Mohammad Shahrokh Esfahani

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Small samples are commonplace in genomic/proteomic classification, the result being inadequate classifier design and poor error estimation. The problem has recently been addressed by utilizing prior knowledge in the form of a prior distribution on an uncertainty class of feature-label distributions. A critical issue remains: how to incorporate biological(More)
MOTIVATION Measurements are commonly taken from two phenotypes to build a classifier, where the number of data points from each class is predetermined, not random. In this 'separate sampling' scenario, the data cannot be used to estimate the class prior probabilities. Moreover, predetermined class sizes can severely degrade classifier performance, even for(More)
BACKGROUND Accumulation of gene mutations in cells is known to be responsible for tumor progression, driving it from benign states to malignant states. However, previous studies have shown that the detailed sequence of gene mutations, or the steps in tumor progression, may vary from tumor to tumor, making it difficult to infer the exact path that a given(More)
Contemporary high-throughput technologies provide measurements of very large numbers of variables but often with very small sample sizes. This paper proposes an optimization-based paradigm for utilizing prior knowledge to design better performing classifiers when sample sizes are limited. We derive approximate expressions for the first and second moments of(More)
Phenotype classification via genomic data is hampered by small sample sizes that negatively impact classifier design. Utilization of prior biological knowledge in conjunction with training data can improve both classifier design and error estimation via the construction of the optimal Bayesian classifier. In the genomic setting, gene/protein signaling(More)
Previous work by Del Re et al. describing the emergence of KRAS mutations following treatment of non-small cell lung cancer patients with EGFR tyrosine kinase inhibitors was inadvertently omitted from the reference list of this Article and should have been cited as follows. The statement in the Results section 'While it is well established that KRAS(More)
Circulating tumour DNA (ctDNA) analysis facilitates studies of tumour heterogeneity. Here we employ CAPP-Seq ctDNA analysis to study resistance mechanisms in 43 non-small cell lung cancer (NSCLC) patients treated with the third-generation epidermal growth factor receptor (EGFR) inhibitor rociletinib. We observe multiple resistance mechanisms in 46% of(More)