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BCL2 and JUNB abnormalities in primary cutaneous lymphomas.
X Mao1, G Orchard, D M Lillington
1Skin Tumour Unit, St John's Institute of Dermatology, St Thomas' Hospital, London SE1 7EH, UK. mxmayo@yahoo.co.uk
The British Journal of Dermatology
|September 21, 2004
Summary
This study reveals that BCL2 loss and JUNB gain occur in primary cutaneous lymphomas (PCLs), particularly in T-cell lymphomas. These genetic alterations suggest a specific molecular pathway driving certain PCLs.
Area of Science:
- Oncology
- Molecular Biology
- Dermatology
Background:
- BCL2 upregulation is common in B-cell lymphomas, promoting anti-apoptotic effects.
- Loss of BCL2 has been observed in some malignancies, indicating diverse pathogenic mechanisms.
Purpose of the Study:
- To investigate the genomic and protein expression of BCL2 and JUNB in primary cutaneous lymphomas (PCLs).
- To compare the expression patterns of BCL2 and JUNB in different types of PCLs.
Main Methods:
- Analysis of BCL2 and JUNB gene copy number using real-time PCR in 88 PCL samples.
- Immunohistochemistry (IHC) to assess BCL2 and JUNB protein expression.
- Fluorescent in situ hybridization (FISH) and gene expression microarray studies for further validation.
Main Results:
- BCL2 gene loss was found in 28% of PCL cases, with significant prevalence in Sézary syndrome/mycosis fungoides (SS/MF).
- JUNB gain was observed in 25% of PCL cases, often co-occurring with BCL2 loss in SS/MF.
- Absent BCL2 protein expression was frequent in SS/MF and C-ALCL, contrasting with BCL2 expression in PCBCL.
Conclusions:
- Findings provide a comprehensive view of BCL2 and JUNB status in PCLs.
- Suggests a selection pressure for BCL2 loss and JUNB upregulation in a subset of cutaneous T-cell lymphomas (CTCLs).
- Highlights the role of chromosomal deletion and amplification in PCL pathogenesis.