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Article ; Online: Image-guided radiotherapy in an orthotopic mouse model of rectal cancer.

Nicolas, Adele M / Pesic, Marina / Rödel, Franz / Fokas, Emmanouil / Greten, Florian R

STAR protocols

2022 Volume 3, Issue 4, Page(s) 101749

Abstract: Radiobiology research in rectal cancer has been limited to cell lines, patient-derived organoids (PDOs), or xenografts. Here, we describe a protocol which recapitulates more efficiently the complex contributions of the tumor microenvironment. This ... ...

Abstract	Radiobiology research in rectal cancer has been limited to cell lines, patient-derived organoids (PDOs), or xenografts. Here, we describe a protocol which recapitulates more efficiently the complex contributions of the tumor microenvironment. This approach establishes a preclinical mouse model of rectal cancer by intrarectal transplantation of genetically modified organoids into immunocompetent mice followed by precise image-guided radiotherapy (IGRT) of organoid-induced tumors. This model represents a useful platform to study the cellular and molecular determinants of therapy resistance in rectal cancer. For complete details on the use and execution of this protocol, please refer to Nicolas et al. (2022).
MeSH term(s)	Humans ; Mice ; Animals ; Radiotherapy, Image-Guided/methods ; Rectal Neoplasms ; Disease Models, Animal ; Heterografts ; Tumor Microenvironment
Language	English
Publishing date	2022-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101749
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Article ; Online: ACO/ARO/AIO-21 - Capecitabine-based chemoradiotherapy in combination with the IL-1 receptor antagonist anakinra for rectal cancer Patients: A phase I trial of the German rectal cancer study group.

Fleischmann, Maximilian / Diefenhardt, Markus / Nicolas, Adele M / Rödel, Franz / Ghadimi, Michael / Hofheinz, Ralf-Dieter / Greten, Florian R / Rödel, Claus / Fokas, Emmanouil

Clinical and translational radiation oncology

2022 Volume 34, Page(s) 99–106

Abstract: Purpose: Recent advances in the treatment algorithm of locally advanced rectal cancer (LARC) have significantly improved complete response (CR) rates and disease-free survival (DFS), but therapy resistance, with its substantial impact on outcomes and ... ...

Abstract	Purpose: Recent advances in the treatment algorithm of locally advanced rectal cancer (LARC) have significantly improved complete response (CR) rates and disease-free survival (DFS), but therapy resistance, with its substantial impact on outcomes and survival, remains a major challenge. Our group has recently unraveled a critical role of interleukin-1α (IL-1α) signaling in activating inflammatory cancer-associated fibroblasts (iCAFs) and mediating radiation-induced senescence, extracellular matrix (ECM) accumulation, and ultimately therapy resistance. We here summarize the recently initiated ACO/ARO/AIO-21 phase I trial, testing the IL-1 receptor antagonist (IL-1 RA) anakinra in combination with fluoropyrimidine-based chemoradiotherapy (CRT) for advanced rectal cancer. Methods/design: The ACO/ARO/AIO-21 is an investigator-driven, prospective, open-labeled phase I drug-repurposing trial assessing the maximum tolerated dose (MTD) of capecitabine administered concurrently to standard preoperative radiotherapy (45 Gy in 25 fractions followed by 9 Gy boost in 5 fractions) in combination with fixed doses of the IL1-RA anakinra (100 mg, days -10 to 30). Capecitabine will be administered using a 3 + 3 dose-escalation design (500 mg/m Discussion: Based on extensive preclinical research, the ACO/ARO/AIO-21 phase I trial will assess whether the IL-1RA anakinra can be safely combined with fluoropyrimidine-based CRT in rectal cancer. It will further explore the potential of IL-1 inhibition to overcome therapy resistance and improve response rates. A comprehensive translational research program will expand our understanding from a clinical perspective and may help translate the results into a randomized phase II trial.
Language	English
Publishing date	2022-04-06
Publishing country	Ireland
Document type	Journal Article
ISSN	2405-6308
ISSN (online)	2405-6308
DOI	10.1016/j.ctro.2022.04.003
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Article ; Online: Combining ferroptosis induction with MDSC blockade renders primary tumours and metastases in liver sensitive to immune checkpoint blockade.

