Our patient developed CD30+ cutaneous large cell lymphoma two years after initiation of Fingolimod treatment and her symptoms regressed following the cessation of treatment.
Although CD30 is not a specific RS cell marker, its characterization has assumed an important role not only in the differential diagnosis of HD, but also in the identification of a morphologically and clinically distinct type of large cell lymphoma, now designated as anaplastic large cell lymphoma (ALCL) (2).
The aggregate results of these studies indicate that the t(2;5) translocation or other somatic mutations resulting in inappropriate expression of ALK are involved rarely if at all in the pathogenesis of Hodgkin's disease, but may be present in about 10% of cases of lymphomatoid papulosis and 20% of cases of CD30+ primary cutaneous large cell lymphoma.
The specimens studied included fresh-frozen lesional tissues obtained from 16 patients with MF, seven with lymphomatoid papulosis, seven with primary cutaneous CD30+ large cell lymphoma of T-cell lineage, and five with Hodgkin's disease.
Lesional DNA from patients with lymphomatoid papulosis (fourteen cases), Hodgkin's disease (twelve cases), and CD30+ large-cell lymphoma (nine cases) was tested for the HTLV-I proviral pX region using a genomic PCR assay followed by confirmatory Southern blot analysis with a nested oligonucleotide pX probe.All cases were uniformly negative.
This observation in a CD30 negative large cell lymphoma of B cell lineage further extends the relationship of anaplastic large cell morphology, ALK activation, lymphoid lineage, and expression of the CD30 antigen.
Here, we describe six cases of follicular lymphoma, large cell in five cases and mixed in one case, that transformed into a diffuse or sinusoidal CD30 antigen-positive large cell lymphoma with anaplastic cytologic features.
Primary cutaneous CD30 (Ki-1)+ large cell lymphoma (KiL) and lymphomatoid papulosis (LyP) type A are collectively termed as primary cutaneous CD30-positive lymphoproliferative disorders.
Primary cutaneous CD30+ lymphoproliferative disorders (LPDs), including lymphomatoid papulosis (LyP), anaplastic and nonanaplastic CD30+ large-cell lymphoma, and borderline cases, comprise a clinical and histologic spectrum.
To determine the role of the t(2;5) translocation in these diseases, we developed a DNA-based polymerase chain reaction (PCR)/Southern blot assay to detect this translocation at the genomic level in lymphomatoid papulosis (14 cases), primary cutaneous CD30+ large cell lymphoma of T-lineage (10 cases) and Hodgkin's disease (13 cases).
These findings are significant for several reasons: 1) they demonstrate the common clonal origin of lymphomatoid papulosis and CD30+ large-cell lymphoma or mycosis fungoides occurring in individual patients; 2) they confirm that co-migrating PCR/DGGE bands exhibit identical nucleotide sequences; and 3) they provide a method for determining the sequence of a tumor-derived TCR-gamma gene rearrangement in early lesions containing a low tumor clone density.
The contig was nucleated using FISH mapped cosmid clones shown to flank the t(2;5)(p23;q35) translocation breakpoint in a CD30-positive large cell lymphoma cell line.
After topical nitrogen mustard and total skin electron beam therapy for progressive generalized CD3+CD4+ patch/plaque lesions, he developed nodules of Ki-1+ (CD30+) T-LCL at age 72.