To assess telomerase as a cancer therapeutic target and determine adaptive mechanisms to telomerase inhibition, we modeled telomerase reactivation and subsequent extinction in T cell lymphomas arising in Atm−/− mice engineered with an inducible telomerase reverse transcriptase allele.
In certain conditional transgenic models, reactivation of c-Myc after transient disruption restores tumor growth [57], which may involve activation of dormant cancer stem cells.
In this model, reactivation of infection upon immune suppression provides evidence for the presence of viable bacilli in the tissue even in animals where bacilli may not have been detected prior to immune suppression by the CFU assay [32].
In this model, reactivation occurs spontaneously resulting in the formation of readily scored lesions.
In this model, reactivation of c-Myc after a brief period of tumour regression led to extensive apoptosis of osteoblasts rather than restoration of the tumour phenotype.
In contrast to the osteogenic sarcoma model, reactivation of c-Myc in growth arrested, redifferentiated keratinocytes did not result in increased apoptosis, despite the absence of an anti-apoptotic lesion, but again resulted in increased levels of suprabasal proliferation extending beyond the basal compartment; but as in the c-Myc 'on', no replicating cells were present in the granular layer.
Centrifuge analogue experiments are used to model the reactivation of pre-existing crustal fabrics during extension.
Objective: In this review we discuss three models for reactivation from latency and present evidence in favor of the model that reactivation is a multi-step process which is initiated by the allogeneic response to the transplanted organ.
Hence, we have modeled the application of reactivation drug as a positive input into Tat that represents increasing the relative amount of acetylated nucleosome 1 (Results are confirmed implementing the drug as an inhibitor of HDAC1 - see later).
Conclusion In a mouse model, CMV reactivation leads to the switch from a non-lethal to a lethal staphylococcal pneumonia, increases bacterial lung count and favors the occurrence of staphylococcal lung abscesses.
