Do the reduced ROS levels caused by SOD1 in ovarian chemotherapy results in the resistant phenotype as well We may make a reasonable assump tion that this phenomenon occurs in ovarian chemore sistance. Based on this biological evidence and our computational experiment results, we can infer that SOD1 plays a critical role in ovarian chemoresistance. As shown in Figure 4, CEBPD interacts with KRAS as well and led to a domino effect that may cause che moresistance. It was found that mutations in this candi date gene, KRAS, are one of the most frequent genetic abnormalities in ovarian carcinoma. In other words, KRAS mutation is a common event in ovarian cancer primarily in carcinomas characterized by lower grade, lower FIGO stage, and mucinous histotype.

The KRAS mutational status is not a prognostic factor for patients treated with standard therapy. However, in line with experience from colorectal cancer and NSCLC, it may prove important for predicting the response to EGFR targeted therapies. Thus far, there is no biological evidence directly indicating KRAS gene is involved in platinum based chemoresistance but, from the computa tional experiment results, we may infer that KRAS plays a critical role in chemoresistance. More computational results with high scores of intersected pathways are pro vided in Additional file 4, and analysis of these data may reveal new chemoresistant mechanisms. Conclusions Although platinum based chemotherapeutic agents are widely used for the treatment of endometrial, cervical and breast cancers, chemoresistance caused by molecu lar mechanisms still remains a major therapeutic problem.

The platinum based anti tumor agent is a DNA reactive reagent which causes cell cycle arrest at various phases in the cell cycle and induces apoptosis. Hence, the drug active pathway plays an important role in drug resistance in the cellular system. It is also a very important issue in the identification and validation of drug target genes by supplying their interactive relation ships. This approach elucidated the particular chemore sistance associated pathways in large biological interaction networks. Genes deemed relevant for che motherapy resistance were also likewise determined. After identifying the chemoresistance associated path ways, the scoring procedure filtered the significant path ways according to the genes differential expressions.

Consequently, this allowed for the identification of dis similarities between the responses of chemosensitivity to the chemoresistance expression cancer data. In particu lar, we identified genes and pathway components such Brefeldin_A as the Hedgehog signalling pathway, the WNT signalling pathway, and the notch signalling pathway, that are rele vant to chemoresistance for ovarian and lung cancer. The advantage of comparison analysis is in recognizing the divergent and convergent mechanisms of chemore sistance between cancers.