Federal regulation of human embryonic stem cell research

President George W. Bush's 2001 statement, which laid out guidelines for research that uses human embryonic stem cells to qualify for federal funding, intends to prevent new embryonic stem cell lines from being developed, by prohibiting the federal funding of research that uses embryonic stem cell lines other than those that existed at the time of the policy's inception and were approved by the National Institutes of Health. This policy raises questions of medical and technological ethics and the governments' role in making decisions regarding the advancement of science based on moral and political opinions. Federal stem cell usage policy directly affects scientific research efforts that are currently on the path to understanding the mechanisms of cell differentiation and could potentially offer answers and therapies for disabilities and many chronic diseases. By reviewing the current literature on the background information on human embryonic stem cells, including what they are, where they come from, how they are used for research purposes, and the ethical controversy surrounding their use, I have researched and reported the impact of the 2001 policy on medical research. ^ Both those who support the current policy on human embryonic stem cell research and those who are advocates for policy change have relevant arguments and varying opinions on human embryonic stem cell usage itself. The ethical implication of how embryonic stem cells are obtained has led to fierce debate. This paper presents many arguments for and against hESC research in addition to the policy governing their use. This analysis concludes that the current policy on federal funding of human embryonic stem cell research should be revised to allow research using new stem lines to be eligible for federal funding under specific guidelines. Supporting evidence for this recommendation is provided.^

Effects of exogeneous p53 on growth suppression, apoptosis, and differentiation in oral cancer cell lines

The p53 gene is known to be one of the most commonly mutated genes in human cancers. Many squamous cell carcinomas of the head and neck (SCCHNs) have been shown to contain nonfunctional p53 as well. The use of p53-mediated gene therapy to treat such cancers has become an intensive area of research. Although there have been varied treatment responses to p53 gene therapy, the role that endogenous p53 status plays in this response has not been thoroughly examined. Because of this, the hypothesis of this study examined the role that the endogenous p53 status of cells plays in their response to p53 gene therapy. To test this, an adenoviral vector containing p53 (p53FAd) was administered to three squamous cell carcinoma lines with varied endogenous p53. The SCC9 cell line demonstrates no p53 protein expression, the SCC4 cell line displays overexpression of a mutant p53 protein, and the 1986LN cell line displays low to no expression of wild-type p53 protein as a consequence of human papillomavirus infection. After treatment with p53FAd, the cells were examined for evidence of exogenous p53 expression, growth suppression, alterations in cellular proteins, G1 growth arrest, apoptosis, and differentiation state. Each cell line exhibited exogenous p53 protein. Growth suppression was seen most prominently in the SCC9 cells, to some extent in the 1986LN cells, and little was seen with the SCC4 cells. WAF1/p21 protein was induced in all three cell lines, while PCNA, bcl-2, and bax expression was not significantly affected in any of the lines. Apoptosis developed first in SCC9 cells, next in 1986LN cells, with little seen in the SCC4 cells. The SCC9 line was the only line to show significant GI growth arrest. No significant differences were observed in the overall expression of differentiation markers, aside from increased keratin 13 mRNA levels in all three lines indicating a possible tendency toward differentiation. This study indicates that the endogenous p53 status of squamous cell carcinomas appears to play a critical role in determining the response to p53 adenoviral gene therapy. ^