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As more patients are included in clinical trials that include longitudinal genome sequencing of tumor samples, this hypothesis will be tested in the near future.
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While this appears to hold true within the Lecanoromycetes with the current sampling, this hypothesis cannot explain the apparent loss of the genes in Endocarpon pallidulum (Chaetothyriomycetidae) or Arthonia rubrocincta (Arthoniomycetes).
The crucial role of CXCR4 in WM cell homing in the BM has been recently described [ 10] and our results, even though obtained in a small number of patients and samples, confirm this hypothesis.
For the AF samples, this null hypothesis was rejected with the Garrigan and Hammers' low-migration model (P = 0.00380 0.00420) and Voight's models with most severe bottleneck (P = 0.00118 0.00052).
While our observations suggest that certain domain types tend to be conserved or disrupted in the event of recombination and that this observation is unlikely to be explained by chance, a greater number of domain types will need to be sampled for this hypothesis to be tested with the necessary rigor.
Our analysis of this ratio in two large, population-based samples strongly supports this hypothesis.
We could, however, not dispose of patient's biological samples to proof this hypothesis.
High GPC levels found in vivo, both in xenograft tissue and clinical samples, suggests that this hypothesis has to be refined.
However, there were no changes in the expression of SDF-1 α and CXCR4 in the lung tissue or protein levels of SDF-1 α in the lung and serum samples, indicating that this hypothesis is not applicable for our model.
Only more extensive sampling can confirm this hypothesis.
Mammographic density data are not available in the CIMBA sample to test this hypothesis explicitly.
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