Molecular studies have demonstrated that primary
translocations occur in the early stage of MM, followed
by large number of secondary translocations during
tumor progression [27]. It is believed that the secondary
genomic aberrations are responsible for a more proliferative phenotype in the advanced stage of MM. Certain
genetic aberrations, such as MYC rearrangements, del
(13q), del (17p), and the deletion of 1p and/or amplification of 1q, have been identified as the most common
secondary aberrations in MM [27-29]. The chromosome
13 deletion or chromosome 13 monosomy occurs in
50% of the patients with advanced MM and are associated with an aggressive clinical course and an unfavorable prognosis [30,31]. Deletion of 17P13, presumably
resulting in LOH (loss of heterozygosity) of P53, has
been determined to be associated with a very poor clinical outcome [32,33]. Chromosome 1p deletion or 1q
amplification is the most common structural aberration
found in MM and is associated with an unfavorable
prognosis