Tandem repeats are found in both coding and non-coding sequences of higher 
organisms. These sequences can be used in cancer genetics and diagnosis to 
unravel the genetic basis of tumor formation and progression. In this study, a 
possible relationship between SSR distributions and lung cancer was studied by 
comparative analysis of EST-SSRs in normal and lung cancerous tissues. While the 
EST-SSR distribution was similar between tumorous tissues, this distribution was 
different between normal and tumorous tissues. Trinucleotides tandem repeats 
were highly different; the number of trinucleotides in ESTs of lung cancer was 3 
times higher than normal tissue. Significant negative correlation between normal 
and cancerous tissue showed that cancerous tissue generates different types of 
trinucleotides. GGC and CGC were the more frequent expressed trinucleotides in 
cancerous tissue, but these SSRs were not expressed in normal tissue. Similar to 
the EST level, the expression pattern of EST-SSRs-derived amino acids was 
significantly different between normal and cancerous tissues. Arg, Pro, Ser, 
Gly, and Lys were the most abundant amino acids in cancerous tissues, and Leu, 
Cys, Phe, and His were significantly more abundant in normal tissues than in 
cancerous tissues. Next, the putative functions of triplet SSR-containing genes 
were analyzed. In cancerous tissue, EST-SSRs produce different types of 
proteins. Chromodomain helicase DNA binding proteins were one of the major 
protein products of EST-SSRs in the cancerous library, while these proteins were 
not produced from EST-SSRs in normal tissue. For the first time, the findings of 
this study confirmed that EST-SSRs in normal lung tissues are different than in 
unhealthy tissues, and tagged ESTs with SSRs cause remarkable differences in 
amino acid and protein expression patterns in cancerous tissue. We suggest that 
EST-SSRs and EST-SSRs differentially expressed in cancerous tissue may be 
suitable candidate markers for lung cancer diagnosis and prediction.