Conche, Claire / Finkelmeier, Fabian / Pešić, Marina / Nicolas, Adele M / Böttger, Tim W / Kennel, Kilian B / Denk, Dominic / Ceteci, Fatih / Mohs, Kathleen / Engel, Esther / Canli, Özge / Dabiri, Yasamin / Peiffer, Kai-Henrik / Zeuzem, Stefan / Salinas, Gabriela / Longerich, Thomas / Yang, Huan / Greten, Florian R

Gut

2023 Volume 72, Issue 9, Page(s) 1774–1782

Abstract: Objective: Investigating the effect of ferroptosis in the tumour microenvironment to identify combinatory therapy for liver cancer treatment.: Design: Glutathione peroxidase 4 (GPx4), which is considered the master regulator of ferroptosis, was ... ...

Abstract	Objective: Investigating the effect of ferroptosis in the tumour microenvironment to identify combinatory therapy for liver cancer treatment. Design: Glutathione peroxidase 4 (GPx4), which is considered the master regulator of ferroptosis, was genetically altered in murine models for hepatocellular carcinoma (HCC) and colorectal cancer (CRC) to analyse the effect of ferroptosis on tumour cells and the immune tumour microenvironment. The findings served as foundation for the identification of additional targets for combine therapy with ferroptotic inducer in the treatment of HCC and liver metastasis. Results: Surprisingly, hepatocyte-restricted GPx4 loss does not suppress hepatocellular tumourigenesis. Instead, GPx4-associated ferroptotic hepatocyte death causes a tumour suppressive immune response characterised by a CXCL10-dependent infiltration of cytotoxic CD8 Conclusion: Our data highlight a context-specific ferroptosis-induced immune response that could be therapeutically exploited for the treatment of primary liver tumours and liver metastases.
MeSH term(s)	Mice ; Animals ; Carcinoma, Hepatocellular/pathology ; Liver Neoplasms/pathology ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Myeloid-Derived Suppressor Cells ; HMGB1 Protein/therapeutic use ; CD8-Positive T-Lymphocytes ; Ferroptosis ; Programmed Cell Death 1 Receptor ; Tumor Microenvironment
Chemical Substances	Immune Checkpoint Inhibitors ; HMGB1 Protein ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2023-01-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2022-327909
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Article ; Online: A Wnt-Induced Phenotypic Switch in Cancer-Associated Fibroblasts Inhibits EMT in Colorectal Cancer.

Mosa, Mohammed H / Michels, Birgitta E / Menche, Constantin / Nicolas, Adele M / Darvishi, Tahmineh / Greten, Florian R / Farin, Henner F

Cancer research

2020 Volume 80, Issue 24, Page(s) 5569–5582

Abstract: Tumor progression is recognized as a result of an evolving cross-talk between tumor cells and their surrounding nontransformed stroma. Although Wnt signaling has been intensively studied in colorectal cancer, it remains unclear whether activity in the ... ...

Abstract	Tumor progression is recognized as a result of an evolving cross-talk between tumor cells and their surrounding nontransformed stroma. Although Wnt signaling has been intensively studied in colorectal cancer, it remains unclear whether activity in the tumor-associated stroma contributes to malignancy. To specifically interfere with stromal signals, we generated Wnt-independent tumor organoids that secrete the Wnt antagonist Sfrp1. Subcutaneous transplantation into immunocompetent as well as immunodeficient mice resulted in a strong reduction of tumor growth. Histologic and transcriptomic analyses revealed that Sfrp1 induced an epithelial-mesenchymal transition (EMT) phenotype in tumor cells without affecting tumor-intrinsic Wnt signaling, suggesting involvement of nonimmune stromal cells. Blockage of canonical signaling using Sfrp1, Dkk1, or fibroblast-specific genetic ablation of β-catenin strongly decreased the number of cancer-associated myofibroblasts (myCAF). Wnt activity in CAFs was linked with distinct subtypes, where low and high levels induced an inflammatory-like CAF (iCAF) subtype or contractile myCAFs, respectively. Coculture of tumor organoids with iCAFs resulted in significant upregulation of EMT markers, while myCAFs reverted this phenotype. In summary, we show that tumor growth and malignancy are differentially regulated via distinct fibroblast subtypes under the influence of juxtacrine Wnt signals. SIGNIFICANCE: This study provides evidence for Wnt-induced functional diversity of colorectal cancer-associated fibroblasts, representing a non-cell autonomous mechanism for colon cancer progression. GRAPHICAL ABSTRACT: http://cancerres.aacrjournals.org/content/canres/80/24/5569/F1.large.jpg.
MeSH term(s)	Animals ; Cancer-Associated Fibroblasts/metabolism ; Cell Survival/genetics ; Coculture Techniques ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Culture Media, Conditioned ; Disease Progression ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Organoids/metabolism ; Organoids/transplantation ; Phenotype ; Transduction, Genetic ; Wnt Signaling Pathway/genetics ; Wnt3 Protein/genetics ; Wnt3 Protein/metabolism
Chemical Substances	Culture Media, Conditioned ; Membrane Proteins ; Sfrp1 protein, mouse ; Wnt3 Protein ; Wnt3 protein, mouse
Language	English
Publishing date	2020-10-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-0263
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Article ; Online: Expansion of T memory stem cells with superior anti-tumor immunity by Urolithin A-induced mitophagy.

