Similarly, there is a rough correspendence between the clinical course of patients and the development of chromosomal abnormalities in their clones. Recurrent chromosomal lesions typically found in B-CLL patients include deletion at 13q14.3,11q22-23,17p13, and 6q21, and amplifications of all or portions of chromosome 12. Deletion at 13q14.3 is found in greater than half of B-CLL cases over time and is linked to loss of two micro-RNAs that can regulate Bcl-2 expression. However, thus particular chromosomal abnormality is not especially dangerous because patients exhibiting this deletion on one allele and no other DNA lesions in their clones have a clinical course that is benign and comparable to normal age-stratified individuals. In contrast, deletions at 11q22-23, 17p13, and 6q21 are generally associated with more aggressive disease, perhaps because these deletions may affect important genes such as p53 (17p13 deletion), and ataxia telangiectasia mutated (ATM; 11q22-23 deletion). Longitudinal studies, albeit on a relatively limited number of patients, demonstrated that these ominuous cytogenetic abnormalities accumulate progressively in the course of the disease and more frequently in patients with U-CLL.