The primary goal of the Yale SPORE in Skin Cancer Developmental Research Program (DRP) is to provide limited support (maximum of $50,000/year, typically for no more than two years) for a broad spectrum of innovative skin cancer pilot projects (involving research, resources, and technology development applicable to human skin cancer risk, prevention, diagnosis, prognosis, or treatment). Such feasibility/pilot projects must have promising translational research potential, i.e., there must be the expectation that they can evolve, or be incorporated into, full projects with an unequivocal translational component, such that they could replace other completed or sub-optimally progressing projects previously funded within this SPORE. An alternative satisfactory outcome for a funded pilot project would be its development into a research project capable of successfully competing for independent, ROI-type funding. A total of at least $250,000/year will be utilized for Developmental Research Projects ($100,000 in direct costs;, $100,000 in institutional matching funds guaranteed by the Yale Cancer Center, and at least $50,000/year guaranteed by the Department of Dermatology to specifically be used to help support translation to early phase clinical trials of scientific advances made as a result of YSPORE primary/full, developmental or career development projects. A second goal of this DRP is broaden the base of investigators within the Yale research community who are actively engaged in research related to human skin cancer. During Its initial five-year funding period, from 31 new applications for funding, the YSPORE DRP has funded 16 different projects (15 related to melanoma, 1 to cutaneous T cell lymphoma) involving 27 different investigators from 12 different departments/sections. Six additional pilot projects (9 investigators from 8 departments) received more limited support via the YSPORE Administrative Core discretionary funds. A very generous gift from a grateful patient allowed the establishment of the Milstein Meyer Center for Melanoma Research, funds from which were used to further diversify YSPORE pilot/developmental research in melanoma by providing support for five additional projects (8 investigators in five departments).
The Developmental Research Program represent a critically important component of this SPORE, by providing limited support for new, innovative studies of human skin cancers. The goal is for these studies to generate enough new data that they can either obtain funding from the NIH or other equivalent sources to support additional research or be incorporated into full researh projects conducted within this SPORE.
|Brash, Douglas E (2015) UV signature mutations. Photochem Photobiol 91:15-26|
|Jilaveanu, Lucia B; Parisi, Fabio; Barr, Meaghan L et al. (2015) PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis. Clin Cancer Res 21:2138-47|
|Kong, Yong; Krauthammer, Michael; Halaban, Ruth (2014) Rare SF3B1 R625 mutations in cutaneous melanoma. Melanoma Res 24:332-4|
|Taube, Janis M; Klein, Alison; Brahmer, Julie R et al. (2014) Association of PD-1, PD-1 ligands, and other features of the tumor immune microenvironment with response to anti-PD-1 therapy. Clin Cancer Res 20:5064-74|
|Zito, Giovanni; Saotome, Ichiko; Liu, Zongzhi et al. (2014) Spontaneous tumour regression in keratoacanthomas is driven by Wnt/retinoic acid signalling cross-talk. Nat Commun 5:3543|
|Leonhardt, Ralf M; Abrahimi, Parwiz; Mitchell, Susan M et al. (2014) Three tapasin docking sites in TAP cooperate to facilitate transporter stabilization and heterodimerization. J Immunol 192:2480-94|
|Sanmamed, Miguel F; Chen, Lieping (2014) Inducible expression of B7-H1 (PD-L1) and its selective role in tumor site immune modulation. Cancer J 20:256-61|
|Ho, Ping-Chih; Meeth, Katrina M; Tsui, Yao-Chen et al. (2014) Immune-based antitumor effects of BRAF inhibitors rely on signaling by CD40L and IFN?. Cancer Res 74:3205-17|
|Paglino, Justin C; Andres, Wells; van den Pol, Anthony N (2014) Autonomous parvoviruses neither stimulate nor are inhibited by the type I interferon response in human normal or cancer cells. J Virol 88:4932-42|
|Troche, Jose Ramon; Ferrucci, Leah M; Cartmel, Brenda et al. (2014) Systemic glucocorticoid use and early-onset basal cell carcinoma. Ann Epidemiol 24:625-7|
Showing the most recent 10 out of 86 publications