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Article ; Online: Targeting CAFs to Improve Anti-PD-1 Checkpoint Immunotherapy.

Tauriello, Daniele V F

2023 Volume 83, Issue 5, Page(s) 655–656

Abstract: The tumor microenvironment is a complex ecosystem that drives cancer progression and restrains immunity. Although immune checkpoint inhibitors have shown strong potential in a subset of patients, a better understanding of suppressive mechanisms may ... ...

Abstract	The tumor microenvironment is a complex ecosystem that drives cancer progression and restrains immunity. Although immune checkpoint inhibitors have shown strong potential in a subset of patients, a better understanding of suppressive mechanisms may inspire ways to improve immunotherapeutic efficacy. A new study in this issue of Cancer Research focuses on targeting cancer-associated fibroblasts in preclinical models of gastric tumors. Aiming to rebalance anticancer immunity and enhance treatment responses to checkpoint-blocking antibodies, this work also addresses the potential for multitarget tyrosine kinase inhibitors in treating gastrointestinal cancer. See related article by Akiyama et al., p. 753.
MeSH term(s)	Humans ; Receptor, Platelet-Derived Growth Factor alpha ; Ecosystem ; Immunotherapy ; Stomach Neoplasms ; Antibodies, Blocking ; Receptor Protein-Tyrosine Kinases ; Tumor Microenvironment
Chemical Substances	Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1) ; Antibodies, Blocking ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-3677
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Article ; Online: From poor prognosis to promising treatment.

Tauriello, Daniele V F

Science (New York, N.Y.)

2019 Volume 363, Issue 6431, Page(s) 1051

MeSH term(s)	Animals ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/therapy ; Disease Models, Animal ; Immunotherapy ; Neoplasm Metastasis ; Neoplasms, Experimental ; Organoids/transplantation ; Prognosis ; Transforming Growth Factor beta/antagonists & inhibitors
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2019-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aaw3609
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 77: Show issues

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Article ; Online: Overcoming TGFβ-mediated immune evasion in cancer.

Tauriello, Daniele V F / Sancho, Elena / Batlle, Eduard

Nature reviews. Cancer

2021 Volume 22, Issue 1, Page(s) 25–44

Abstract: Transforming growth factor-β (TGFβ) signalling controls multiple cell fate decisions during development and tissue homeostasis; hence, dysregulation of this pathway can drive several diseases, including cancer. Here we discuss the influence that TGFβ ... ...

Abstract	Transforming growth factor-β (TGFβ) signalling controls multiple cell fate decisions during development and tissue homeostasis; hence, dysregulation of this pathway can drive several diseases, including cancer. Here we discuss the influence that TGFβ exerts on the composition and behaviour of different cell populations present in the tumour immune microenvironment, and the context-dependent functions of this cytokine in suppressing or promoting cancer. During homeostasis, TGFβ controls inflammatory responses triggered by exposure to the outside milieu in barrier tissues. Lack of TGFβ exacerbates inflammation, leading to tissue damage and cellular transformation. In contrast, as tumours progress, they leverage TGFβ to drive an unrestrained wound-healing programme in cancer-associated fibroblasts, as well as to suppress the adaptive immune system and the innate immune system. In consonance with this key role in reprogramming the tumour microenvironment, emerging data demonstrate that TGFβ-inhibitory therapies can restore cancer immunity. Indeed, this approach can synergize with other immunotherapies - including immune checkpoint blockade - to unleash robust antitumour immune responses in preclinical cancer models. Despite initial challenges in clinical translation, these findings have sparked the development of multiple therapeutic strategies that inhibit the TGFβ pathway, many of which are currently in clinical evaluation.
MeSH term(s)	Humans ; Immune Evasion ; Immunotherapy ; Neoplasms/pathology ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/therapeutic use ; Tumor Microenvironment
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2021-10-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-021-00413-6
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Zs.A 5563: 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: Mutant RAS and the tumor microenvironment as dual therapeutic targets for advanced colorectal cancer.

Janssen, Jorien B E / Medema, Jan Paul / Gootjes, Elske C / Tauriello, Daniele V F / Verheul, Henk M W

Cancer treatment reviews

2022 Volume 109, Page(s) 102433

Abstract: RAS genes are the most frequently mutated oncogenes in cancer. These mutations occur in roughly half of the patients with colorectal cancer (CRC). RAS mutant tumors are resistant to therapy with anti-EGFR monoclonal antibodies. Therefore, patients with ... ...

