The Diverse Applications of Pancreatic Ductal Adenocarcinoma Organoids

2021 Sunrise member publications

The Diverse Applications of Pancreatic Ductal Adenocarcinoma Organoids

Ronnie Ren Jie Low, Wei Wen Lim , Paul M. Nguyen , Belinda Lee , Michael Christie, Antony W. Burgess ,Peter Gibbs ,Sean M. Grimmond ,Frédéric Hollande andTracy L. Putoczki

Cancers 2021, 13(19), 4979

Simple Summary

Patients diagnosed with pancreatic cancer have very few treatment options. In order to identify new treatment opportunities, and develop new drugs for clinical use, appropriate model systems that take into account the complexities of a tumor are required. In this review, we summarize the current and emerging opportunities to accurately model pancreatic cancer using organoid technologies. We highlight the need for continued development of these complex model systems in order to inform personalized treatment.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies. While immortalized cancer cell lines and genetically engineered murine models have increased our understanding of PDAC tumorigenesis, they do not recapitulate inter- and intra-patient heterogeneity. PDAC patient derived organoid (PDO) biobanks have overcome this hurdle, and provide an opportunity for the high throughput screening of potential new therapies. This review provides a summary of the PDAC PDO biobanks established to date, and discusses how they have advanced our understanding of PDAC biology. Looking forward, the development of coculturing techniques for specific immune or stromal cell populations will enable a better understanding of the crosstalk that occurs within the tumor microenvironment, and the impact of this crosstalk on treatment response.

22/11/2021

Integrative Analysis to Identify Genes Associated with Stemness and Immune Infiltration in Glioblastoma

2021 Sunrise member publications

Neerada Meenakshi Warrier,Prasoon Agarwal and Praveen Kumar

Abstract

It is imperative to identify the mechanisms that confer stemness to the cancer cells for more effective targeting. Moreover, there are not many studies on the link between stemness characteristics and the immune response in tumours. Therefore, in the current study involving GBM, we started with the study of BIRC5 (one of the rare genes differentially expressed in normal and cancer cells) and CXCR4 (gene involved in the survival and proliferation of CSCs). Together, these genes have not been systematically explored. We used a set of 27 promoter methylated regions in GBM. Our analysis showed that four genes corresponding to these regions, namely EOMES, BDNF, HLA-A, and PECAM1, were involved with BIRC5 and CXCR4. Interestingly, we found EOMES to be very significantly involved in stemness and immunology and it was positively correlated to CXCR4. Additionally, BDNF, which was significant in methylation, was negatively correlated to BIRC5

22/11/2021

CD44v6 Defines a New Population of Circulating Tumor Cells Not Expressing EpCAM

2021 Sunrise member publications

Simple Summary

In the present work, we describe (for the first time) the use of the transmembrane protein, CD44v6, to detect CTCs from blood samples of several patients with colorectal or breast cancer. We used CD44v6 antibodies to demonstrate that live CTCs can be specifically purified from CRC patient blood samples via magnetic bead- or FACS-based isolation techniques. Finally, we demonstrated that CD44v6-positive CTCs rarely expressed EpCam, which is currently the gold standard to enumerate CTCs, suggesting the need to use a combination of markers for a more comprehensive view of CTC heterogeneity.

Abstract

Circulating tumor cells (CTCs) are promising diagnostic and prognostic tools for clinical use. In several cancers, including colorectal and breast, the CTC load has been associated with a therapeutic response as well as progression-free and overall survival. However, counting and isolating CTCs remains sub-optimal because they are currently largely identified by epithelial markers such as EpCAM. New, complementary CTC surface markers are therefore urgently needed. We previously demonstrated that a splice variant of CD44, CD44 variable alternative exon 6 (CD44v6), is highly and specifically expressed by CTC cell lines derived from blood samples in colorectal cancer (CRC) patients. Two different approaches—immune detection coupled with magnetic beads and fluorescence-activated cell sorting—were optimized to purify CTCs from patient blood samples based on high expressions of CD44v6. We revealed the potential of the CD44v6 as a complementary marker to EpCAM to detect and purify CTCs in colorectal cancer blood samples. Furthermore, this marker is not restricted to colorectal cancer since CD44v6 is also expressed on CTCs from breast cancer patients. Overall, these results strongly suggest that CD44v6 could be useful to enumerate and purify CTCs from cancers of different origins, paving the way to more efficacious combined markers that encompass CTC heterogeneity.

