NASA Scientific and Technical Aerospace Reports

changes in SFOAEs due to noise can be detected from artifact and test-retest variability. WU# 50309 Evoked Otoacoustic
Emissions in Military Hearing Conservation Programs.
DTIC
Acoustic Emission; Acoustics; Audio Frequencies; Auditory Signals; Frequencies; Hearing; Noise (Sound); Reliability
20040073554 California Univ., Los Angeles, CA
Role of Androgen Receptor in Growth of Androgen Independent Prostate Cancer
Chen, Charlie D.; Jan. 2004; 6 pp.; In English; Original contains color illustrations
Contract(s)/Grant(s): DAMD17-02-1-0024
Report No.(s): AD-A422345; No Copyright; Avail: CASI; A02, Hardcopy
Hormone therapy is an effective treatment for advanced hormone sensitive (HS) prostate cancer. However, the treatment
is short-lived and hormone refractory (HR) cancer eventually develops. Through gene profiling using seven pairs of HS and
HR xenografts, we identified overexpression of androgen receptor (AR) is the only consistent change in the progression of
prostate cancer. In the first grand period (01/02-10/03), we confirmed that AR protein is elevated in HR tumors. Using
lentivirus and retrovirus systems, we were able to overexpress AR in HS prostate cancer cells. In vitro and in vivo experiments
demonstrated that overexpression of AR is sufficient for HS-to-HR transition. We also developed a system (shRNA) to
knockdown AR in HR LNCaP cells and shown that AR- knockdown abolished HR phenotype in vitro. In the last grand period
(01/03-01/04), we demonstrated that overexpression of AR is required for hormone refractory prostate cancer in vivo using
both LAPC4 and LNCaP cells. Although, we were unable to obtain conclusive results to determine the mechanisms for AR
overexpression, we demonstrated that gene amplification is not the sole cause of the overexpression.
DTIC
Cancer; Hormones; Males; Prostate Gland
20040073572 Case Western Reserve Univ., Cleveland, OH
EphA2 Kinase Agonists as Novel Suppressors of Both Prostate Cancer Cell Motility and Growth: Structure-Function
Relations and the Role of RAS/MPK pathway
Wang, Bingcheng; Sep. 2003; 54 pp.; In English; Original contains color illustrations
Contract(s)/Grant(s): DAMD17-99-1-9019
Report No.(s): AD-A422402; No Copyright; Avail: CASI; A04, Hardcopy
There are three goals in this proposal. 1) To establish the expression profile of EphA2 during TRAMP prostate cancer
development and progression, which will help determine the optimal window of EphA2 targeting. 2) To target EphA2 with
its native and artificial agonists to see if they can suppress TRAMP prostate cancer development and/or progression. 3) To
investigate the role of EphA2 during prostate cancer development by crossing EphA2- null mice with TRAMP mice. During
the past 6 months since this modified grant was reactivated, we have made significant progress breeding and genotyping large
number of animals required for achieving the goals.
DTIC
Cancer; Locomotion; Prostate Gland; Suppressors
20040073573 Texas Univ. Health Science Center, San Antonio, TX
Cell Motility and Invasiveness of Neurofibromin- Deficient Neural Crest Cells and Malignant Triton Tumor Lines
Vogel, Kristine S.; Oct. 2003; 20 pp.; In English
Contract(s)/Grant(s): DAMD17-99-1-9499
Report No.(s): AD-A422403; No Copyright; Avail: CASI; A03, Hardcopy
Our purpose is to examine the role of the NF1 gene product, neurofibromin, in modulating the migratory and invasive
properties of neural crest cells (NCC) and neural crest-derived sarcoma cells. As a negative regulator of Ras signaling,
neurofibromin may influence the responses of NC- derived cells to growth factors and extracellular matrix (ECM) molecules
that affect motility. We use embryonic NCC and NC- derived sarcoma lines isolated from cisNf1;p53 mice to compare integrin
ECM receptor expression patterns, ECM adhesion preferences, migration on ECM substrata, invasion through ECM barriers,
and dispersal along NCC pathways in vivo for wild- type and neurofibromin-deficient cells. In the past year, we have
completed studies on the invasiveness of branchial arch mesenchymal cells and trigeminal neural crest cells isolated from
Nf-/-, +/-, and +/+ mouse embryos. Consistent with published results for neurofibromin deficient astrocytes, mast cells, and
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