It might be a secondary event or an early primary event in tumourigenesis depending on how one defines it. On average cancers that use hTERT as their mechanism for telomere maintenance tend to have shorter telomeres than the paired "normal" tissue, suggesting that upon "transformation" the cells underwent several cell divisions which shortened their telomeres by some amount prior to activating hTERT expression for telomere maintenance, suggesting perhaps that the cells already had uncontrolled growth prior to gaining their limitless replicative potential. Whether you consider hTERT activation in this case a primary or secondary event can be debated. Certain types of neuroblastoma which spontaneously regress do not express hTERT, yet other types that do not spontaneously regress do express hTERT.
Conversely, there is also an hTERT independent mechanism of telomere maintenance called ALT found in approximately 10% of certain cancers. Tumour cells with ALT phenotype tend to have much longer telomeres than their paired normal tissue.
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