人急性髓性嗜酸性粒细胞白血病细胞EOL-1

Bone metastases are a common occurrence in several malignancies, including breast, prostate, and lung. Once established in bone, tumors are responsible for significant morbidity and mortality. Thus, there is a significant need to understand the molecular mechanisms controlling the establishment, growth and activity of tumors in bone. Several in vivo models have been established to study these events and each has specific benefits and limitations. The most commonly used model utilizes intracardiac inoculation of tumor cells directly into the arterial blood supply of athymic (nude) BalbC mice. This procedure can be applied to many different tumor types (including PC-3 prostate cancer, lung carcinoma, and mouse mammary fat pad tumors); however, in this manuscript we will focus on the breast cancer model, MDA-MB-231. In this model we utilize a highly bone-selective clone, originally derived in Dr. Mundys group in San Antonio, that has since been transfectedbacteria interaction. Not surprisingly, there have been numerous genes identiied that are within IBD risk loci that contribute to the autophagic pathway [reviewed in (208)]. The most well-known and studied is the autophagy gene ATG16L1 which in Crohn’s patients is encoded asamissense variant ATG16L1 T300A (30– 33). ATG16L1 functions as a core autophagy factor (Figure 1) and individuals carrying the variant ATG16L1  T300A  display immune dysregulation and intestinal barrier defects (79, 80, 82,