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Exact(5)
Tumor progression is an evolutionary process which starts from a single cell and results in the selection of more aggressive subclones [ 119].
They conclude that tumors can remain dormant for long intervals despite constant cellular turnover and that high apoptosis rates perturb the intrinsic tumor dynamics and shift the population towards more aggressive subclones.
This effect is due to resistance emergence in more aggressive subclones for larger tumours, such that the tumour relapses more deterministically (i.e., with less variability and faster on average).
The number of subclonal mutations increases in treated compared with untreated cases; thus, the therapy would be a trigger for natural selection leading to the emergence of more aggressive subclones.
A hallmark of myeloid cancers is the ability of the malignant clone to evolve into multiple, frequently more aggressive subclones, as a result of either the natural history of the disease or the selective pressure of chemotherapy.
Similar(55)
The gene expression differences that do occur may be due to a combination of different amounts of epithelial/stromal cells (Fig. 1, Supplemental Table 1), and/or clonal expansion of a more aggressive subclone of a tumor [ 4, 29].
Theoretically, it should be possible to target a cancer in which co-deletion of a gene or of a gene function associated with a more aggressive subclone is expected to arise with high probability due to constraints from external selection and tumor cell architecture on lineage selection.
With respect to BTL2 cells, the cytogenetic data suggest that the first recurrence is derived from the more aggressive subclone of the primary tumour, which might be reflected by chromosomal changes that are borderline in BTL1 but reach significance in BTL2 (losses in chromosomes 2, 6q, and 12q).
One alternative therapeutic approach could be the introduction of a metabolic restriction by a drug which drives the tumor cell population into a newly rearranged genotype which then may not be able to evolve further into the more aggressive subclone due to restriction by the genome architecture of the selected genotype.
Also the long-term passaged subclones displayed variations in phenotypic marker expression and showed an increased growth rate in vitro and a more aggressive growth in vivo.
He is more aggressive.
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