Charles Spruck, Ph.D.

Charles Spruck's Research Focus

Breast Cancer, Cancer, Lung Cancer, Molecular Biology
Cancer Biology, Cancer Epigenetics, Cell Biology, Cell Cycle Progression, Cell Signaling, Cellular Senescence, Genomic Instability, Innate Immunity, Metastasis, Posttranslational Modification, Proteolytic Pathways
Cultured Cell Lines, Human Cell Lines, Mouse, Mouse Cell Lines
Cell Biology, Drug Discovery, In vivo Modeling, Gene Knockout (Complete and Conditional)

Dr. Spruck’s laboratory is focused on developing new, effective, and non-toxic treatments for patients with advanced cancers. The lab focuses on defining the molecular networks that regulate cancer cell division and drive metastasis progression. A long-standing interest of the lab is exploring the role of ubiquitin ligases in cancer initiation and metastasis. Recent studies have focused on identifying therapeutic approaches that activate dormant endogenous retroviruses and retrotransposons in cancer cells to enhance the efficacy of immune checkpoint blockade immunotherapy and DNA damaging therapies. The laboratory utilizes various biochemical and molecular approaches, CRISPR gene editing, and animal models of cancer. An emphasis of the lab is studies of breast, lung, and brain tumors.

Charles Spruck's Research Report

Developing 'viral mimicry' therapeutic approaches for cancer: Approximately 45% of the human genome is composed of repetitive elements (REs), including endogenous retroviruses and retrotransposons, that are transcriptionally silenced in normal somatic cells. Recent studies have demonstrated that the transcriptional reactivation of REs beyond a threshold level of tolerance in cancer cells induces antiviral pathways that can enhance the efficacy of certain therapies. We recently discovered an epigenetic regulatory pathway called FBXO44/SUV39H1 that is essential for RE silencing in cancer cells. Preclinical studies showed that inactivation of this pathway induced viral mimicry in cancer cells, leading to increased immunogenicity and decreased tumorigenicity, and enhanced the efficacy of immune checkpoint blockade therapy. We are currently exploring therapeutic approaches to target this pathway to prevent tumor growth and enhance immunotherapy response.

Targeting metastasis: Metastasis is a major cause of mortality in cancer. Through genomic screens and biochemical studies, we are identifying novel molecular pathways that drive cancer cell motility, invasion, and metastasis. Recently, we identified a novel molecular pathway that promotes cancer cell motility and cancer stem cell self-renewal and suppresses cancer cell immunogenicity, and found its targeting can prevent metastasis and stimulate anti-tumor immune responses in preclinical mouse models.

Charles Spruck's Bio

"Despite recent advances in treatment, patients with advanced metastatic cancers have few effective treatment options. Our lab is focused on developing new effective and non-toxic treatments for these patients."

Charles Spruck earned his B.S. in Biology at UCLA and Ph.D. in Molecular Biology at the University of Southern California. He worked as a postdoctoral fellow at The Scripps Research Institute in La Jolla and was recruited to the Sidney Kimmel Cancer Center in San Diego as an Assistant Professor in 2003. He joined Sanford Burnham Prebys in 2010.
 

Education and Training

Post-doc, The Scripps Research Institute, 2003
Ph.D., University of Southern California, 1995 B.S. University of California at Los Angeles, 1986
 

Prestigious Funding Awards / Major Collaborative Grants

NIH/NCI DoD BCRP CBCRP TRDRP
 

Honors and Recognition

ACS Scholar


TIM Accessory

Publications

FBXO44 promotes DNA replication-coupled repetitive element silencing in cancer cells.

Shen JZ, Qiu Z, Wu Q, Finlay D, Garcia G, Sun D, Rantala J, Barshop W, Hope JL, Gimple RC, Sangfelt O, Bradley LM, Wohlschlegel J, Rich JN, Spruck C

Cell 2021 Jan 21 ;184(2):352-369.e23

CKS1 Germ Line Exclusion Is Essential for the Transition from Meiosis to Early Embryonic Development.

Ellederova Z, Del Rincon S, Koncicka M, Susor A, Kubelka M, Sun D, Spruck C

Mol Cell Biol 2019 Jul 1 ;39(13)

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FBXO44 promotes DNA replication-coupled repetitive element silencing in cancer cells.

Shen JZ, Qiu Z, Wu Q, Finlay D, Garcia G, Sun D, Rantala J, Barshop W, Hope JL, Gimple RC, Sangfelt O, Bradley LM, Wohlschlegel J, Rich JN, Spruck C

Cell 2021 Jan 21 ;184(2):352-369.e23

Triple‑negative breast cancer therapy: Current and future perspectives (Review).

Won KA, Spruck C

Int J Oncol 2020 Dec ;57(6):1245-1261

PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer.

Brunner A, Suryo Rahmanto A, Johansson H, Franco M, Viiliäinen J, Gazi M, Frings O, Fredlund E, Spruck C, Lehtiö J, Rantala JK, Larsson LG, Sangfelt O

Elife 2020 Jul 6 ;9

CKS1 Germ Line Exclusion Is Essential for the Transition from Meiosis to Early Embryonic Development.

Ellederova Z, Del Rincon S, Koncicka M, Susor A, Kubelka M, Sun D, Spruck C

Mol Cell Biol 2019 Jul 1 ;39(13)

CKS protein overexpression renders tumors susceptible to a chemotherapeutic strategy that protects normal tissues.

Tat J, Loriot C, Henze M, Spruck C, Felding BH, Reed SI

Oncotarget 2017 Dec 29 ;8(70):114911-114923

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