This finding was supported by a re cent study that SM22 overexpression activated the Rb E2F pathway through elevating MT1G expression in human hepatocarcinoma cells. Conclusions MLN2238 In summary, our data showed that MT1G acted as a tumor suppressor, which was frequently inactivated by epigenetic alterations, such as promoter methylation and histone modification, in thyroid cancer. MT1G contributes to suppression of thyroid carcinogenesis by inhibiting cell growth and invasiveness, and inducing cell cycle arrest and apoptosis mainly through modulating the PI3K Akt signaling pathway and partially through regulating the Rb E2F pathway. Background Globally, is the third most common diagnosed cancer in men and second in women Jemal, 2011 316. With the annual worldwide incidence rate of colon cancer rising to over 1.

2 million in 2008, up from less than 0. 95 million in 2005, the number of annual deaths has also risen by 100,000 in the same three year span. Surgical resection is the only curative treatment option for local regional disease. Clinical outcome is dependent upon extent of disease at presentation, also known as tumor stage. Five year survival rates according to tumor stage at diagnosis based on the patient data collected in the SEER database between 1991 and 2000 were as follows, 72 85% for stage II patients, 44 83% for stage III patients, and 8% for stage IV. For patients that have undergone potentially curative resection, disease recurrence has been attributed to clinically occult micro metastases present at the time of surgery, which are targeted by postoperative therapy.

However, despite multi modality therapy, survival rates are still modest. As a result multiple hypotheses have been developed to account for the limitations in current treatment modalities. One argument described discusses the impact of genetic aberrations that arise during the development of CRC, which can lead to a reduced susceptibility to apoptosis which could account for the resistance to chemotherapy. thing Raf kinase inhibitor protein is a member of the phosphatidylethanolamine binding protein family and is an inhibitor of the mitogen activated protein kin ase cascade initiated by Raf 1. RKIP can affect vari ous diseases including cancer, Alzheimers disease, and pancreatitis, which makes it a logical target for individu alized therapy and disease specific interventions. The antagonizing effects of RKIP on cell survival also extends to the NFB and GRK2 pathways. RKIP is induced upon exposure to many chemotherapeutic agents and plays a key role in the apoptosis of tumor cells.