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Individual variants present at <10 % allele fraction or in regions with <50X coverage were flagged for manual review and evaluated/interpreted by the reviewing laboratory scientists and molecular pathologists based on a variety of factors, including, but not limited to, overall tumor percentage, read depth, complexity of alteration, and evidence for associated copy number alterations.
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Cancer is a heterogeneous disease often requiring a complexity of alterations to drive a normal cell to a malignancy and ultimately to a metastatic state.
Given the complexity of alterations in cells and tissues expressing expanded polyQ/htt, gene perturbation screens are expected to shed light on the mechanisms that may be critical for cell response to mutant polyQ expression.
Examples for specific genes are depicted in Figure 7B and Supplementary Figure 7A and demonstrate a striking complexity of alterations of binding patterns mediated by RUNX1 induction whereby the actual formation of non-adherent precursor cells does not yet take place.
Currently, the S2FCP2 is not well studied due to the risk and complexity of routing alteration.
Historically, a two-pathway model had been applied to distinguish low- and high-grade urothelial carcinoma, although significant overlap and increasing complexity of molecular alterations has been recently described.
Recently, the first cancer genomes to be completely sequenced have revealed an unanticiapted breadth and complexity of somatic alterations [1], [2], [3].
However, the underlying mechanism remains undetermined, given the complexity of genetic alterations and accumulating changes upon passaging in such immortalized cells.
Our data provide evidence on the complexity of genetic alterations during the development of cancer.
These findings underscore the difficulty in capturing the complexity of molecular alterations associated with MBC subtypes using single protein markers.
Our results indicate the complexity of genetic alterations involving various molecular pathways that might be associated with intrinsic and/or acquired resistance to chemotherapy in breast cancer.
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