22/11/2021

Dependence receptors: new targets for cancer therapy

15/10/2021

GNS561, a New Autophagy Inhibitor Active against Cancer Stem Cells in Hepatocellular Carcinoma and Hepatic Metastasis from Colorectal Cancer

2021 Sunrise member publications

15/10/2021

The Diverse Applications of Pancreatic Ductal Adenocarcinoma Organoids

2011 Sunrise member publications

The Diverse Applications of Pancreatic Ductal Adenocarcinoma Organoids

Ronnie Ren Jie Low 1,2,3,Wei Wen Lim 3,Paul M. Nguyen 3,Belinda Lee 1,2,Michael Christie 1,2,Antony W. Burgess 1,2,Peter Gibbs 1,2,4,Sean M. Grimmond 3,5,Frédéric Hollande 3,5 andT racy L. Putoczki 1,2

1 The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia
2 Department of Medical Biology, The University of Melbourne, Melbourne, VIC 3052, Australia
3 Victorian Comprehensive Cancer Centre, University of Melbourne Centre for Cancer Research, Melbourne, VIC 3000, Australia
4 Department of Medical Oncology, Western Health, Melbourne, VIC 3052, Australia
5 Department of Clinical Pathology, University of Melbourne, Melbourne, VIC 3000, Australia

Simple Summary

Patients diagnosed with pancreatic cancer have very few treatment options. In order to identify new treatment opportunities, and develop new drugs for clinical use, appropriate model systems that take into account the complexities of a tumor are required. In this review, we summarize the current and emerging opportunities to accurately model pancreatic cancer using organoid technologies. We highlight the need for continued development of these complex model systems in order to inform personalized treatment.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies. While immortalized cancer cell lines and genetically engineered murine models have increased our understanding of PDAC tumorigenesis, they do not recapitulate inter- and intra-patient heterogeneity. PDAC patient derived organoid (PDO) biobanks have overcome this hurdle, and provide an opportunity for the high throughput screening of potential new therapies. This review provides a summary of the PDAC PDO biobanks established to date, and discusses how they have advanced our understanding of PDAC biology. Looking forward, the development of coculturing techniques for specific immune or stromal cell populations will enable a better understanding of the crosstalk that occurs within the tumor microenvironment, and the impact of this crosstalk on treatment response.

15/10/2021

A stem cell population at the anorectal junction maintains homeostasis and participates in tissue regeneration

2021 Sunrise member publications

doi: 10.1038/s41467-021-23034-x.

A stem cell population at the anorectal junction maintains homeostasis and participates in tissue regeneration

Affiliations

Abstract

At numerous locations of the body, transition zones are localized at the crossroad between two types of epithelium and are frequently associated with neoplasia involving both type of tissues. These transition zones contain cells expressing markers of adult stem cells that can be the target of early transformation. The mere fact that transition zone cells can merge different architecture with separate functions implies for a unique plasticity that these cells must display in steady state. However, their roles during tissue regeneration in normal and injured state remain unknown. Here, by using in vivo lineage tracing, single-cell transcriptomics, computational modeling and a three-dimensional organoid culture system of transition zone cells, we identify a population of Krt17+ basal cells with multipotent properties at the squamo-columnar anorectal junction that maintain a squamous epithelium during normal homeostasis and can participate in the repair of a glandular epithelium following tissue injury.

