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PAX2 plays an important role in kidney development; although small studies have demonstrated PAX2 expression in Wilms tumors (WT), comprehensive studies on formalin-fixed tissue are lacking. Thus, we systematically evaluated PAX2 immunohistochemical staining in a retrospective study of pediatric WT, as compared with other pediatric tumors. We stained formalin-fixed, paraffin-embedded sections from 39 WT, 6 nephrogenic rests, 8 non-Wilms renal tumors, and 43 nonrenal pediatric small round cell tumors with 2 different PAX2 polyclonal antibodies. PAX2 demonstrated strong, diffuse staining of epithelial and blastema components of WT (97% of cases). PAX2 stained WT stroma in fewer cases (23%), but 80% of anaplastic foci were positive. Nephrogenic rests, 1 case of metanephric adenoma, and 1 pediatric renal cell carcinoma were also PAX2 positive; other pediatric renal tumors were negative. Neuroblastoma, primitive neuroectodermal tumor/Ewings, and T-cell acute lymphoblastic lymphoma (ALL) were PAX2 negative. However, PAX2 weakly stained some cases of B-cell ALL rhabdomyosarcoma (RMS) was also stained, especially alveolar RMS (83%), with less staining of embryonal RMS (13%). One of the antibodies also stained maturing myoid cytoplasm of WT and RMS. This study shows that PAX2 is a sensitive marker of WT (sensitivity 97%), but PAX2 shows weak-to-moderate-intensity nuclear staining of RMS and B-cell ALL, somewhat limiting its utility. However, PAX2 may be a helpful marker in certain diagnostic situations. We speculate that RMS and B-cell ALL staining could be due to antibody cross-reactivity with PAX family members with known expression in RMS and B-cell ALL.

Radiation therapy is an important adjunct to breast-conserving surgery, but the diagnosis of recurrent/de novo carcinoma in a background of radiation atypia can be difficult, especially on small biopsies. Immunostaining for myoepithelial cell proteins is often used to assess invasion in nonirradiated breast tissue, yet these stains have not been investigated specifically in irradiated breast. We studied 29 irradiated breast resection specimens, some with carcinoma in situ (CIS, n=13) and/or invasive carcinoma (n=13). Representative blocks were stained for the myoepithelial proteins p63, smooth muscle myosin heavy chain (SMM), calponin, CK5/6, the proliferative marker Ki-67, and the tumor-suppressor p53. Nonirradiated control tissue was also stained with Ki-67 and p53 (CIS, normal, contralateral). Areas of radiation atypia/atrophy and nearly all CIS in irradiated breast tissue had abundant myoepithelial cells as evidenced by SMM, calponin, and p63 stains, with focal staining attenuation or gaps with SMM and calponin and frequently absent CK5/6 staining. As predicted, myoepithelial cell staining was absent in invasive carcinoma. p63 staining revealed postradiation myoepithelial nuclear morphologic changes. p53 staining was increased, although weak, in irradiated non-neoplastic breast (12% irradiated; 4% nonirradiated); however, irradiated CIS had less p53 staining when compared with control CIS (3% irradiated; 38% nonirradiated). As expected, Ki-67 was increased in carcinoma as compared with non-neoplastic irradiated tissue. Thus, myoepithelial immunostaining is a useful diagnostic adjunct in irradiated breast, with caveats similar to nonirradiated breast. Ki-67 may be helpful in some postradiation specimens; however, p53 staining is not reliable in this setting.