Finally Lee et al demonstrated that intestine specific expression of DGAT1 in the DGAT1

arresten may also vary depending on its level. To date, the systemic or local concentration of arresten is not known, although a pilot study by Ramazani et al. suggests that the normal circulatory level of collagen IV is around 100 ng/ml in healthy humans giving us some cues on the level or arresten. We show here for the first time that arresten directly modulates the behavior of carcinoma cells, and propose that this occurs at least partially via binding to integrin a1b1. Oral squamous cell carcinoma and breast carcinoma cells overexpressing arresten changed to a more epithelial-like phenotype, possibly reflecting ongoing MET-like events, and subsequently became less motile and more apoptotic. However, the MET-like events may not always be beneficial for survival, as MET has also been reported during the establishment of metastases. Furthermore, some ECM molecules have been found to contribute to the formation of premetastatic niches. In summary, since arresten is a potent inhibitor of angiogenesis, and also exerts strong anti-invasive effects on carcinoma cells, it could be considered a candidate for drug development efforts. However, the MET-inducing property of arresten and its role in primary tumors and metastases should be first characterized in detail. Nucleotide excision repair can be considered as an old friend, but is in fact a new enemy in the context of cancer. In normal cells, NER removes many types of DNA lesions, protecting cell Leucomethylene blue (Mesylate) integrity. However, in cancer cells exposed to DNA damaging agents that distort the DNA helix or form bulky injuries to the genome, NER comes into play and removes the damage, thus protecting cancer cells from death. A striking example of this mechanism is represented by the use of platinum compounds such as cisplatin, the backbone for many treatments of solid tumors including testicular, bladder, ovarian, head and neck, cervical, lung and colorectal cancer. It has been demonstrated that NER is the major DNA repair mechanism that removes cisplatin-induced DNA damage, and that ITE resistance to platinum-based therapy correlates with high expression of ERCC1, a major element of the NER machinery. In this context, one way to increase the efficacy of platinum therapy and decrease drug resistance is to regulate NER by inhibiti