Abstract
The morphologic changes in early-stage mycosis fungoides (MF) might overlap with benign inflammatory dermatitis (BID). Previous studies have described altered expression patterns of several proteins in MF, but their diagnostic significance is uncertain. This study aims at examining the frequency of expression of CD45RO, NFkB-p105/p50, JAK3, TOX, and IL-17 proteins by immunohistochemistry. The cohorts included 21 patients of early-stage MF and 19 with benign BID as a control group. CD45RO was positive in all patients of MF and BID. NFkB-p105/p50 showed normal cytoplasmic staining, indicating an inactive status in all patients of both groups. JAK3 was positive in 3 (14%) MF and in 17 (89%) BID patients (p = 0.003). TOX was expressed in 19 (90%) and 13 (68%) patients of MF and BID, respectively (p = 0.120). IL-17 was detected in 13 (62%) MF and in 7 (37%) BID patients (p = 0.056). Co-expression of TOX and IL-17 was seen in 11 (52%) MF patients but in only 3 (16%) BID patients, which was statistically significant (p = 0.021). We conclude that a double expression of TOX and IL-17 may support the diagnosis of MF in the right clinicopathologic setting, while none of the immunohistochemical stains alone provided a significant discrimination between MF and BID.
Highlights
Mycosis fungoides (MF) is a mature T-cell neoplasm that arises in the skin
It is noteworthy to mention that the best assessment of immunophenotypic alterations should be at the epidermal lymphocytes, as the number of lymphoma cells in the dermis is low in early MF [7]
The results of our study showed that Cluster of differentiation-45RO (CD45RO) is a very sensitive marker of MF, it was expressed in all benign inflammatory dermatitis (BID) patients, discounting its diagnostic value
Summary
Mycosis fungoides (MF) is a mature T-cell neoplasm that arises in the skin. It is the most common type of primary cutaneous lymphoma, comprising 50–90% of skin lymphomas [1,2]. The cell of origin of MF is believed to be a CD45RO-positive effector memory T-cell that normally resides in the skin. These cells have many subsets such as TH1, TH2, and TH17 lymphocytes, which explains the heterogeneity of the immunophenotypic characteristics of MF [3]. Examples include mutations in the tumor suppressor gene p53, CDKN2A, and CDKN2B; increased expression of NAV3, JUNB, and c-MYC; and hypermethylation of mismatch repair genes, while chromosomal aberrations are rare [4]
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