To date reports from the COSMIC database sellckchem describe mutations of SMG-1 in human breast cancer cell lines and hSMG-1 RNA is detected only at low levels in lung carcinoma and melanoma cell lines [14], [20]. These reports together with our new functional findings indicate SMG-1 is likely to be a potential human tumour suppressor gene product. Give
The basic armamentarium for induction therapy for Crohn’s disease includes: 5-ASAs, antibiotics, budesonide, systemic corticosteroids, thiopurines, methotrexate, and anti-TNF agents. These drugs can be used alone or combined in different treatment algorithms to optimize therapy. The approach to induction therapy can be categorized into three main groups: (1) corticosteriod induction, (2) steroid-free ��bridge�� induction therapy to immunomodulators, and (3) anti-TNF induction.

Corticosteroid Induction Prednisone is highly effective for inducing remission in patients with Crohn’s disease. In the National Cooperative Crohn’s Disease Study (NCCDS), a large randomized controlled trial from the 1970s, at the end of 15 weeks 60% of patients were in remission when treated with prednisone as compared to 30% of those in the placebo group (p < 0.001) [1]. There is not much debate about the effectiveness of corticosteroids for improving symptoms, but once initiated, the long-term outcomes are disappointing. In a cohort of patients from Olmsted County (Minn., USA) although over 80% of patients had either a complete or partial response to corticosteroids at 30 days, at the end of one year, only 28% had a prolonged response, 32% were steroid dependent, and 38% required surgery [2].

Even if patients respond, adverse effects are common. Approximately 50% of patients receiving corticosteroids stop taking this medication due to some side effect. Common events that are typically quickly reversible upon cessation of therapy include acne, moon facies, easy bruising, and ankle edema. More serious long-term problems related to steroid use include osteoporosis, cataracts and diabetes [3,4]. Furthermore, in a recent population based study including almost 6,000 patients from the United Kingdom, the highest risk of death were in those patients treated with corticosteroids (HR 2.48, 95% CI 1.85�C3.31). Although ��bias by indication�� might be in part responsible (e.g. sicker patients received corticosteroids), the hazard ratio of those receiving thiopurines was 0.83, and although not statistically significant to be protective it strengthens the argument of a detrimental effect Entinostat of corticosteroids.