In order to avoid laborious and time intensive subcloning, we determined that mA% could be accurately estimated by measurements of the relative peak heights present on the electropherograms of routine sequencing for mutation detection. While mA% could be determined accurately in cell lines by these simple techniques, tumor samples present a much greater problem because of contamination with highly variable percentages of non-malignant cells. Reports of molecular studies often provide estimates of the percentage of tumor cells by histologic examination, but these are usually performed rapidly and are relatively inaccurate. In addition, because of the frequent presence of tumor cell polyploidy, most genetic analyses require determination of the percentage of tumor DNA in the examined sample, rather than the percentage of tumor cells. For our studies, we used SNP array data for determinations of tumor cell DNA percentages. While this approach has been used by others, we refined the methodology. We found a mean value of 57% tumor DNA in the samples having SNP data, with a wide range of values. We arbitrarily used a slightly more conservative estimate for tumor cell DNA of 50% for the tumor samples lacking SNP data. While we 
used such estimates for copy number determinations in tumors, recognition of tumor homozygosity, including UPD, was limited to the tumor subsets with SNP data. Four types of inter-relationships between mA and wA were found: a) balanced type, with mutant: wild type Gentamycin Sulfate allele ratio of approximately one ; b) MASI with CNG; c) uniparental disomy ; and d) reverse MASI. For 75 mutations present in 68 cell lines the overall incidence of MASI was 48%, while only a single example of reverse MASI was identified. Thus allelic imbalance almost invariably targets the mutant allele. Our previous observations regarding allelic imbalance are consistent with our present findings. While MASI was convincingly demonstrated in cell lines the true incidence in Cinoxacin tumors could only be determined with accuracy for the subset of lung tumors having SNP array data and mutational status of the KRAS and EGFR genes. The incidences of MASI in lung cancer cell lines and tumors for these two genes were not significantly different. However, the incidences of MASI for individual oncogenes showed differences, with high frequencies for EGFR and KRAS, intermediate for BRAF and low for PIK3CA. These differences may reflect variations in the oncogenic potential of the individual gene mutations. The frequencies of the two major forms of MASI also demonstrated individual gene differences. For EGFR and BRAF, the most frequent type was MASI with CNGs, while for KRAS, the frequencies of MASI with CNGs and UPD were similar. While mutations of the KRAS and EGFR genes and CNGs of the EGFR gene are well described, the literature regarding KRAS CNGs in human tumors is sparse. While less common than mutations in the present study, KRAS CNGs were relatively frequent. Of interest, KRAS CNGs showed the same clinico-pathological associations as those previously described for KRAS mutations �C relationship to smoking status, nonAsian ethnicity and mutual exclusivity with EGFR mutations. While inherited UPD is associated with developmental disorders. the role of acquired UPD in cancer development is poorly understood. Although UPD has been reported to be related to inactivation of tumor suppressor genes, its presence with activating oncogenic mutations has rarely been described in tumors. To date, UPD has been mainly reported in hematopoietic malignancies for a few oncogenes such as JAK2.