Established in 2020 with funding from the National Institute of Aging, part of the National Institutes of Health, the San Diego Nathan Shock Center of Excellence in the Basic Biology of Aging is a consortium of Sanford Burnham Prebys, Salk Institute for Biological Studies and the University of California San Diego.
The center focuses on the heterogeneity of aging, the fact that cells, organs and people age at different rates and that this “biological age” is a better indicator of an individual’s susceptibility to age-related declines and diseases.
The center provides resources to scientist-members to develop new human cell models of aging, enabling deeper analyses of molecular, cellular and tissue heterogeneity and support of basic biology of aging research through development, training and mentoring activities.
Samarra A, Renwick S, Arzamasov AA, Rodionov DA, Spann K, Cabrera-Rubio R, Acuna-Gonzalez A, Martínez-Costa C, Hall L, Segata N, Osterman AL, Bode L, Collado M
Like any complex machine comprised of multifarious but highly synchronized parts, cancer is the creation of diverse but organized cells and molecules driven by disinformation and dysfunction to produce malignant tissues and tumors.
Our program focuses on determining how nutrients and the microenvironment surrounding tumors interact to direct the formation, growth and spread of cancer cells. From individual metabolites to stromal cells, such as fibroblasts and immune cells, our goal is to discern the basic workings of tumors that cause disease, revealing a more comprehensive view of cancer biology that can be a guide to new therapies.
Director’s Statement
“We live and work in the tumor ecosystem, probing its nooks, crannies and complexities for new insights into how tumors begin and grow—and how best to prevent or stop both. We study paramount processes in cancer, including metabolism, signal transduction, tumor-stroma crosstalk and molecular machines. We want to know what different parts of a tumor do, how they work alone or together and why so that we can, ultimately, fix the problems that result in cancer. ”
Samarra A, Renwick S, Arzamasov AA, Rodionov DA, Spann K, Cabrera-Rubio R, Acuna-Gonzalez A, Martínez-Costa C, Hall L, Segata N, Osterman AL, Bode L, Collado M
Lamm V, Huang K, Deng R, Cao S, Wang M, Soleymanjahi S, Promlek T, Rodgers R, Davis D, Nix D, Escudero GO, Xie Y, Chen CH, Gremida A, Rood RP, Liu TC, Baldridge MT, Deepak P, Davidson NO, Kaufman RJ, Ciorba MA
All cancers depend upon dysregulation and dysfunction of normal cell processes. These processes are often controlled by the cell nucleus, specifically by DNA sequence (the genome) and its regulation (the epigenome).
Dysregulation of nuclear processes encoded within the genome and/or epigenome drive many of the detrimental properties of cancer cells, such as defective DNA repair and mutation accumulation, altered inflammatory signaling and immune regulation, unrestrained cell growth and survival, tissue invasion, metastasis and drug resistance. Understanding these processes, including their dysregulation in aging and differences between races and ethnicities, can lead to new approaches for patient- and population-specific risk assessment, early detection and diagnoses of cancer, as well as novel therapeutic interventions.
Director’s Statement
“We bring together experts in nuclear dysfunction in cancer. Analysis of the genome and epigenome is intensive, and so too is our program. Our faculty pursue diverse research interests, and share a fundamental focus on how nuclear dysregulation drives cancer growth—all intended to lead to breakthrough discoveries and treatments for cancer.”
Rohm TV, Dos Reis FCG, Cunha E Rocha K, Isaac R, Strayer S, Murphy C, Bandyopadhyay G, Gao H, Ganguly S, Nguyen T, Wang J, Youhanna JE, Pack D, Liu X, Kim HY, Jeelani I, Dhar D, Kisseleva T, Ying W, Olefsky JM