Abstract	RAS genes are the most frequently mutated oncogenes in cancer. These mutations occur in roughly half of the patients with colorectal cancer (CRC). RAS mutant tumors are resistant to therapy with anti-EGFR monoclonal antibodies. Therefore, patients with RAS mutant CRC currently have few effective therapy options. RAS mutations lead to constitutively active RAS GTPases, involved in multiple downstream signaling pathways. These alterations are associated with a tumor microenvironment (TME) that drives immune evasion and disease progression by mechanisms that remain incompletely understood. In this review, we focus on the available evidence in the literature explaining the potential effects of RAS mutations on the CRC microenvironment. Ongoing efforts to influence the TME by targeting mutant RAS and thereby sensitizing these tumors to immunotherapy will be discussed as well.
MeSH term(s)	Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; ErbB Receptors/genetics ; Genes, ras ; Humans ; Mutation ; Tumor Microenvironment/genetics
Chemical Substances	Antibodies, Monoclonal ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2022-06-30
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	125102-8
ISSN	1532-1967 ; 0305-7372
ISSN (online)	1532-1967
ISSN	0305-7372
DOI	10.1016/j.ctrv.2022.102433
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Zs.A 1022: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 611: Show issues

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Article ; Online: Lost in translation: Revisiting the use of tyrosine kinase inhibitors in colorectal cancer.

Iyer, Kirti K / van Erp, Nielka P / Tauriello, Daniele V F / Verheul, Henk M W / Poel, Dennis

Cancer treatment reviews

2022 Volume 110, Page(s) 102466

Abstract: Patients with advanced or metastatic colorectal cancer ((m)CRC) have limited effective treatment options resulting in high mortality rates. A better understanding of the molecular basis of this disease has led to growing interest in small molecule ... ...

Abstract	Patients with advanced or metastatic colorectal cancer ((m)CRC) have limited effective treatment options resulting in high mortality rates. A better understanding of the molecular basis of this disease has led to growing interest in small molecule tyrosine kinase inhibitors (TKIs) for its treatment. However, of around 42 TKIs demonstrating preclinical anti-tumour activity, and despite numerous clinical trials, only 1 has been approved for clinical use in mCRC. Clearly, there is a huge gap in the translation of these targeted therapies to the clinic. This underlines the limitations of preclinical models to predict clinical drug efficacy and to fully characterize the mechanism of action. Moreover, several relevant topics remain poorly resolved. Do we know the actual intracellular concentrations that are required for anticancer efficacy, and what range of intra-tumoral drug concentrations is reached in clinical setting? Are the intended targeted kinases responsible for the anti-cancer activity or are other unexpected cellular targets involved? Do we have any idea of the effect of these drugs on the tumour microenvironment and does this help explain therapy success, failure or heterogeneity? In this review, we address these questions and discuss concepts that jointly complicate the clinical translation of TKIs for CRC. Finally, we will argue that an integrated approach with more sophisticated preclinical models and techniques may improve the prediction of clinical treatment efficacy.
MeSH term(s)	Colorectal Neoplasms/drug therapy ; Humans ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Tumor Microenvironment
Chemical Substances	Protein Kinase Inhibitors
Language	English
Publishing date	2022-09-21
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	125102-8
ISSN	1532-1967 ; 0305-7372
ISSN (online)	1532-1967
ISSN	0305-7372
DOI	10.1016/j.ctrv.2022.102466
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Zs.A 1022: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 611: Show issues

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Article ; Online: Targeting the Microenvironment in Advanced Colorectal Cancer.

Tauriello, Daniele V F / Batlle, Eduard

Trends in cancer

2016 Volume 2, Issue 9, Page(s) 495–504

Abstract: Colorectal cancer (CRC) diagnosis often occurs at late stages when tumor cells have already disseminated. Current therapies are poorly effective for metastatic disease, the main cause of death in CRC. Despite mounting evidence implicating the tumor ... ...