15/10/2021

USP22 promotes HER2-driven mammary carcinoma aggressiveness by suppressing the unfolded protein response

Prokakis E, Dyas A, Grün R, Fritzsche S, U Bedi, Kazerouni ZB, Kosinsky RL, Johnsen SA, Wegwitz F

Oncogene 2021 May 18.

The Ubiquitin-Specific Protease 22 (USP22) is a deubiquitinating subunit of the mammalian SAGA transcriptional co-activating complex. USP22 was identified as a member of the so-called “death-from-cancer” signature predicting therapy failure in cancer patients. However, the importance and functional role of USP22 in different types and subtypes of cancer remain largely unknown. In the present study, we leveraged human cell lines and genetic mouse models to investigate the role of USP22 in HER2-driven breast cancer (HER2⁺-BC) and demonstrate for the first time that USP22 is required for the tumorigenic properties in murine and human HER2⁺-BC models. To get insight into the underlying mechanisms, we performed transcriptome-wide gene expression analyses and identified the Unfolded Protein Response (UPR) as a pathway deregulated upon USP22 loss. The UPR is normally induced upon extrinsic or intrinsic stresses that can promote cell survival and recovery if shortly activated or programmed cell death if activated for an extended period. Strikingly, we found that USP22 actively suppresses UPR induction in HER2⁺-BC cells by stabilizing the major endoplasmic reticulum (ER) chaperone HSPA5. Consistently, loss of USP22 renders tumor cells more sensitive to apoptosis and significantly increases the efficiency of therapies targeting the ER folding capacity. Together, our data suggest that therapeutic strategies targeting USP22 activity may sensitize tumor cells to UPR induction and could provide a novel, effective approach to treat HER2⁺-BC.

29/07/2021

Store-Operated Calcium Channels Control Proliferation and Self-Renewal of Cancer Stem Cells from Glioblastoma

Elodie Terrié ¹ Nadine Déliot ¹ Yassine Benzidane ¹ Thomas Harnois ¹ Laëtitia Cousin ¹ Patrick Bois ¹ Lisa Oliver ² Patricia Arnault ¹ François Vallette ^{2, 3} Bruno Constantin ^{1, 3} Valérie Coronas

Cancers 2021, 13(14), 3428

1 STIM – Signalisation et Transports Ioniques Membranaires

2 CRCINA-ÉQUIPE 9 – Apoptosis and Tumor Progression, CRCINA – Centre de Recherche en Cancérologie et Immunologie Nantes-Angers

3 CNRS GDR 3697 MicroNiT – Microenvironnement des niches tumorales [UNIV Tours]

Glioblastoma is the most frequent and deadly form of primary brain tumors. Despite multimodal treatment, more than 90% of patients experience tumor recurrence. Glioblastoma contains a small population of cells, called glioblastoma stem cells (GSC) that are highly resistant to treatment and endowed with the ability to regenerate the tumor, which accounts for tumor recurrence. Transcriptomic studies disclosed an enrichment of calcium (Ca²⁺) signaling transcripts in GSC. In non-excitable cells, store-operated channels (SOC) represent a major route of Ca²⁺ influx. As SOC regulate the self-renewal of adult neural stem cells that are possible cells of origin of GSC, we analyzed the roles of SOC in cultures of GSC previously derived from five different glioblastoma surgical specimens. Immunoblotting and immunocytochemistry experiments showed that GSC express Orai1 and TRPC1, two core SOC proteins, along with their activator STIM1. Ca²⁺ imaging demonstrated that SOC support Ca²⁺ entries in GSC. Pharmacological inhibition of SOC-dependent Ca²⁺ entries decreased proliferation, impaired self-renewal, and reduced expression of the stem cell marker SOX2 in GSC. Our data showing the ability of SOC inhibitors to impede GSC self-renewal paves the way for a strategy to target the cells considered responsible for conveying resistance to treatment and tumor relapse.

