Although tremendous strides have been made towards understanding the basic biology of breast cancer, very few of these advances have directly translated into improved outcome for the breast cancer patient. Several reasons may account for the inability to turn research findings into clinical applications. 1. A successful translational breast cancer program requires several elements: a critical mass of basic scientists, breast cancer clinicians who function in a multi-disciplinary setting, administrative support, and adequate resources. The SPORE program was designed to facilitate the merging of these elements. 2. Research technology has become increasingly complex and specialized. This trend can limit the kinds of questions any individual investigator can ask, and collaboration between investigators is absolutely required. For example, if the chemotherapist wishes to investigate p53 mutation and response to chemotherapy, collaboration with a skilled molecular biologist will be necessary. The molecular biologist may wish to study breast cancer tissues, which requires collaboration with a breast cancer pathologist. Real advances in improving patient outcome will come from a collaborative team approach, drawing together the various basic science disciplines (molecular biology, cell biology, protein chemistry, etc.) and the clinical disciplines. 3. Research and clinical training has become highly specialized. The Ph.D. investigator often trains in a very narrow field of technology and application. Such training may leave the investigator ill-prepared to approach the complex clinical questions posed by the breast cancer patient. Similarly, the M.D. investigator can become narrowly focused in clinical areas such that the potential applications of basic research findings are not understood or utilized. In order to more rapidly translate basic science advances into clinical advances, a special type of investigator is required. There are still relatively few investigators who can operate at the critical interface between basic science research and clinical medicine. Several barriers evident in the current training of scientists may be responsible for this observation.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Specialized Center (P50)
Project #
Application #
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Baylor College of Medicine
United States
Zip Code
Yu, L; Liang, Y; Cao, X et al. (2017) Identification of MYST3 as a novel epigenetic activator of ER? frequently amplified in breast cancer. Oncogene 36:2910-2918
Holloway, Kimberly R; Sinha, Vidya C; Bu, Wen et al. (2016) Targeting Oncogenes into a Defined Subset of Mammary Cells Demonstrates That the Initiating Oncogenic Mutation Defines the Resulting Tumor Phenotype. Int J Biol Sci 12:381-8
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
Erdem, Cemal; Nagle, Alison M; Casa, Angelo J et al. (2016) Proteomic Screening and Lasso Regression Reveal Differential Signaling in Insulin and Insulin-like Growth Factor I (IGF1) Pathways. Mol Cell Proteomics 15:3045-57
Chaluvally-Raghavan, Pradeep; Jeong, Kang Jin; Pradeep, Sunila et al. (2016) Direct Upregulation of STAT3 by MicroRNA-551b-3p Deregulates Growth and Metastasis of Ovarian Cancer. Cell Rep 15:1493-1504
Dobrolecki, Lacey E; Airhart, Susie D; Alferez, Denis G et al. (2016) Patient-derived xenograft (PDX) models in basic and translational breast cancer research. Cancer Metastasis Rev 35:547-573
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
Canfield, Kaleigh; Li, Jiaqi; Wilkins, Owen M et al. (2015) Receptor tyrosine kinase ERBB4 mediates acquired resistance to ERBB2 inhibitors in breast cancer cells. Cell Cycle 14:648-55
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

Showing the most recent 10 out of 295 publications