Abstract	Colorectal cancer (CRC) diagnosis often occurs at late stages when tumor cells have already disseminated. Current therapies are poorly effective for metastatic disease, the main cause of death in CRC. Despite mounting evidence implicating the tumor microenvironment in CRC progression and metastasis, clinical practice remains predominantly focused on targeting the epithelial compartment. Because CRCs remain largely refractory to current therapies, we must devise alternative strategies. Transforming growth factor (TGF)-β has emerged as a key architect of the microenvironment in poor-prognosis cancers. Disseminated tumor cells show a strong dependency on a TGF-β-activated stroma during the establishment and subsequent expansion of metastasis. We review and discuss the development of integrated approaches focused on targeting the ecosystem of poor-prognosis CRCs.
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2016.08.001
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Article ; Online: The Therapeutic Potential of Tackling Tumor-Induced Dendritic Cell Dysfunction in Colorectal Cancer.

Subtil, Beatriz / Cambi, Alessandra / Tauriello, Daniele V F / de Vries, I Jolanda M

Frontiers in immunology

2021 Volume 12, Page(s) 724883

Abstract: Colorectal cancer (CRC) is the third most diagnosed malignancy and the second leading cause of cancer-related deaths worldwide. Locally advanced and metastatic disease exhibit resistance to therapy and are prone to recurrence. Despite significant ... ...

Abstract	Colorectal cancer (CRC) is the third most diagnosed malignancy and the second leading cause of cancer-related deaths worldwide. Locally advanced and metastatic disease exhibit resistance to therapy and are prone to recurrence. Despite significant advances in standard of care and targeted (immuno)therapies, the treatment effects in metastatic CRC patients have been modest. Untreatable cancer metastasis accounts for poor prognosis and most CRC deaths. The generation of a strong immunosuppressive tumor microenvironment (TME) by CRC constitutes a major hurdle for tumor clearance by the immune system. Dendritic cells (DCs), often impaired in the TME, play a critical role in the initiation and amplification of anti-tumor immune responses. Evidence suggests that tumor-mediated DC dysfunction is decisive for tumor growth and metastasis initiation, as well as for the success of immunotherapies. Unravelling and understanding the complex crosstalk between CRC and DCs holds promise for identifying key mechanisms involved in tumor progression and spread that can be exploited for therapy. The main goal of this review is to provide an overview of the current knowledge on the impact of CRC-driven immunosuppression on DCs phenotype and functionality, and its significance for disease progression, patient prognosis, and treatment response. Moreover, present knowledge gaps will be highlighted as promising opportunities to further understand and therapeutically target DC dysfunction in CRC. Given the complexity and heterogeneity of CRC, future research will benefit from the use of patient-derived material and the development of
MeSH term(s)	Animals ; Cells, Cultured ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Humans ; Immunotherapy/methods ; Organ Culture Techniques ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology
Language	English
Publishing date	2021-10-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.724883
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Article ; Online: Multiomics of Colorectal Cancer Organoids Reveals Putative Mediators of Cancer Progression Resulting from SMAD4 Inactivation.

Dijkstra, Jelmer J / Neikes, Hannah K / Rezaeifard, Somayeh / Ma, Xuhui / Voest, Emile E / Tauriello, Daniele V F / Vermeulen, Michiel

Journal of proteome research

2022 Volume 22, Issue 1, Page(s) 138–151

Abstract: The development of metastasis severely reduces the life expectancy of patients with colorectal cancer (CRC). Although loss of SMAD4 is a key event in CRC progression, the resulting changes in biological processes in advanced disease and metastasis are ... ...

Abstract	The development of metastasis severely reduces the life expectancy of patients with colorectal cancer (CRC). Although loss of SMAD4 is a key event in CRC progression, the resulting changes in biological processes in advanced disease and metastasis are not fully understood. Here, we applied a multiomics approach to a CRC organoid model that faithfully reflects the metastasis-supporting effects of SMAD4 inactivation. We show that loss of SMAD4 results in decreased differentiation and activation of pro-migratory and cell proliferation processes, which is accompanied by the disruption of several key oncogenic pathways, including the TGFβ, WNT, and VEGF pathways. In addition, SMAD4 inactivation leads to increased secretion of proteins that are known to be involved in a variety of pro-metastatic processes. Finally, we show that one of the factors that is specifically secreted by
MeSH term(s)	Humans ; Multiomics ; Cell Line, Tumor ; Colorectal Neoplasms/pathology ; Transforming Growth Factor beta/metabolism ; Cell Proliferation/genetics ; Smad4 Protein/genetics
Chemical Substances	Transforming Growth Factor beta ; Smad4 Protein ; SMAD4 protein, human
Language	English
Publishing date	2022-11-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/acs.jproteome.2c00551
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Article ; Online: cDC2 plasticity and acquisition of a DC3-like phenotype mediated by IL-6 and PGE2 in a patient-derived colorectal cancer organoids model.

