Sample A: Cover Page of Thesis, Project, or Dissertation Proposal

Kruppel-like factor 5 (KLF5) has also been implicated in carcinogenesis pathways. In particular,
it activates in response to DNA damage to induce apoptosis or DNA repair, through the p53
dependent pathways [48]. Increased KLF5 expression accelerates G2/M phase transitions by
activating cyclin B1 [49]. Similarly, PPP2R5C also participates in p53 activation after the
induction of DNA damage, acting as a mitotic checkpoint to suppress cancer growth [50, 51].
DNA damage activates ATM (ataxia telangiectasia mutated), which phosphorylates p53 at Ser15.
The phosphorylation promotes the p53 and PPP2R5C interaction, thereby causing the
dephosphorylation of p53-Thr55 and cell cycle arrest [50, 51]. Both KLF5 and PPP2R5C have
elevated levels of mRNA transcript in the squamous cells, which supports the hypothesis that the
squamous carcinomas have undergone DNA damage. Finally the TSC22D3, or GILZ, ProbeSet
demonstrates significant up-regulation in the normal samples. This gene regulates a number of
cell functions, including cell proliferation, and has been identified has a tumor suppressor gene.
Conclusion
Cancer is a complex disease that can affect nearly every pattern of expression of a cells genes,
depending on the stage. This obscures important mechanisms that discriminate the types of
disease and perhaps possible points of control. We have shown that by application of the BaFL
cleansing routine, followed by straightforward machine learning methods for down-selection
criteria and clustering parameters, even very simple classification methods reveal a distinct
picture of tumorogenesis for the Bhattacharjee NSCLC samples. While the complexity of the
disease cannot be overstated, this picture is much simpler and amenable to straightforward assays
for confirmation. For example, a significant proportion of the identified genes have been
documented to have alternative transcripting events, oncogenic genomic amplification,
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