29/07/2021

Identification of CRYAB + KCNN3 + SOX9 + Astrocyte-Like and EGFR + PDGFRA + OLIG1 + Oligodendrocyte-Like Tumoral Cells in Diffuse IDH1-Mutant Gliomas and Implication of NOTCH1 Signalling in Their Genesis

2021 Sunrise member publications

Meera Augustus, Donovan Pineau, Franck Aimond, Safa Azar, Davide Lecca, Frédérique Scamps², Sophie Muxel¹, Amélie Darlix^1 4, William Ritchie⁵, Catherine Gozé^1 6, Valérie Rigau^1 7, Hugues Duffau^1 8, Jean-Philippe Hugnot

Abstract

Diffuse grade II IDH-mutant gliomas are slow-growing brain tumors that progress into high-grade gliomas. They present intratumoral cell heterogeneity, and no reliable markers are available to distinguish the different cell subtypes. The molecular mechanisms underlying the formation of this cell diversity is also ill-defined. Here, we report that SOX9 and OLIG1 transcription factors, which specifically label astrocytes and oligodendrocytes in the normal brain, revealed the presence of two largely nonoverlapping tumoral populations in IDH1-mutant oligodendrogliomas and astrocytomas. Astrocyte-like SOX9⁺ cells additionally stained for APOE, CRYAB, ID4, KCNN3, while oligodendrocyte-like OLIG1⁺ cells stained for ASCL1, EGFR, IDH1, PDGFRA, PTPRZ1, SOX4, and SOX8. GPR17, an oligodendrocytic marker, was expressed by both cells. These two subpopulations appear to have distinct BMP, NOTCH1, and MAPK active pathways as stainings for BMP4, HEY1, HEY2, p-SMAD1/5 and p-ERK were higher in SOX9⁺ cells. We used primary cultures and a new cell line to explore the influence of NOTCH1 activation and BMP treatment on the IDH1-mutant glioma cell phenotype. This revealed that NOTCH1 globally reduced oligodendrocytic markers and IDH1 expression while upregulating APOE, CRYAB, HEY1/2, and an electrophysiologically-active Ca²⁺-activated apamin-sensitive K⁺ channel (KCNN3/SK3). This was accompanied by a reduction in proliferation. Similar effects of NOTCH1 activation were observed in nontumoral human oligodendrocytic cells, which additionally induced strong SOX9 expression. BMP treatment reduced OLIG1/2 expression and strongly upregulated CRYAB and NOGGIN, a negative regulator of BMP. The presence of astrocyte-like SOX9⁺ and oligodendrocyte-like OLIG1⁺ cells in grade II IDH1-mutant gliomas raises new questions about their role in the pathology.

Keywords: BMP; NOTCH1 pathway; brain tumors; cellular heterogeneity; diffuse IDH1-mutant gliomas; diffuse grade II IDH-mutant glioma.

26/07/2021

FTO-Mediated Cytoplasmic m6Am Demethylation Adjusts Stem-Like Properties in Colorectal Cancer Cell

2021 Sunrise member publications

Sébastien Relier¹, Julie Ripoll², Hélène Guillorit^1 3, Amandine Amalric¹, Cyrinne Achour^4 5, Florence Boissière⁶, Jérôme Vialaret^7 8, Aurore Attina^7 8, Françoise Debart⁹, Armelle Choquet¹, Françoise Macari¹, Virginie Marchand¹⁰, Yuri Motorin¹⁰, Emmanuelle Samalin^1 6, Jean-Jacques Vasseur⁹, Julie Pannequin¹, Francesca Aguilo^4 5, Evelyne Lopez-Crapez⁶, Christophe Hirtz^7 8, Eric Rivals¹¹, Amandine Bastide¹², Alexandre David^13 14