Subtil, Beatriz / van der Hoorn, Iris A E / Cuenca-Escalona, Jorge / Becker, Anouk M D / Alvarez-Begue, Mar / Iyer, Kirti K / Janssen, Jorien / van Oorschot, Tom / Poel, Dennis / Gorris, Mark A J / van den Dries, Koen / Cambi, Alessandra / Tauriello, Daniele V F / de Vries, I Jolanda M

European journal of immunology

2024 , Page(s) e2350891

Abstract: Metastatic colorectal cancer (CRC) is highly resistant to therapy and prone to recur. The tumor-induced local and systemic immunosuppression allows cancer cells to evade immunosurveillance, facilitating their proliferation and dissemination. Dendritic ... ...

Abstract	Metastatic colorectal cancer (CRC) is highly resistant to therapy and prone to recur. The tumor-induced local and systemic immunosuppression allows cancer cells to evade immunosurveillance, facilitating their proliferation and dissemination. Dendritic cells (DCs) are required for the detection, processing, and presentation of tumor antigens, and subsequently for the activation of antigen-specific T cells to orchestrate an effective antitumor response. Notably, successful tumors have evolved mechanisms to disrupt and impair DC functions, underlining the key role of tumor-induced DC dysfunction in promoting tumor growth, metastasis initiation, and treatment resistance. Conventional DC type 2 (cDC2) are highly prevalent in tumors and have been shown to present high phenotypic and functional plasticity in response to tumor-released environmental cues. This plasticity reverberates on both the development of antitumor responses and on the efficacy of immunotherapies in cancer patients. Uncovering the processes, mechanisms, and mediators by which CRC shapes and disrupts cDC2 functions is crucial to restoring their full antitumor potential. In this study, we use our recently developed 3D DC-tumor co-culture system to investigate how patient-derived primary and metastatic CRC organoids modulate cDC2 phenotype and function. We first demonstrate that our collagen-based system displays extensive interaction between cDC2 and tumor organoids. Interestingly, we show that tumor-corrupted cDC2 shift toward a CD14+ population with defective expression of maturation markers, an intermediate phenotype positioned between cDC2 and monocytes, and impaired T-cell activating abilities. This phenotype aligns with the newly defined DC3 (CD14
Language	English
Publishing date	2024-03-21
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202350891
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 85: Show issues

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Article ; Online: Dendritic cell phenotype and function in a 3D co-culture model of patient-derived metastatic colorectal cancer organoids.

Subtil, Beatriz / Iyer, Kirti K / Poel, Dennis / Bakkerus, Lotte / Gorris, Mark A J / Escalona, Jorge Cuenca / van den Dries, Koen / Cambi, Alessandra / Verheul, Henk M W / de Vries, I Jolanda M / Tauriello, Daniele V F

Frontiers in immunology

2023 Volume 14, Page(s) 1105244

Abstract: Colorectal cancer (CRC) remains one of the most aggressive and lethal cancers, with metastasis accounting for most deaths. As such, there is an unmet need for improved therapies for metastatic CRC (mCRC). Currently, the research focus is shifting towards ...

Abstract	Colorectal cancer (CRC) remains one of the most aggressive and lethal cancers, with metastasis accounting for most deaths. As such, there is an unmet need for improved therapies for metastatic CRC (mCRC). Currently, the research focus is shifting towards the reciprocal interactions within the tumor microenvironment (TME), which prevent tumor clearance by the immune system. Dendritic cells (DCs) play a key role in the initiation and amplification of anti-tumor immune responses and in driving the clinical success of immunotherapies. Dissecting the interactions between DCs and CRC cells may open doors to identifying key mediators in tumor progression, and possible therapeutic targets. This requires representative, robust and versatile models and tools. Currently, there is a shortage of such
MeSH term(s)	Humans ; Coculture Techniques ; Colonic Neoplasms/pathology ; Rectal Neoplasms/pathology ; Dendritic Cells ; Organoids ; Phenotype ; Tumor Microenvironment
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1105244
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