Accounting for 1.2 million deaths each year, non-small cell lung cancer (NSCLC) is the primary cause of cancer mortality in both sexes, with an overall five-year survival rate of only 10–15%. Despite therapeutic advances in recent years, the high mortality of patients with NSCLC has not been substantially reduced, largely because of the potential of invasion, metastasis, and frequent recurrence. Thus there is an urgent need for developing therapeutic methods to improve the outcome of patients with lung cancer. In NSCLC, the leading death cause is chemotherapy resistance and metastasis, yet the underlying mechanisms of them remain largely unclear¹.

Therapeutic responses to drugs such as gefitinib may persist for as long as 2–3 years; however, drug resistance eventually emerges and this limits the mean duration of response to 6–8 months. Recent advances in bioinformatics and high-throughput technologies, such as microarray analysis, are increasing the understanding of the molecular mechanisms underlying drug sensitivity and biological processes².

Prostate cancer (PCa) has become one of the most common malignancies in men worldwide, with strongly varying rates of tumor progression and responses to treatment. If the tumor is confined to the prostate, patients can be treated by surgical removal of the tumor or by radiation, with high efficacy. By contrast, therapy for unconfined tumors still represents a major problem¹.

Though cancer metastasis is a highly complex multi-step process facilitated by several key events and molecular players, the most effective way known to prevent this progression is by identifying and targeting the various genes involved in the process(es)².

A number of techniques are currently available for assessing prostate health, the most common of which include digital rectal exam (DRE), trans-rectal ultrasonography (TRUS), and prostate specific antigen-based testing (PSA), however, miRNA expression “signatures” are expected to offer serious potential for diagnosing and prognosing cancers in the near future³.

Pancreatic cancer exhibits aggressive features with 1-year relative survival rate of only 21% . Such high mortality of pancreatic cancer could in part be due to the capacity of pancreatic cancer cells to acquire rapid cell proliferative, invasive, and metastatic characteristics during the development and progression of pancreatic cancer. Only early pancreatic cancers can be removed by surgery. Unfortunately, early pancreatic cancer only accounts for a very small numbers of patients (about 20% of all pancreatic cancer diagnosed). Moreover, chemotherapies for unresectable pancreatic cancer are not effective for most patients. Therefore, it is important to understand the molecular mechanism(s) involved in the aggressive growth characteristics of pancreatic cancer. By knowing the altered molecular signaling in pancreatic cancer, novel targeted and combination therapies could be designed to inhibit the aggressiveness of pancreatic cancer so that the patients with pancreatic cancers could be treated with better outcome¹.