¹IGF, Univ. Montpellier, CNRS, INSERM, Montpellier, France.
²LIRMM, Univ. Montpellier, CNRS, Montpellier, France.
³Stellate Therapeutics, Paris, France.
⁴Wallenberg Centre for Molecular Medicine (WCMM), Umea University, Umea, Sweden.
⁵Department of Medical Biosciences, Umea University, Umea, Sweden.
⁶ICM, Montpellier, France.
⁷IRMB-PPC, Univ. Montpellier, INSERM, CHU Montpellier, CNRS, Montpellier, France.
⁸INM, Univ. Montpellier, INSERM, Montpellier, France.
⁹IBMM, CNRS, Univ. Montpellier, ENSCM, Montpellier, France.
¹⁰Université de Lorraine, IMoPA UMR7365 CNRS-UL and UMS2008/US40 IBSLor, UL-CNRS-INSERM, BioPole, Vandoeuvre-les-Nancy, France.
¹¹LIRMM, Univ. Montpellier, CNRS, Montpellier, France. rivals@lirmm.fr.
¹²IGF, Univ. Montpellier, CNRS, INSERM, Montpellier, France. amandine.bastide@igf.cnrs.fr.
¹³IGF, Univ. Montpellier, CNRS, INSERM, Montpellier, France. alexandre.david@igf.cnrs.fr.
¹⁴IRMB-PPC, Univ. Montpellier, INSERM, CHU Montpellier, CNRS, Montpellier, France. alexandre.david@igf.cnrs.fr.

Cancer stem cells (CSCs) are a small but critical cell population for cancer biology since they display inherent resistance to standard therapies and give rise to metastases. Despite accruing evidence establishing a link between deregulation of epitranscriptome-related players and tumorigenic process, the role of messenger RNA (mRNA) modifications in the regulation of CSC properties remains poorly understood. Here, we show that the cytoplasmic pool of fat mass and obesity-associated protein (FTO) impedes CSC abilities in colorectal cancer through its N⁶,2′-O-dimethyladenosine (m⁶A_m) demethylase activity. While m⁶A_m is strategically located next to the m⁷G-mRNA cap, its biological function is not well understood and has not been addressed in cancer. Low FTO expression in patient-derived cell lines elevates m⁶A_m level in mRNA which results in enhanced in vivo tumorigenicity and chemoresistance. Inhibition of the nuclear m⁶A_m methyltransferase, PCIF1/CAPAM, fully reverses this phenotype, stressing the role of m⁶A_m modification in stem-like properties acquisition. FTO-mediated regulation of m⁶A_m marking constitutes a reversible pathway controlling CSC abilities. Altogether, our findings bring to light the first biological function of the m⁶A_m modification and its potential adverse consequences for colorectal cancer management.

19/04/2021

The Role of Cancer Stem Cells in Colorectal Cancer: From the Basics to Novel Clinical Trials

2021 Sunrise member publications

Céline Hervieu, Niki Christou, Serge Battu, Muriel Mathonnet

EA 3842 CAPTuR “Control of Cell Activation in Tumor Progression and Therapeutic Resistance”, Faculty of Medicine, Genomics, Environment, Immunity, Health and Therapeutics (GEIST) Institute, University of Limoges, 87025 Limoges CEDEX, France.
Department of General, Endocrine and Digestive Surgery, University Hospital of Limoges, 87025 Limoges CEDEX, France.

Abstract

The treatment options available for colorectal cancer (CRC) have increased over the years and have significantly improved the overall survival of CRC patients. However, the response rate for CRC patients with metastatic disease remains low and decreases with subsequent lines of therapy. The clinical management of patients with metastatic CRC (mCRC) presents a unique challenge in balancing the benefits and harms while considering disease progression, treatment-related toxicities, drug resistance and the patient’s overall quality of life. Despite the initial success of therapy, the development of drug resistance can lead to therapy failure and relapse in cancer patients, which can be attributed to the cancer stem cells (CSCs). Thus, colorectal CSCs (CCSCs) contribute to therapy resistance but also to tumor initiation and metastasis development, making them attractive potential targets for the treatment of CRC. This review presents the available CCSC isolation methods, the clinical relevance of these CCSCs, the mechanisms of drug resistance associated with CCSCs and the ongoing clinical trials targeting these CCSCs. Novel therapeutic strategies are needed to effectively eradicate both tumor growth and metastasis, while taking into account the tumor microenvironment (TME) which plays a key role in tumor cell plasticity.

