Approximately 50% of patients with newly diagnosed sarcoma eventually die of disease. The purpose of the Developmental Research Program of the MSKCC SPORE in Soft Tissue Sarcoma is to support innovative translational research projects in sarcoma. The translational research projects in this program aim to use knowledge of animal and human sarcoma biology to develop and test interventions related to improving diagnosis, prognosis, and treatment of pafients with soft fissue sarcoma. This program will allow us to respond quickly to new opportunifies in translational research and will help us recruit new scientific talent into our SPORE and, more broadly, into sarcomarelevant research.
The specific aims of the Developmental Research Program are: 1) to provide seed funding for innovative, investigator-initiated research in the biology, pathogenesis, progression, and natural history of sarcoma, 2) to fund research with exceptional potential to advance the translational research goals of the SPORE, and 3) to establish a mechanism for strategic interactions with other SPOREs and other major national and international research centers. We are budgeting $450,000 yeariy for this program including $50,000 from the SPORE award itself and $400,000 in MSKCC institutional funds. The priority for funding will be those inifiafives considered most creafive and of the highest scientific quality. Preference will be given to projects that complement the long-term research goals of the SPORE and advance our translational research objecfives. The executive committee can also solicit and fund experimental or clinical initiatives that address an urgent and specific need in the MSKCC SPORE in Soft Tissue Sarcoma program or a unique research opportunity. The internal scientific advisory committee, under the chairmanship of Murray F. Brennan, MD, will review applications to determine priorities for use of these funds and will annually select projects for one to two years of funding. The projects that appear most promising after two years of funding will be considered for incorporation into the SPORE as Research Projects, either in current or future funding cycles.
|Agaram, Narasimhan P; Chen, Chun-Liang; Zhang, Lei et al. (2014) Recurrent MYOD1 mutations in pediatric and adult sclerosing and spindle cell rhabdomyosarcomas: evidence for a common pathogenesis. Genes Chromosomes Cancer 53:779-87|
|Antonescu, Cristina R; Chen, Hsiao-Wei; Zhang, Lei et al. (2014) ZFP36-FOSB fusion defines a subset of epithelioid hemangioma with atypical features. Genes Chromosomes Cancer 53:951-9|
|Kohsaka, Shinji; Shukla, Neerav; Ameur, Nabahet et al. (2014) A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations. Nat Genet 46:595-600|
|Kim, Teresa S; Cavnar, Michael J; Cohen, Noah A et al. (2014) Increased KIT inhibition enhances therapeutic efficacy in gastrointestinal stromal tumor. Clin Cancer Res 20:2350-62|
|Qin, Li-Xuan; Breeden, Linda; Self, Steven G (2014) Finding gene clusters for a replicated time course study. BMC Res Notes 7:60|
|Brennan, Murray F; Antonescu, Cristina R; Moraco, Nicole et al. (2014) Lessons learned from the study of 10,000 patients with soft tissue sarcoma. Ann Surg 260:416-21; discussion 421-2|
|Patwardhan, Parag P; Surriga, Oliver; Beckman, Michael J et al. (2014) Sustained inhibition of receptor tyrosine kinases and macrophage depletion by PLX3397 and rapamycin as a potential new approach for the treatment of MPNSTs. Clin Cancer Res 20:3146-58|
|Weinreb, Ilan; Zhang, Lei; Tirunagari, Laxmi M S et al. (2014) Novel PRKD gene rearrangements and variant fusions in cribriform adenocarcinoma of salivary gland origin. Genes Chromosomes Cancer 53:845-56|
|Antonescu, Cristina R; Sung, Yun-Shao; Chen, Chun-Liang et al. (2014) Novel ZC3H7B-BCOR, MEAF6-PHF1, and EPC1-PHF1 fusions in ossifying fibromyxoid tumors--molecular characterization shows genetic overlap with endometrial stromal sarcoma. Genes Chromosomes Cancer 53:183-93|
|Lee, William; Teckie, Sewit; Wiesner, Thomas et al. (2014) PRC2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors. Nat Genet 46:1227-32|
Showing the most recent 10 out of 37 publications