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Ama1 variants have recently been shown to cluster into six genetically distinct subgroups on the basis of antibody cross-reactivity, with all subgroups being found worldwide.
Breakpoints of these chromosome translocations have been shown to cluster within restricted regions in or around the genes implicated in the translocations.
In human breast cancer samples, NAT1 mRNA levels have been shown to cluster with a group of genes that included the estrogen receptor, being highest in luminal-type carcinomas and lowest in basal-like carcinomas [7], [8], [9].
Fibrosarcomas, like the MPNST, have been shown to cluster with the SS [ 7, 10].
In protein kinases, they have been shown to cluster into the functionally important catalytic core [ 11, 12].
To put our findings into perspective, we note that SM breakpoints have previously been shown to cluster in gene regions in the majority of cancer types [ 5].
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Over 5300 genes were differentially expressed between CMCs and PBMCs, and these two populations were shown to cluster independently by unsupervised hierarchical clustering analyses.
The outlying sequence (ch 5) was shown to cluster robustly (bootstrap values 100, ML and NJ) with G2 sequences but with a far greater branch length than other members of this cluster.
Biological replicates were shown to cluster together.
All of the families have been placed in a phylogenetic framework and are shown to cluster together to the exclusion of non- Capsaspora families.
M. neglectum was shown to cluster differently to M. contortum [ 24], on the same branch as Podohedriella falcata [ 25], also known as Ankistrodesmus falcatus.
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