Thus, our data suggest that higher inclusion levels of ECT2-Ex5 promote tumor growth of MCF7-DoxoR cells, and indicate that the growth of Doxo-resistant tumors can be inhibited by combined Doxo and VMO-ECT2-Ex5 treatments, although it is unclear for statistical reasons, whether VMO-ECT2-Ex5 may decrease MCF7-DoxoR tumor growth preferentially in the presence of Doxo. This evidence concerns the gene ECT2 and neoplasm.