CONCLUSIONS: Quantitative flow cytometry can detect significant differences in CD10 expression between normal follicular cells and follicular or diffuse large B-cell lymphoma. The use of CD10 intensity of expression as well as the fraction of CD10-expressing B cells should help distinguish reactive from neoplastic B-cell processes.