19/04/2021

ERK-Mediated Loss of miR-199a-3p and Induction of EGR1 Act as a “Toggle Switch” of GBM Cell Dedifferentiation into NANOG- and OCT4-Positive Cells

2020 Sunrise member publications

Fabien Almairac , Laurent Turchi , Nathalie Sakakini , David Nicolas Debruyne , Sarah Elkeurti , Elisabet Gjernes , Beatrice Polo , Laurence Bianchini , Denys Fontaine , Philippe Paquis , Herve Chneiweiss , Marie-Pierre Junier , Patrick Verrando , Fanny Burel-Vandenbos , Thierry Virolle.

There is great interest in understanding how the cancer stem cell population may be maintained in solid tumors. Here, we show that tumor cells exhibiting stem-like properties and expression of pluripotency markers NANOG and OCT4 can arise from original differentiated tumor cells freshly isolated from human glioblastomas (GBM) and that have never known any serum culture conditions. Induction of EGR1 by EGFR/ERK signaling promoted cell conversion from a less aggressive, more differentiated cellular state to a self-renewing and strongly tumorigenic state, expressing NANOG and OCT4. Expression of these pluripotency markers occurred before the cells re-entered the cell cycle, demonstrating their capacity to change and dedifferentiate without any cell divisions. In differentiated GBM cells, ERK-mediated repression of miR-199a-3p induced EGR1 protein expression and triggered dedifferentiation. Overall, this signaling pathway constitutes an ERK-mediated “toggle switch” that promotes pluripotency marker expression and stem-like features in GBM cells. SIGNIFICANCE: This study defines an ERK-mediated molecular mechanism of dedifferentiation of GBM cells into a stem-like state, expressing markers of pluripotency

doi: 10.1158/0008-5472.CAN-19-0855. Epub 2020 May 4.

22/01/2021

Organotypic Modeling of the Tumor Landscape

2020 Sunrise member publications

Maria Haykal, Clara Nahmias, Christine Varon, Océane Martin

Cancer is a complex disease and it is now clear that not only epithelial tumor cells play a role in carcinogenesis. The tumor microenvironment is composed of non-stromal cells, including endothelial cells, adipocytes, immune and nerve cells, and a stromal compartment composed of extracellular matrix, cancer-associated fibroblasts and mesenchymal cells. Tumorigenesis is a dynamic process with constant interactions occurring between the tumor cells and their surroundings. Even though all connections have not yet been discovered, it is now known that crosstalk between actors of the microenvironment drives cancer progression. Taking into account this complexity, it is important to develop relevant models to study carcinogenesis. Conventional 2D culture models fail to represent the entire tumor microenvironment properly and the use of animal models should be decreased with respect to the 3Rs rule. To this aim, in vitro organotypic models have been significantly developed these past few years. These models have different levels of complexity and allow the study of tumor cells alone or in interaction with the microenvironment actors during the multiple stages of carcinogenesis. This review depicts recent insights into organotypic modeling of the tumor and its microenvironment all throughout cancer progression. It offers an overview of the crosstalk between epithelial cancer cells and their microenvironment during the different phases of carcinogenesis, from the early cell autonomous events to the late metastatic stages. The advantages of 3D over classical 2D or in vivo models are presented as well as the most promising organotypic models. A particular focus is made on organotypic models used for studying cancer progression, from the less complex spheroids to the more sophisticated body-on-a-chip. Last but not least, we address the potential benefits of these models in personalized medicine which is undoubtedly a domain paving the path to new hopes in terms of cancer care and cure.

