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It has been proposed that the divergence might result from a modified cell cycle processes in A. gossypii [ 4- 6].
Possible contributing effects caused by different and/or modified cell cycle regulation in tumour vs. normal cells have not been investigated.
An endoreduplication cycle is a modified cell cycle with repeated replication of the genome without mitosis and cytokinesis, resulting in polyploid cells with increased DNA content and cell volume.
With regard to radioresistance, malignant characteristics of cancer cells such as resistance to apoptosis, reduced intracellular adhesion, increased cell matrix adhesion, and modified cell cycle are considered to be important features.
It is known that larval growth is largely based on an increase in cell size, which is accomplished by endoreplication, a modified cell cycle, consisting of successive rounds of DNA synthesis without intervening mitoses.
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A previous study also indicated that a different HDAC inhibitor, LBH589, modified cell cycle-controling proteins, especially cyclin D1 and p21, and powerfully inhibited the progress of ATC in a xenograft model; this was involved by a powerful decrease in Ki-67 expression in tissues from LBH589-treated animals [ 37].
A number of studies assert that EBV overrides or modifies cell cycle checkpoints in G1, G2 and mitosis (reviewed in O'Nions and Allday [28]).
While there is evidence that RB and p53 function in related/partially overlapping pathways to modify cell cycle checkpoints, this point remains unresolved and is likely modified by discrete forms of DNA damage.
For example, matrix metalloproteinases may act in transformation by inducing apoptosis in anchorage-dependent cells and/or by modifying cell cycle checkpoints through alterations in cell adhesion.
This is achieved most likely by modifying cell cycle and transcriptional regulation, for instance, the infection of cabbage leaf curl geminivirus (CaLCUV) has been shown to induce changes in the cell cycle in virus infected cells [ 47].
Recent study has demonstrated that an altered peptide ligand derived from HSP60 induces the activation of T cells by modifying cell cycle phase's distribution of CD4+ T cells from RA patients [ 26].
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