NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
NASA Scientific and Technical Aerospace Reports
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people discover an interest in BCR <strong>and</strong> are going on to graduate school or medical school <strong>and</strong> are actively involved with BCR<br />
at the next stage of their career. The Summer Undergraduate Research Programs at the Albany Medical College is designed<br />
to recruit highly talented undergraduates <strong>and</strong> expose them to career-defining opportunities. That talented students are being<br />
recruited is evident from the diversity of undergraduate schools (39 in number), the quality of the matriculants (average GPA<br />
3.75), <strong>and</strong> the number of applications (104) received. Students spent 90% of their time in the laboratory of a funded<br />
investigator doing authentic, meaningful, mentored BCR. Students also participated in a variety of Enrichment Activities, all<br />
focused on breast cancer.<br />
DTIC<br />
Cancer; Education; Mammary Gl<strong>and</strong>s; Research Management; Summer<br />
20040111672 Indiana Univ., Indianapolis, IN<br />
Targeting Nuclear Factor kappa B for the Treatment of Prostate Cancer<br />
Sweeney, Christopher J.; Feb. 2004; 16 pp.; In English; Original contains color illustrations<br />
Contract(s)/Grant(s): DAMD17-02-1-0072<br />
Report No.(s): AD-A425799; No Copyright; Avail: CASI; A03, Hardcopy<br />
This report details our progress to date describing the inhibition of the transcription factor, Nuclear Factor kappa B<br />
(NFkB) with parthenolide. To date, we have shown that NFkB is constitutively active in prostate cancer cell lines <strong>and</strong><br />
endothelial cells <strong>and</strong> that NFkB DNA binding is inhibited by parthenolide. Moreover, we have found that NFkB is<br />
over-expressed in human prostatectomy speciments at both the prostatic intraepithelial neoplasia <strong>and</strong> invasive adenocarcinoma<br />
stages. With the use of cDNA array technology, we have shown that multiple genes associated with the hallmarks of cancer<br />
<strong>and</strong> that are under NFkB control are decreased when cancer <strong>and</strong> endothelial cells are treated with parthenolide. We have<br />
subsequently shown that parthenolide is able to decrease cancer cell proliferation <strong>and</strong> enhance the cytotoxic effect of taxanes<br />
in vitro. Finally, we have shown that parthenolide is bioactive in vivo as it is able to inhibit angiogenesis as a single agent,<br />
enhance the cytotoxic effects of docetaxel <strong>and</strong> restore sensitivity of the hormone independent cell line, CWR22Rvl, to the<br />
anti-<strong>and</strong>rogen, bicalutamide.<br />
DTIC<br />
Cancer; Prostate Gl<strong>and</strong><br />
20040111673 Texas Univ., Houston, TX<br />
Wilms’ Tumor 1 (WT1) as Novel Molecular Target in Breast Cancer<br />
Tari, Ana M.; Apr. 2004; 27 pp.; In English<br />
Contract(s)/Grant(s): DAMD17-02-1-0459<br />
Report No.(s): AD-A425800; No Copyright; Avail: CASI; A03, Hardcopy<br />
High levels of Wilms’ Tumor 1 (WT1) mRNA in breast tumors have been linked with poor prognosis for breast cancer<br />
patients. However, the function of WT1 protein in breast cancer was not known. We demonstrated that WT1 protein is vital<br />
to the proliferation of breast cancer cells since downregulation of WT1 protein expression led to breast cancer growth<br />
inhibition. We also demonstrated that the WT1 protein expression is increased by 17-estradiol, but inhibited by tamoxifen or<br />
all-trans retinoic acid. We have exp<strong>and</strong>ed our studies <strong>and</strong> found that two other poor prognostic indicators of breast cancer<br />
patients: HER2/neu <strong>and</strong> Insulin-like Growth Factor-I use the Akt pathway to increase WT1 expression. WT1 has been shown<br />
to undergo two splicing events, which result in four different isoforms. We have preliminary data indicating that the two<br />
isoforms ‘A’ <strong>and</strong> ‘D’ are stimulate the proliferation of MCF-7 breast cancer cells. However, the WT1 isoforms do not appear<br />
to modulate the sensitivities of MCF-7 cells to doxorubicin <strong>and</strong> taxol. We plan to determine the mechanisms <strong>and</strong> the isoforms<br />
by which WT1 deregulates breast cancer cell proliferation.<br />
DTIC<br />
Cancer; Mammary Gl<strong>and</strong>s; Targets; Tumors<br />
20040111674 Pennsylvania State Univ., Hershey, PA<br />
Development of km23-Based Diagnostics <strong>and</strong> Therapeutics<br />
Mulder, Kathleen M.; May 2004; 135 pp.; In English; Original contains color illustrations<br />
Contract(s)/Grant(s): DAMD17-03-1-0287<br />
Report No.(s): AD-A425801; No Copyright; Avail: CASI; A07, Hardcopy<br />
Similar to other solid tumors, ovarian cancers are resistant to the growth inhibitory effects of the natural epithelial growth<br />
inhibitor TGF beta, suggesting that alterations in TGF beta pathways contribute to ovarian cancer progression. The TGF beta<br />
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