The purpose of the Administrative Core is to provide support for the integrated Program on Lung Cancer Targeted Therapies, whose ultimate goal is to translate genomic events into the therapy of patients with nonsmall cell lung cancer (NSCLC) by discovery, testing, and validating kinase inhibitors as targeted therapies for genomically selected NSCLC . Specifically, the Core Director and Co-Director will provide guidance and oversight to the Projects and shared research Cores and will lead the evaluation of research progress including consultation with an Internal Advisory Committee and an External Advisory Board. The Administrative Core of this Program Project application is to coordinate these interrelated complementary research projects to maximize their scientific synergy and to share the findings with the scientific community. The Core Directors will co-ordinate staff assistance to projects including administrative support to facilitate scientific progress including meeting arrangements, editorial services for manuscript preparation, and web development services for internal and external communications.
The specific aims of the Administrative Core are summarized below.
Specific Aim 1 : Monitor projects and shared resource cores and to evaluate overall research progress.
Specific Aim 2 : Foster collaboration and communication among the projects and shared resource cores.
Specific Aim 3; Provide fiscal oversight and support for the program.
Specific Aim 4 : Promote the clinical translation of diagnostic and therapeutic discoveries from the program.
To accomplish a complex, multi-investigator research effort such as the Program in Lung Cancer Targeted Therapies, which could achieve a real impact on lung cancer treatment, requires significant co-ordination among Projects, Cores, and investigators within the Program. The Administrative Core will accomplish this necessary co-ordination and oversight.
|Gannon, Hugh S; Kaplan, Nathan; Tsherniak, Aviad et al. (2016) Identification of an ""Exceptional Responder"" Cell Line to MEK1 Inhibition: Clinical Implications for MEK-Targeted Therapy. Mol Cancer Res 14:207-15|
|Jia, Yong; Yun, Cai-Hong; Park, Eunyoung et al. (2016) Overcoming EGFR(T790M) and EGFR(C797S) resistance with mutant-selective allosteric inhibitors. Nature 534:129-32|
|Kim, Eejung; Ilic, Nina; Shrestha, Yashaswi et al. (2016) Systematic Functional Interrogation of Rare Cancer Variants Identifies Oncogenic Alleles. Cancer Discov 6:714-26|
|Aguirre, Andrew J; Meyers, Robin M; Weir, Barbara A et al. (2016) Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting. Cancer Discov 6:914-29|
|Zhang, Haikuo; Qi, Jun; Reyes, Jaime M et al. (2016) Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer. Cancer Discov 6:1006-21|
|Yang, Shenghong; Imamura, Yu; Jenkins, Russell W et al. (2016) Autophagy Inhibition Dysregulates TBK1 Signaling and Promotes Pancreatic Inflammation. Cancer Immunol Res 4:520-30|
|Wu, Hong; Wang, Aoli; Zhang, Wei et al. (2015) Ibrutinib selectively and irreversibly targets EGFR (L858R, Del19) mutant but is moderately resistant to EGFR (T790M) mutant NSCLC Cells. Oncotarget 6:31313-22|
|Lim, Sang Min; Xie, Ting; Westover, Kenneth D et al. (2015) Development of small molecules targeting the pseudokinase Her3. Bioorg Med Chem Lett 25:3382-9|
|Tricker, Erin M; Xu, Chunxiao; Uddin, Sharmeen et al. (2015) Combined EGFR/MEK Inhibition Prevents the Emergence of Resistance in EGFR-Mutant Lung Cancer. Cancer Discov 5:960-71|
|Shen, R R; Zhou, A Y; Kim, E et al. (2015) TRAF2 is an NF-*B-activating oncogene in epithelial cancers. Oncogene 34:209-16|
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