NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
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iotechniques to identify the gene located in mouse chromosome 1 that is involved in the regulation of peak bone density. B.<br />
<strong>Technical</strong> Objective 2: Our second technical objective has been focused on identifying the key genes that are involved in soft<br />
tissue repair/regeneration using inbred strains of mice as model systems. C. <strong>Technical</strong> Objective 3: The goal of our third<br />
technical objective is to identify <strong>and</strong> characterize novel genes, using ENU mutagenesis techniques <strong>and</strong> to elucidate the<br />
function of known genes that play a key role in the metabolism of bone <strong>and</strong> soft tissue.<br />
DTIC<br />
Bones; Fracturing; Genes; Maintenance; Wound Healing<br />
20040050677 University of South Florida, Tampa, FL<br />
Advanced Cancer Detection Center<br />
Krischer, Jeffrey P.; Oct. 2003; 135 pp.; In English<br />
Contract(s)/Grant(s): DAMD17-01-2-0056<br />
Report No.(s): AD-A420948; No Copyright; Avail: CASI; A07, Hardcopy<br />
The goals of the Advanced Cancer Detection Center include the discovery of molecular <strong>and</strong> genetic markers of cancer<br />
risk, the identification of individuals at high risk for cancer through screening <strong>and</strong> the testing of methods to prevent cancer.<br />
DTIC<br />
Cancer<br />
20040050678 General Hospital Corp., Boston, MA<br />
Mitochondria Polymorphism in Neurofibromatosis Type 1<br />
Kurtz, Andreas C.; Nov. 2003; 47 pp.; In English; Original contains color illustrations<br />
Contract(s)/Grant(s): DAMD17-00-1-0535<br />
Report No.(s): AD-A420949; No Copyright; Avail: CASI; A03, Hardcopy<br />
NF1 is characterized clinically by the development of plexiform <strong>and</strong> multiple cutaneous neurofibromas. There is no<br />
correlation between the numbers, size or prevalence of neurofibromas <strong>and</strong> the type of mutations in the NF1 gene, suggesting<br />
a role for genetic modifiers. Genetic polymorphism in mitochondria could cause variability in the observed tumor phenotype<br />
in NF1. Here, we analyzed somatic mitochondrial DNA mutations in cutaneous <strong>and</strong> plexiform neurofibromas to determine if<br />
certain mutations are found predominantly in tumors. We found somatic mutations in 9 of 18 plexiform neurofibromas <strong>and</strong><br />
9 of 19 cutaneous neurofibromas. All mutations detected were in the hypervariable D-loop region, where origin of replication<br />
<strong>and</strong> transcriptional regulators are located. Most mutations appeared to be homoplasmic in the tumors. In addition, pre-existing<br />
soamtic mtDNA mutations were detected in healthy skin of NF1 patients. Our analysis found that these pre-existing somatic<br />
mtDNA mutations accumulate in the tumor, suggesting a selection for the mutated mitochondria in all cell types present in<br />
neurofibromas. In a second ongoing set of experiments we analyze the proportion of germ line mitochondrial DNA variants<br />
in a cohort of 500 NF1 patients with high numbers <strong>and</strong> low numbers of cutaneous neurofibromas.<br />
DTIC<br />
Deoxyribonucleic Acid; Genetic Engineering; Mitochondria; Neoplasms; Polymorphism<br />
20040050679 Cornell Univ., Ithaca, NY<br />
Characterization of the Hen as a Model for Human Ovarian Cancer<br />
Johnson, Patricia A.; Sep. 2003; 13 pp.; In English; Original contains color illustrations<br />
Contract(s)/Grant(s): DAMD17-00-1-0560<br />
Report No.(s): AD-A420950; No Copyright; Avail: CASI; A03, Hardcopy<br />
Investigation of basic factors involved in malignant transformation of the ovary has been hampered by the lack of an<br />
appropriate animal model. Most animals, with the exception of the domestic hen, do not spontaneously develop ovarian cancer.<br />
The use of two related genetic strains, which differ in spontaneous incidence of ovarian cancer may reveal an important<br />
difference between the two strains that could underlie the differential susceptibility to ovarian cancer. We have examined many<br />
hens of both strains <strong>and</strong> have observed that the marked difference in incidence between the strains has been maintained. We<br />
have characterized the tumors in terms of ovalburnin expression as an indication of site or origin. We have also examined the<br />
expression of markers in the tumors. Our second approach was to manipulate the rate of follicle development <strong>and</strong> ovulation<br />
to examine the effect of repetitive ovulation on incidence. This experiment was not possible so we have instead focused on<br />
hormones related to ovulation. We found that the C strain has higher circulating levels of progesterone as compared to the K<br />
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