Denk, Dominic / Petrocelli, Valentina / Conche, Claire / Drachsler, Moritz / Ziegler, Paul K / Braun, Angela / Kress, Alena / Nicolas, Adele M / Mohs, Kathleen / Becker, Christoph / Neurath, Markus F / Farin, Henner F / Buchholz, Christian J / Andreux, Pénélope A / Rinsch, Chris / Greten, Florian R

Immunity

2022 Volume 55, Issue 11, Page(s) 2059–2073.e8

Abstract: T memory stem cells ( ... ...

Abstract	T memory stem cells (T
MeSH term(s)	Mice ; Animals ; Mitophagy ; Coumarins/pharmacology ; Wnt Signaling Pathway ; Stem Cells ; Immunologic Memory
Chemical Substances	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one (1143-70-0) ; Coumarins
Language	English
Publishing date	2022-10-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2022.09.014
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Inflammatory fibroblasts mediate resistance to neoadjuvant therapy in rectal cancer.

Nicolas, Adele M / Pesic, Marina / Engel, Esther / Ziegler, Paul K / Diefenhardt, Markus / Kennel, Kilian B / Buettner, Florian / Conche, Claire / Petrocelli, Valentina / Elwakeel, Eiman / Weigert, Andreas / Zinoveva, Anna / Fleischmann, Maximilian / Häupl, Björn / Karakütük, Cem / Bohnenberger, Hanibal / Mosa, Mohammed H / Kaderali, Lars / Gaedcke, Jochen /

Ghadimi, Michael / Rödel, Franz / Arkan, Melek C / Oellerich, Thomas / Rödel, Claus / Fokas, Emmanouil / Greten, Florian R

Cancer cell

2022 Volume 40, Issue 2, Page(s) 168–184.e13

Abstract: Standard cancer therapy targets tumor cells without considering possible damage on the tumor microenvironment that could impair therapy response. In rectal cancer patients we find that inflammatory cancer-associated fibroblasts (iCAFs) are associated ... ...

Abstract	Standard cancer therapy targets tumor cells without considering possible damage on the tumor microenvironment that could impair therapy response. In rectal cancer patients we find that inflammatory cancer-associated fibroblasts (iCAFs) are associated with poor chemoradiotherapy response. Employing a murine rectal cancer model or patient-derived tumor organoids and primary stroma cells, we show that, upon irradiation, interleukin-1α (IL-1α) not only polarizes cancer-associated fibroblasts toward the inflammatory phenotype but also triggers oxidative DNA damage, thereby predisposing iCAFs to p53-mediated therapy-induced senescence, which in turn results in chemoradiotherapy resistance and disease progression. Consistently, IL-1 inhibition, prevention of iCAFs senescence, or senolytic therapy sensitizes mice to irradiation, while lower IL-1 receptor antagonist serum levels in rectal patients correlate with poor prognosis. Collectively, we unravel a critical role for iCAFs in rectal cancer therapy resistance and identify IL-1 signaling as an attractive target for stroma-repolarization and prevention of cancer-associated fibroblasts senescence.
MeSH term(s)	Animals ; Biomarkers ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Cell Line, Tumor ; Cellular Senescence/drug effects ; Cellular Senescence/genetics ; Cytokines/genetics ; Cytokines/metabolism ; DNA Damage ; Disease Models, Animal ; Disease Susceptibility ; Drug Resistance, Neoplasm ; Gene Expression Profiling ; Heterografts ; High-Throughput Nucleotide Sequencing ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Mice ; Neoadjuvant Therapy ; Prognosis ; Rectal Neoplasms/drug therapy ; Rectal Neoplasms/etiology ; Rectal Neoplasms/metabolism ; Rectal Neoplasms/pathology ; Signal Transduction ; Tumor Microenvironment/genetics
Chemical Substances	Biomarkers ; Cytokines
Language	English
Publishing date	2022-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2022.01.004
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Disruption of Prostaglandin E2 Signaling in Cancer-Associated Fibroblasts Limits Mammary Carcinoma Growth but Promotes Metastasis.

