p63 is a recently described p53 homologue. It is involved in survival and differentiation of reserve/stem cells in epithelia. To obtain new insights into the role of p63 in malignant lymphomas (MLs), immunohistochemical staining for p63 and p53 was performed in 126 cases of MLs. p63 was expressed in 38 cases of MLs (30.2%) including 32/61 cases (52.5%) of diffuse large B-cell lymphoma (DLBCL), 1/8 cases (12.5%) of precursor T-lymphoblastic lymphoma (T-LBL), 4/14 cases (28.6%) of follicular lymphoma, 1/6 cases (16.7%) of T/NK cell lymphoma. Among p63 positive cases, p63 was strongly expressed in 15/32 cases of DLBCL and 1/1 case of T-LBL. p63 was not expressed in mantle cell lymphomas, peripheral T-cell lymphomas, marginal zone B-cell lymphomas, plasma cell myelomas and Hodgkin's lymphomas. p63 was coexpressed with p53 in 18/38 p63 positive cases in which only 4 cases were strongly coexpressed. All p63+/p53+ cases were DLBCL. p63 overexpression (above 30%) cases showed significant poor survival (p=0.0228) in DLBCL. However, there was no statistically significant correlation between p63 expression and IPI score on Multivariate analysis. We could speculate that p63 could act indirectly as an oncogene by inhibiting p53 functions. Stage of differentiation of neoplastic lymphocytes appears to have a correlation with p63 expression in MLs.

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A case of salivary gland type pleomorphic adenoma of the trachea in a 48-year-old woman is presented. Pleomorphic adenoma is extremely rare in the trachea. The behavior of this tumor in the trachea appears to be similar to its counterpart in other sites and distinctly different from the more frequently encountered epithelial tumors.

Recently diffuse large B cell lymphoma (DLBCLs) was reported to be subdivided into germinal center B-cell-like (GCB) and activated B-cell-like (ABC) subgroups by using cDNA microarray and immunohistochemical markers. Tissue microarray blocks were created from 51 nodal DLBCLs with c ntrol tissue. Immunohistochemical staining for the above markers were performed. The median follow-up period was 26 months. Nodal DLBCLs were subclassified into GCB [CD10+ or CD10-/Bcl-6+/MUM1-, n=17 (33%)] and non-GC subgroups [CD10-/Bcl-6- or CD10-/Bcl- 6+/MUM1+, n=35 (67%)], and were alternatively subclassified into pattern A [+ for GCB marker only, n=12 (23%)], B [Co-positive for both markers, n=13 (33%)], C [+ for activation marker only, n=18 (35%)], and D [- for both markers, n=9 (17%)]. Upon survival analysis, the GCB groups showed a relatively better survival than non-GC groups (p=0.0748). Also, pattern C (p=0.0055) and CD138+ (p=0.0008) patients had significantly lower survival rates. By multivariate analysis, CD138 expression alone was considered as an independent risk factor (p=0.031). In summary, our results add to the registration of prognostic implications for previously reported DLBCL subgroups. CD138 may play an important role as a poor prognostic marker. By using immunohistochemistry, a prognostically important subclassification of DLBCLs is possible.

These results suggest that the expression of TS in primary colorectal cancer might be an important prognostic factor for chemotherapy response and survival, and might be a useful therapeutic marker for the response of chemotherapy.