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Allelic deletion at 9p21-22 in primary cutaneous CD30(+) large cell lymphoma
1Department of Dermatology, University Hospital, Zürich, Switzerland. rboeni@derm.unizh.ch
Abstract:
The genetic alterations responsible for the development of cutaneous lymphoma are largely unknown. Chromosome region 9p21 contains a gene locus encoding an inhibitor of cyclin-dependent kinase 4, and heterozygous deletions of this tumor suppressor gene (p16) have been shown in a variety of malignant tumors. We studied 11 randomly selected cutaneous CD30-positive large cell lymphomas. Several areas containing 20-50 CD30-positive lymphocytes were microdissected in each case and subjected to single-step DNA extraction. Loss of heterozygosity analysis was performed using polymorphic markers at 9p21 (IFNA, D9S171, D9S169) and 17p13 (TP53). Samples from normal cells apart from CD30-positive lymphocytes, e.g., CD30-negative lymphohistiocytic infiltrates and normal epidermal layer, were also obtained in all cases from the same slide for comparison with the tumor samples. Expression of CD30 and T-lineage antigens (CD3, CD45Ro) was confirmed in all cases. Immunohistochemical staining for p16 and p53 was performed using the monoclonal antibodies sc-1661 and DO-7, respectively. Of the 11 informative cases, seven (64%) exhibited loss of heterozygosity at least for one marker at 9p21 (p16), whereas no allelic deletions were found for the polymorphic marker at 17p13 (p53). On immunohistochemistry loss of the p16 protein was detected in two of 11 cases. Nuclear staining for p53 protein was found in four of 11 cases. Here, we provide the first evidence of the involvement of the tumor suppressor gene p16 in primary cutaneous large cell lymphoma. Whether p16 deletion in these lymphomas is associated with disease progression and whether this method could serve as an early marker to detect lymphomas at an early stage needs to be addressed in future studies. J Invest Dermatol 115:1104-1107 2000
Insights
Genetic alterations in cutaneous lymphoma are unclear. This study found evidence of the tumor suppressor gene p16 involvement in primary cutaneous large cell lymphoma, suggesting a potential role in disease development.
Area of Science:
- Dermatology
- Oncology
- Genetics
Background:
- The genetic basis of cutaneous lymphoma remains largely unknown.
- The tumor suppressor gene p16, located at chromosome region 9p21, is implicated in various malignancies.
- Understanding genetic alterations is crucial for diagnosing and treating cutaneous lymphomas.
Purpose of the Study:
- To investigate the potential role of the tumor suppressor gene p16 in primary cutaneous CD30-positive large cell lymphomas.
- To analyze loss of heterozygosity at 9p21 (p16) and 17p13 (p53) in cutaneous lymphoma samples.
- To assess the expression of p16 and p53 proteins in these lymphomas.
Main Methods:
- Microdissection of CD30-positive lymphocytes from 11 cutaneous lymphoma cases.
- Loss of heterozygosity analysis using polymorphic markers at 9p21 and 17p13.
- Immunohistochemical staining for p16 and p53 protein expression.
Main Results:
- Loss of heterozygosity at 9p21 (p16) was observed in 64% of informative cases.
- No allelic deletions were found at 17p13 (p53).
- Loss of p16 protein was detected in two cases, and p53 nuclear staining in four cases.
Conclusions:
- This study provides the first evidence implicating the tumor suppressor gene p16 in primary cutaneous large cell lymphoma.
- Further research is needed to determine if p16 deletion correlates with disease progression or can serve as an early diagnostic marker.