| Popis: |
The paper addresses the topic of the clonal origin of neoplasms that frequently present as multiple lesions, such as Kaposi's sarcoma in patients with human immunodeficiency virus infection. The authors used a statistical analysis that showed the low likelihood that their findings would occur by chance. We suggest caution in the interpretation of these calculations because of the skewing of X-chromosome methylation in different tissues. Synchronic or metachronic tumors can be shown to be truly monoclonal (derived from the same clone) only if several molecular markers are concordant. An analysis of X-chromosome inactivation cannot distinguish metastatic tumors (arising from a single clone) from synchronic tumors arising from different clones but expressing the same inactivated X chromosome. The results obtained by analyzing a single molecular marker prove clonal expansion of a subgroup of tumor cells with proliferative advantages, but they do not prove actual clonality, especially when the assay is based on patterns of methylation that may be influenced by the functional status of the cell, tumor progression, or both. |