Frontiers in Cell and Developmental Biology, Frontiers media, 2020, 8,

Online ahead of print. ff10.3389/fcell.2020.606039f

21/01/2021

Autophagy in Osteosarcoma Cancer Stem Cells Is Critical Process which Can Be Targeted by the Antipsychotic Drug Thioridazine

2020 Sunrise member publications

Olivier Camuzard, Marie-Charlotte Trojani, Sabine Santucci-Darmanin, Sophie Pagnotta , Véronique Breuil, Georges F Carle, Valérie Pierrefite-Carle

Cancer stem cells (CSCs) represent a minor population of cancer cells with stem cell-like properties which are able to fuel tumor growth and resist conventional treatments. Autophagy has been described to be upregulated in some CSCs and to play a crucial role by maintaining stem features and promoting resistance to both hostile microenvironments and treatments. Osteosarcoma (OS) is an aggressive bone cancer which mainly affects children and adolescents and autophagy in OS CSCs has been poorly studied. However, this is a very interesting case because autophagy is often deregulated in this cancer. In the present work, we used two OS cell lines showing different autophagy capacities to isolate CSC-enriched populations and to analyze the autophagy in basal and nutrient-deprived conditions. Our results indicate that autophagy is more efficient in CSCs populations compared to the parental cell lines, suggesting that autophagy is a critical process in OS CSCs. We also showed that the antipsychotic drug thioridazine is able to stimulate, and then impair autophagy in both CSC-enriched populations, leading to autosis, a cell death mediated by the Na+/K⁺ ATPase pump and triggered by dysregulated accumulation of autophagosomes. Taken together, our results indicate that autophagy is very active in OS CSCs and that targeting this pathway to switch their fate from survival to death could provide a novel strategy to eradicate these cells in osteosarcoma.

Cancers, 2020 Dec 7;12(12):3675

doi: 10.3390/cancers12123675.

21/01/2021

Progastrin production transitions from Bmi1+/Prox1+ to Lgr5high cells during early intestinal tumorigenesis.

2020 Sunrise member publications

Giraud J, Foroutan M, Boubaker-Vitre J, Grillet F, Homayed Z, Jadhav U, Crespy P, Breuker C, Bourgaux JF, Hazerbroucq J, Pignodel C, Brulin B, Shivdasani RA, Jay P, Hollande F, Pannequin J.

Transl Oncol. 2020 Dec 22;14(2):101001. doi: 10.1016/j.tranon.2020.101001.

Online ahead of print. PMID: 33360299

05/01/2021

Direct and Indirect Regulators of Epithelial-Mesenchymal Transition (EMT)-mediated Immunosuppression in Breast Carcinomas

2020 Seminal publications

Anushka Dongre, Mohammad Rashidian, Elinor Ng Eaton, Ferenc Reinhardt, Prathapan Thiru, Maria Zagorulya, Sunita Nepal, Tuba Banaz, Anna Martner, Stefani Spranger and Robert A. Weinberg

Cancer Discov; Published OnlineFirst December 16, 2020; doi:10.1158/2159-8290.CD-20-0603

05/01/2021

CRISPR Screening of CAR T Cells and Cancer Stem Cells Reveals Critical Dependencies for Cell-Based Therapies

2020 Seminal publications

Dongrui Wang, Briana C Prager, Ryan C Gimple, Brenda Aguilar, Darya Alizadeh, Hongzhen Tang, Deguan Lv, Renate Starr, Alfonso Brito, Qiulian Wu, Leo J.Y Kim, Zhixin Qiu, Peng Lin, Michael H. Lorenzini, Behnam Badie, Stephen J Forman, Qi Xie, Christine E Brown and Jeremy N. Rich

Cancer Discov; Published OnlineFirst December 16, 2020; doi:10.1158/2159-8290.CD-20-1243

05/01/2021

Organotypic Modeling of the Tumor Landscape

2020 Reviews, Sunrise member publications

Maria M. Haykal, Clara Nahmias, Christine Varon and Océane C. B. Martin

Front. Cell Dev. Biol., 24 November 2020

18/12/2020

Heterotypic cell–cell communication regulates glandular stem cell multipotency

2020 Seminal publications

Alessia Centonze, Shuheng Lin, Elisavet Tika, Alejandro Sifrim, Marco Fioramonti, Milan Malfait, Yura Song, Aline Wuidart, Jens Van Herck, Anne Dannau, Gaelle Bouvencourt, Christine Dubois, Nina Dedoncker, Amar Sahay, Viviane de Maert elaer, Christian W. Siebel, Alexandra Van Keymeulen, Thierry Voet & Cédric Blanpain

