? CANCER STEM CELLS PROGRAM The Cancer Stem Cells (CSC) Program is based on two pivotal findings made by program members: 1) only a small percentage of cells in tumors, the cancer stem or initiating cells, drive the growth and metastatic capability of tumors. These cells must be eliminated to achieve a complete therapeutic response; and 2) cancers frequently arise as the consequence of changes in self-renewal pathways, such as the Wnt and the Hedgehog signaling cascades. The CSC Program postulates that self-renewal is a critical function of both cancer stem cells and their normal counterparts and that self-renewal pathways may be co-opted in the process of oncogenesis to support tumor growth. Based on these concepts, the overall goal of the Cancer Stem Cells Program is to identify and characterize self-renewal pathways in model systems, normal tissues, and solid tumors. These efforts require the strong integration of basic research with preclinical studies within the program, as well as collaboration with clinical investigators in other programs. Co-led by Michael Clarke, MD and Roel Nusse, PhD, the 20 members represent three schools (the School of Medicine, the School of Humanities & Sciences and the School of Engineering) and 12 departments. The research activities of the 20 investigators are supported by 41 peer-reviewed, investigator-initiated grants (R01s and others). Peer-reviewed funding is a total of $18.3 million in total costs/year of which $3.3 million is from the NCI, $7.4 million from other NIH sources, and $7.7 million from other peer-reviewed support. Since 2009, program investigators have published over 300 manuscripts relevant to cancer stem cell biology in peer-reviewed journals, of which 19% are intra-programmatic and 42% inter-programmatic, as well as numerous externally collaborative manuscripts. The SCI will continue to be invaluable in seeding innovative projects and assisting with the translation of the basic science findings from this program into new clinical approaches for the diagnosis and treatment of patients with cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA124435-13
Application #
9936160
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2020-06-01
Budget End
2021-05-31
Support Year
13
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Stanford University
Department
Type
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305
Nair, Viswam S; Sundaram, Vandana; Desai, Manisha et al. (2018) Accuracy of Models to Identify Lung Nodule Cancer Risk in the National Lung Screening Trial. Am J Respir Crit Care Med 197:1220-1223
She, Richard; Jarosz, Daniel F (2018) Mapping Causal Variants with Single-Nucleotide Resolution Reveals Biochemical Drivers of Phenotypic Change. Cell 172:478-490.e15
Champion, Magali; Brennan, Kevin; Croonenborghs, Tom et al. (2018) Module Analysis Captures Pancancer Genetically and Epigenetically Deregulated Cancer Driver Genes for Smoking and Antiviral Response. EBioMedicine 27:156-166
Zhou, Mu; Leung, Ann; Echegaray, Sebastian et al. (2018) Non-Small Cell Lung Cancer Radiogenomics Map Identifies Relationships between Molecular and Imaging Phenotypes with Prognostic Implications. Radiology 286:307-315
Pollom, Erqi L; Fujimoto, Dylann K; Han, Summer S et al. (2018) Newly diagnosed glioblastoma: adverse socioeconomic factors correlate with delay in radiotherapy initiation and worse overall survival. J Radiat Res 59:i11-i18
Nørgaard, Caroline Holm; Jakobsen, Lasse Hjort; Gentles, Andrew J et al. (2018) Subtype assignment of CLL based on B-cell subset associated gene signatures from normal bone marrow - A proof of concept study. PLoS One 13:e0193249
Im, Hogune; Rao, Varsha; Sridhar, Kunju et al. (2018) Distinct transcriptomic and exomic abnormalities within myelodysplastic syndrome marrow cells. Leuk Lymphoma 59:2952-2962
Huang, Min; Zhu, Li; Garcia, Jacqueline S et al. (2018) Brd4 regulates the expression of essential autophagy genes and Keap1 in AML cells. Oncotarget 9:11665-11676
Chiou, Shin-Heng; Dorsch, Madeleine; Kusch, Eva et al. (2018) Hmga2 is dispensable for pancreatic cancer development, metastasis, and therapy resistance. Sci Rep 8:14008
Breslow, David K; Hoogendoorn, Sascha; Kopp, Adam R et al. (2018) A CRISPR-based screen for Hedgehog signaling provides insights into ciliary function and ciliopathies. Nat Genet 50:460-471

Showing the most recent 10 out of 322 publications