To enable SPORE investigators to rapidly develop new research opportunities which could translate into early benefits for breast cancer patients, and to allow for exploration of new techniques which may require substantial efforts but which are nevertheless not ready for full scale multi-year research funding, we have devoted considerable effort and resources to this SPORE Developmental Research Program. The Executive Committee, together with the advocate members and the Internal Advisory Board, selects proposals for funding as Developmental Projects, based on their scientific merit and relevance to SPORE translational goals. Through the funding of pilot projects, we broaden the scope of research, and allow exploration of high-risk ideas that have the potential for high yields in treatment, prevention, or basic biology of breast cancer. We also attract new investigators with a wide variety of special expertise to apply their expertise to problems and questions in breast cancer research, and we catalyze productive collaborations in which individual skills and approaches combine to create progress that no single investigator could achieve alone. It is important to point out that, although only $50,000 per year is requested from SPORE funds for this program, the Dan L. Duncan Cancer Center is contributing an additional $50,000 per year in recognition of the value of this outreach effort to cancer research in general. During the 21 years of our previous Breast SPORE, initiated in 1992, we funded 97 developmental projects, contributing to 120 publications and providing essential preliminary data for 77 funded grants plus several still pending (including new Projects 3 and 4 In this new SPORE proposal). This mechanism complements the larger and longer-term regular research projects, offering a degree of flexibility which leads to enhanced productivity for the SPORE as a whole.
For the fastest and most efficient progress against breast cancer, we need to draw the broadest possible range of ideas and approaches into the fight. Yet we can't devote a full-scale project to every idea. Thus these developmental projects allow us to take some chances, to attract new ideas and backgrounds into the tent and give them a preliminary tryout, so that the most promising can earn support to become larger successful efforts either within the SPORE or with other major funding.
|Yu, L; Liang, Y; Cao, X et al. (2016) Identification of MYST3 as a novel epigenetic activator of ERÎ± frequently amplified in breast cancer. Oncogene :|
|Malorni, Luca; Giuliano, Mario; Migliaccio, Ilenia et al. (2016) Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance. Mol Cancer Res 14:470-81|
|Fu, Xiaoyong; Jeselsohn, Rinath; Pereira, Resel et al. (2016) FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer. Proc Natl Acad Sci U S A 113:E6600-E6609|
|Eedunuri, Vijay Kumar; Rajapakshe, Kimal; Fiskus, Warren et al. (2015) miR-137 Targets p160 Steroid Receptor Coactivators SRC1, SRC2, and SRC3 and Inhibits Cell Proliferation. Mol Endocrinol 29:1170-83|
|Nardone, Agostina; De Angelis, Carmine; Trivedi, Meghana V et al. (2015) The changing role of ER in endocrine resistance. Breast 24 Suppl 2:S60-6|
|Giuliano, Mario; Hu, Huizhong; Wang, Yen-Chao et al. (2015) Upregulation of ER Signaling as an Adaptive Mechanism of Cell Survival in HER2-Positive Breast Tumors Treated with Anti-HER2 Therapy. Clin Cancer Res 21:3995-4003|
|Shi, Aiping; Dong, Jie; Hilsenbeck, Susan et al. (2015) The Status of STAT3 and STAT5 in Human Breast Atypical Ductal Hyperplasia. PLoS One 10:e0132214|
|Dowst, Heidi; Pew, Benjamin; Watkins, Chris et al. (2015) Acquire: an open-source comprehensive cancer biobanking system. Bioinformatics 31:1655-62|
|Sine, Jessica; Urban, Cordula; Thayer, Derek et al. (2015) Photo activation of HPPH encapsulated in "Pocket" liposomes triggers multiple drug release and tumor cell killing in mouse breast cancer xenografts. Int J Nanomedicine 10:125-45|
|Sinha, Vidya C; Qin, Lan; Li, Yi (2015) A p53/ARF-dependent anticancer barrier activates senescence and blocks tumorigenesis without impacting apoptosis. Mol Cancer Res 13:231-8|
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