For example, miR-127 has been shown to participate in cancer development, miR-145 has been shown to control c-Myc expression through p53, miR-199a Mechlorethamine hydrochloride regulates MET protooncogene and affects NF-KB expression, miR-379 affects brain neuronal development, miR-451 affects erythroid differentiation, miR-126 affects angiogenic signaling and controls blood vessel development, miR-143 regulates ERK5 signaling and targets KRAS gene, miR-298 regulates CYPA3 expression and miR-486 regulates kinase activity and tumor progression. Also, miR-671 and miR-700 are involved cancer growth and development. miR-669 is involved in c-Myc expression through p53, miR-500 regulates MET protooncogenes and affects NF-kB, miR-466 is involved in mammary tumor development, miR-466c is involved in tumor growth, miR-449a regulates breast cancer development and inhibits cell proliferation and miR-Let7b plays a role in myeloid leukemia. Together, such data suggested that TCDD affects a large number of miRs that may be directly or indirectly involved in tumor induction and promotion. The precise role of such miRs in TCDD-induced tumorigenesis and toxicity in vivo can be better addressed by using mice deficient in such miRs. In summary, we demonstrate for the first time that exposure to environmental toxicants such as 
TCDD during pregnancy can have a significant effect on the miR profile of fetal thymus and thereby influence the regulation of a large number of genes that may affect the development of the immune system. Identification of miRs as targets for TCDD-induced modulation of gene expression offers insights into novel pathways to further understand the mechanisms of toxicity. Oxalate is a metabolic end product that is freely filtered at the glomerulus, undergoes bi-directional transport in the renal tubules, and is excreted primarily by the kidney. The most common pathological condition involving oxalate is the formation of calcium oxalate stones in the kidney. While very high levels of urinary oxalate are observed only in subjects with primary hyperoxaluria, a majority of idiopathic kidney stone patients only show a mild elevation in urinary oxalate In addition several other conditions associated with oxalate deposits are: renal cysts in acquired renal cystic disease, proliferating cells in the kidney, hyperplasic thyroid glands, and benign neoplasm of the breast. These considerations suggest that the pathological deposition of calcium oxalate is more complex than a simple physical precipitation of calcium oxalate crystals. In 1994, we were the first group to note that oxalate renal cell interactions involved alterations in gene expression. Over the past two decades, studies have demonstrated that oxalate interactions with renal epithelial cells result in a program of events, including changes in gene expression and cell dysfunction, consistent with cellular stress. Studies from our laboratory demonstrated that oxalate induced changes in renal cells are inhibited by inhibitors of transcription and translation, indicating that the cellular response to oxalate toxicity is dependent on new gene expression and protein synthesis. Moreover, cells of the renal Tulathromycin B tubular epithelium are exposed to an environment with variable and elevated concentrations of the oxalate and must be able to adapt to oxalate stress. Indeed we have shown that many signal transduction pathways, including p38 MAPK and JNK, are activated in renal epithelial cells in response to oxalate and COM crystals. However, the genetic response of renal epithelial cells to oxalate exposure remains ambiguous. HK-2 cells are a line of human proximal tubular epithelial cells immortalized by using the E6/E7 genes of human papilloma virus.