Cancers, Vol. 9, Pages 165: Telomere Shortening in Hematological Malignancies with Tetraploidization —A Mechanism for Chromosomal Instability?

Cancers, Vol. 9, Pages 165: Telomere Shortening in Hematological Malignancies with Tetraploidization—A Mechanism for Chromosomal Instability? Cancers doi: 10.3390/cancers9120165 Authors: Eigil Kjeldsen Aneuploidy, the presence of an abnormal number of chromosomes in a cell, is one of the most obvious differences between normal and cancer cells. There is, however, debate on how aneuploid cells arise and whether or not they are a cause or a consequence of tumorigenesis. Further, it is important to distinguish aneuploidy (the “state” of the karyotype) from chromosomal instability (CIN; the “rate” of karyotypic change). Although CIN leads to aneuploidy, not all aneuploid cells exhibit CIN. One proposed route to aneuploid cells is through an unstable tetraploid intermediate because tetraploidy promotes chromosomal aberrations and tumorigenesis. Tetraploidy or near-tetraploidy (T/NT) (81–103 chromosomes) karyotypes with or without additional structural abnormalities have been reported in acute leukemia, T-cell and B-cell lymphomas, and solid tumors. In solid tumors it has been shown that tetraploidization can occur in response to loss of telomere protection in the early stages of tumorigenesis in colon cancer, Barrett’s esophagus, and breast and cervical cancers. In hematological malignancies T/NT karyotypes are rare and the role of telomere dysfunction for the induction of tetraploidization is less well characterized. To further our understanding of possible ...
Source: Cancers - Category: Cancer & Oncology Authors: Tags: Article Source Type: research