Cancer research

2022 Volume 82, Issue 7, Page(s) 1380–1395

Abstract: The activation and differentiation of cancer-associated fibroblasts (CAF) are involved in tumor progression. Here, we show that the tumor-promoting lipid mediator prostaglandin E2 (PGE2) plays a paradoxical role in CAF activation and tumor progression. ... ...

Abstract	The activation and differentiation of cancer-associated fibroblasts (CAF) are involved in tumor progression. Here, we show that the tumor-promoting lipid mediator prostaglandin E2 (PGE2) plays a paradoxical role in CAF activation and tumor progression. Restricting PGE2 signaling via knockout of microsomal prostaglandin E synthase-1 (mPGES-1) in PyMT mice or of the prostanoid E receptor 3 (EP3) in CAFs stunted mammary carcinoma growth associated with strong CAF proliferation. CAF proliferation upon EP3 inhibition required p38 MAPK signaling. Mechanistically, TGFβ-activated kinase-like protein (TAK1L), which was identified as a negative regulator of p38 MAPK activation, was decreased following ablation of mPGES-1 or EP3. In contrast with its effects on primary tumor growth, disruption of PGE2 signaling in CAFs induced epithelial-to-mesenchymal transition in cancer organoids and promoted metastasis in mice. Moreover, TAK1L expression in CAFs was associated with decreased CAF activation, reduced metastasis, and prolonged survival in human breast cancer. These data characterize a new pathway of regulating inflammatory CAF activation, which affects breast cancer progression. Significance: The inflammatory lipid prostaglandin E2 suppresses cancer-associated fibroblast expansion and activation to limit primary mammary tumor growth while promoting metastasis.
MeSH term(s)	Animals ; Breast Neoplasms/pathology ; Cancer-Associated Fibroblasts/metabolism ; Carcinoma/pathology ; Dinoprostone/metabolism ; Female ; Fibroblasts/metabolism ; Humans ; Mice ; Prostaglandin-E Synthases/genetics ; Prostaglandin-E Synthases/metabolism ; Prostaglandin-E Synthases/pharmacology
Chemical Substances	Prostaglandin-E Synthases (EC 5.3.99.3) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-21-2116
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Article ; Online: Colon tumour cell death causes mTOR dependence by paracrine P2X4 stimulation.

Nature

2022 Volume 612, Issue 7939, Page(s) 347–353

Abstract: Solid cancers exhibit a dynamic balance between cell death and proliferation ensuring continuous tumour maintenance and ... ...

Abstract	Solid cancers exhibit a dynamic balance between cell death and proliferation ensuring continuous tumour maintenance and growth
MeSH term(s)	Humans ; Reactive Oxygen Species ; Cause of Death ; Organoids ; Cell Death ; Colonic Neoplasms ; Tumor Microenvironment ; TOR Serine-Threonine Kinases
Chemical Substances	Reactive Oxygen Species ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-11-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-05426-1
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Article ; Online: Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis.

Canli, Özge / Nicolas, Adele M / Gupta, Jalaj / Finkelmeier, Fabian / Goncharova, Olga / Pesic, Marina / Neumann, Tobias / Horst, David / Löwer, Martin / Sahin, Ugur / Greten, Florian R

Cancer cell

2017 Volume 32, Issue 6, Page(s) 869–883.e5

Abstract: Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment ... ...

Abstract	Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H
MeSH term(s)	Animals ; Apoptosis/drug effects ; DNA Damage/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Hydrogen Peroxide/pharmacology ; Mice ; Mice, Mutant Strains ; Mutagenesis/physiology ; Mutation ; Myeloid Cells/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects
Chemical Substances	Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2017-12-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2017.11.004
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