Aging and Cancer Group

PRECLINICAL & TRANSLATIONAL RESEARCH

We investigate the mechanisms of aging, and its connections to cancer. We work on novel paradigms that can quantify and modulate the processes of cellular senescence, immunosenescence, and organismal aging, and test these in the context of oncology and longevity. Our aim is to deliver new understanding, and novel technology that can improve the lives of cancer patients and increase the number of years spent in good health for all individuals.

With aging, our body accumulates senescent cells, our organs lose circulation and functionality in a process called fibrogenesis, all of these contributing to our decline in health. We have reported that iron accumulation can play a key role in several of these processes (Maus et al., bioRxiv, 2022). Our findings have important implications for the pathobiology of aging and cancer. Currently, we investigate the role, and the diagnostic and therapeutic potential of age-associated iron accumulation in longevity and cancer.

With aging, our immune functions decline in a process that is referred to as immunosenescence. We have reported on regulators of immunometabolism that are key for the preservation of immune function (Maus and Vaeth et al., Immunity, 2017). Currently, we develop approaches to measure and modulate the age of the immune system with the aim to understand the role as well as the diagnostic and therapeutic potential of immunosenescence in aging and cancer.

Deregulated nutrient sensing is a shared characteristic of aged tissues, senescent cells, and cancer cells resulting in excessive accumulation of biomaterials. We have reported on regulators of biomass accumulation (Maus et al., Cell Metabolism, 2017). Currently, we investigate the biology that underlies excessive biomass accumulation in senescent cells with important implications to aging and cancer.

Mate Maus

Group Leader

Biosketch

Research Lines

Aging of the microenvironment and cancer: we investigate processes that drive cellular senescence, fibrotic tissue remodeling and inflammation in aged tissues, and in the tumor microenvironment. Our goal is to better predict the course of aging and cancer, and to provide for new therapeutic modalities.
Immunosenescence and cancer: we investigate cellular changes that accompany the aging of the immune system and ask questions related to the relevance and the therapeutic potential of immunosenescence in aging, and cancer.
Nutrient sensing in cellular senescence in aging and cancer: we investigate the processes that cause excessive nutrient uptake and storage in damaged cells and senescent cells with the aim to improve diagnostics and therapeutics for aging and cancer.

Team

Group Leader

Mate Maus

Publications

Maus M, López-Polo V, Lafarga M, Aguilera M, De Lama E, Meyer K, Manonelles A, Sola A, Lopez Martinez C, López-Alonso I, Hernandez-Gonzales F, Chaib S, Rovira M, Sanchez M, Faner R, Agusti A, Prats N, Albaiceta G, Cruzado JM, Serrano M. Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype. bioRxiv 2022 https://doi.org/10.1101/2022.07.29.501953
Maus M, Serrano M. A novel redox cycle diverts cells from oncogene-induced senescence into cancer. Mol Cell. 2021 Sep 16;81(18):3672-3674.
Kahlfuss S, Kaufmann U, Concepcion AR, Noyer L, Raphael D, Vaeth M, Yang J, Pancholi P, Maus M, Muller J, Kozhaya L, Khodadadi-Jamayran A, Sun Z, Shaw P, Unutmaz D, Stathopulos PB, Feist C, Cameron SB, Turvey SE, Feske S. STIM1-mediated calcium influx controls antifungal immunity and the metabolic function of non-pathogenic Th17 cells. EMBO Mol Med. 2020 Aug 7;12(8):e11592.
Saint Fleur-Lominy S* and Maus M*, Vaeth M, Lange I, Zee I, Suh D, Liu C, Wu X, Tikhonova A, Aifantis I, Feske S. STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia. Cell Rep. 2018 Sep 11;24(11):3045-3060.e5. (*equal contribution)
Vaeth M* and Maus M*, Klein-Hessling S, Freinkman E, Yang J, Eckstein M, Cameron S, Turvey SE, Serfling E, Berberich-Siebelt F, Possemato R, Feske S. Store-Operated Ca2+ Entry Controls Clonal Expansion of T Cells through Metabolic Reprogramming. Immunity. 2017 Oct 17;47(4):664-679.e6. (*equal contribution)
Maus M, Cuk M, Patel B, Lian J, Ouimet M, Kaufmann U, Yang J, Horvath R, Hornig-Do HT, Chrzanowska-Lightowlers ZM, Moore KJ, Cuervo AM, Feske S. Store-Operated Ca2+ Entry Controls Induction of Lipolysis and the Transcriptional Reprogramming to Lipid Metabolism. Cell Metab. 2017 Mar 7;25(3):698-712.
Vaeth M, Zee I, Concepcion AR, Maus M, Shaw P, Portal-Celhay C, Zahra A, Kozhaya L, Weidinger C, Philips J, Unutmaz D, Feske S. Ca2+ Signaling but Not Store-Operated Ca2+ Entry Is Required for the Function of Macrophages and Dendritic Cells. J Immunol. 2015 Aug 1;195(3):1202-17.
Maus M, Jairaman A, Stathopulos PB, Muik M, Fahrner M, Weidinger C, Benson M, Fuchs S, Ehl S, Romanin C, Ikura M, Prakriya M, Feske S. Missense mutation in immunodeficient patients shows the multifunctional roles of coiled-coil domain 3 (CC3) in STIM1 activation. Proc Natl Acad Sci U S A. 2015 May 12;112(19):6206-11.
Maus M, Medgyesi D, Kiss E, Schneider AE, Enyedi A, Szilágyi N, Matkó J, Sármay G. B cell receptor-induced Ca2+ mobilization mediates F-actin rearrangements and is indispensable for adhesion and spreading of B lymphocytes. J Leukoc Biol. 2013 Apr;93(4):537-47.
Maus M, Medgyesi D, Kövesdi D, Csuka D, Koncz G, Sármay G. Grb2 associated binder 2 couples B-cell receptor to cell survival. Cell Signal. 2009 Feb;21(2):220-7.
Sármay G, Angyal A, Kertész A, Maus M, Medgyesi D. The multiple function of Grb2 associated binder (Gab) adaptor/scaffolding protein in immune cell signaling. Immunol Lett. 2006 Apr 15;104(1-2):76-82.

Projects

Project Funding

This group is supported by CaixaResearch and Ayudas para contratos Ramón y Cajal (RYC) (REF: RYC2020-030652-I)