Nature volume 584, pages608–613(2020)

15/09/2020

CD44 regulates epigenetic plasticity by mediating iron endocytosis

2020 Sunrise member publications

Sebastian Müller, Fabien Sindikubwabo, Tatiana Cañeque, Anne Lafon, Antoine Versini, Bérangère Lombard, Damarys Loew, Ting-Di Wu, Christophe Ginestier, Emmanuelle Charafe-Jauffret, Adeline Durand, Céline Vallot, Sylvain Baulande, Nicolas Servant, Raphaël Rodriguez

Nature Chemistry (2020)

15/09/2020

The Epigenetic Progenitor Origin of Cancer Reassessed: DNA Methylation Brings Balance to the Stem Force

2020 Sunrise member publications

Marco Bruschi
U981-Molecular Predictors and New Targets in Oncology, INSERM, Gustave Roussy, University Paris-Saclay, 114 rue Édouard Vaillant, 94800 Villejuif, France
Département de Cancérologie de l’Enfant et de l’Adolescent, Gustave Roussy, Université Paris-Saclay, 94800 Villejuif, France
Epigenomes 2020, 4(2), 8
https://doi.org/10.3390/epigenomes4020008

02/06/2020

Zonation of Ribosomal DNA Transcription Defines a Stem Cell Hierarchy in Colorectal Cancer

2020 Seminal publications

Clara Morral , Jelena Stanisavljevic , Xavier Hernando-Momblona , Elisabetta Mereu , Adrián Álvarez-Varela , Carme Cortina , Diana Stork , Felipe Slebe , Gemma Turon , Gavin Whissell , Marta Sevillano , Anna Merlos-Suárez , Àngela Casanova-Martí , Catia Moutinho , Scott W Lowe , Lukas E Dow , Alberto Villanueva , Elena Sancho , Holger Heyn , Eduard Batlle
PMID: 32396863
DOI: 10.1016/j.stem.2020.04.012

26/05/2020

Transformation Foci in IDH1-mutated Gliomas Show STAT3 Phosphorylation and Downregulate the Metabolic Enzyme ETNPPL, a Negative Regulator of Glioma Growth

2020 Sunrise member publications

Leventoux N1, Augustus M, Azar S, Riquier S, Villemin JP, Guelfi S, Falha L, Bauchet L, Gozé C, Ritchie W, Commes T, Duffau H, Rigau V, Hugnot JP

Sci Rep. 2020 Mar 26;10(1):5504. doi: 10.1038/s41598-020-62145-1.

PMID: 32218467

05/05/2020

Cancer stem cells in solid tumours: accumulating evidence and unresolved questions

2008 Reviews

Visvader JE, Lindeman GJ.

Nat Rev Cancer. 2008 Oct;8(10):755-68. doi: 10.1038/nrc2499. Epub 2008 Sep 11. Review.

PMID: 18784658

06/03/2020

Cancer stem cell definitions and terminology: the devil is in the details.

2012 Reviews

Valent P, Bonnet D, De Maria R, Lapidot T, Copland M, Melo JV, Chomienne C, Ishikawa F, Schuringa JJ, Stassi G, Huntly B, Herrmann H, Soulier J, Roesch A, Schuurhuis GJ, Wöhrer S, Arock M, Zuber J, Cerny-Reiterer S, Johnsen HE, Andreeff M, Eaves C.

Nat Rev Cancer. 2012 Nov;12(11):767-75. doi: 10.1038/nrc3368. Epub 2012 Oct 11. Review.

PMID: 23051844

06/03/2020