The purpose of this Career Development Program is to support promising investigators who will participate in translational breast cancer research projects. There are one to two awardees at any one time, who may be either MD's or PhD's. Candidates are selected based on their previous accomplishments and their potential and desire to pursue a career in academic breast cancer research. While our primary focus is to support promising young investigators at the junior faculty level, it is possible that more established investigators may also be appropriate for support. The general outline of each awardee's research will have been discussed by the applicant and the Selection Committee as a part of the selection process, and a principal mentor from the Program Faculty will be agreed upon. Awardees will receive further guidance from the Executive Committee and the selected mentor in developing their translational research projects throughout the award period. They will also participate in an extensive set of seminars, professional development courses, and clinical opportunities. The research environment at the Baylor Breast Center is ideal for supporting translational activities. Scientific excellence in breast cancer research continues to be reaffirmed by the award of both individual and collaborative grants, while both national and local programs of clinical investigation are well established at the Baylor Breast Center and can serve to assist in the translation of research findings into clinical practice. This is an excellent setting for enhancing and focusing the careers of outstanding investigators on productive translational research in breast cancer. Indeed, of the 17 young investigators who received partial support from this program in the 21 years of our previous SPORE, most are active in academic research positions in breast cancer, and two have important roles in this new SPORE proposal.
The real goal of our translational research is to get the most up to date laboratory research and the most current clinical experience to talk productively to each other, for the most rapid and efficient progress toward controlling and eliminating breast cancer. Thus we have designed this career development program to expose young researchers to the full range of the breast cancer research experience in a vigorously translational environment, whatever their initial training was, as they move towards research independence.
|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|
Showing the most recent 10 out of 12 publications