The pattern of immunohistochemical expression of cytokeratins 7 (CK 7) and 20 (CK 20) is commonly used to assess possible primary sites of metastatic carcinomas. Because pituitary tumors are almost always benign, there has been little interest in their cytokeratin profile. However, we recently reported the use of CK 7/20 expression to document malignant progression and metastasis of a pituitary tumor, indicating the potential diagnostic usefulness of the CK 7/20 profile of pituitary adenomas. We analyzed CK 7/20 expression in 97 pituitary adenomas subclassified by immunohistochemical hormone expression. In about 90% of all subtypes, CK 7 was either negative or reactive in only a few scattered cells. Corticotrophs and sparsely granulated growth hormone-positive adenomas were consistently CK 20 positive (and CK 7 negative) whereas all other subtypes were almost always CK 20 negative. This CK 20-positive, CK 7-negative profile is previously described consistently only in colonic adenocarcinomas. This study documents that subtypes of pituitary adenomas have different CK 7/20 profiles. Whereas this pattern is likely to have diagnostic usefulness in only rare adenomas, the presence of a unique CK signature in corticotrophs and sparsely granulated growth hormone-positive adenomas, subtypes particularly noted for invasive and aggressive behavior, merits further investigation.
17504 Background: Asynchronous expression of immunophenotypic markers on AML myeloblasts has been well described, but the association of aberrant phenotype with morphologic subclasses has not been reported previously. Methods: Multiparameter flow cytometry (MFC) data were analyzed for all patients (pts) diagnosed with AML at our institution from 2000–2006. MFC was done on fresh bone marrow aspirate and/or peripheral blood samples using the following panel of monoclonal antibodies in triple staining: CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11c, CD13, CD14, CD15, CD16, CD19, CD20, CD22, CD24, CD33, CD56, CD34, CD117, HLA-DR and TdT. Identification of myeloblasts was performed using Side Scatter (SS) characteristics and CD45 expression. Acute lymphoblastic leukemia (ALL) cases or cases with mixed lineage acute leukemia were excluded from the study. Results: We identified 76 pts with AML; median age 57, (range 10 weeks to 89 years), with 32 males and 44 females. The patients had the following French American British classification of AML: M0 (n=1), M1 (n=11), M2 (m=10), M3 (n=5), M4 (n=13), M5 (n=14), M6 (n=1), M7 (n=4) and not otherwise categorized non- M3 AML (n=17). Twenty two pts had AML with multilineage dysplasia (AML-MD) as classified by World Health Organization. Coexpression of TdT on myeloblasts was observed in 4 pts, one of these coexpressed CD5. T-cell lymphoid associated antigens (CD2, CD5 and/or CD7) were coexpressed on myeloblasts from12 pts. B cell lymphoid associated antigens (CD19 and/or CD20) were expressed on myeloblasts from11 pts. Both T and B cell lymphoid associated antigens were present on myeloblasts in 4 pts. Myeloblasts from 13 pts demonstrated the presence of the NK cell marker CD56. A total of 43 patients had AML with immunophenotypic lineage infidelity manifested by coexpression of one or more aberrant antigens on myeloblasts. The distribution of cases with lineage infidelity was higher in 22 pts with AML-MD (n=17, 77%) versus in 54 pts with no dysplasia (n=26, 48%), Chi square =5.4, p=0.02. Conclusions: Abnormal coexpression of lymphoid and NK cell markers was observed in significant number of AML pts and correlated with the presence of multilineage dysplasia. This finding may indicate an earlier stem cell origin of AML-MD. No significant financial relationships to disclose.
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