LIVIVO - Search results -

Search results

Result 1 - 10 of total 69

Search options

Article ; Online: Tumor microenvironment and noncoding RNAs as co-drivers of epithelial-mesenchymal transition and cancer metastasis.

Drak Alsibai, Kinan / Meseure, Didier

Developmental dynamics : an official publication of the American Association of Anatomists

2017 Volume 247, Issue 3, Page(s) 405–431

Abstract: Reciprocal interactions between cancer cells and tumor microenvironment (TME) are crucial events in tumor progression and metastasis. Pervasive stromal reprogramming of TME modifies numerous cellular functions, including extracellular matrix (ECM) ... ...

Abstract	Reciprocal interactions between cancer cells and tumor microenvironment (TME) are crucial events in tumor progression and metastasis. Pervasive stromal reprogramming of TME modifies numerous cellular functions, including extracellular matrix (ECM) stiffness, inflammation, and immunity. These environmental factors allow selection of more aggressive cells that develop adaptive strategies associating plasticity and epithelial-mesenchymal transition (EMT), stem-like phenotype, invasion, immunosuppression, and resistance to therapies. EMT is a morphomolecular process that endows epithelial tumor cells with mesenchymal properties, including reduced adhesion and increased motility. Numerous studies have demonstrated involvement of noncoding RNAs (ncRNAs), such as miRNAs and lncRNAs, in tumor initiation, progression, and metastasis. NcRNAs regulate every hallmark of cancer and have now emerged as new players in induction and regulation of EMT. The reciprocal regulatory interactions between ncRNAs, TME components, and cancer cells increase the complexity of gene expression and protein translation in cancer. Thus, deeper understanding of molecular mechanisms controlling EMT will not only shed light on metastatic processes of cancer cells, but enhance development of new therapies targeting metastasis. In this review, we will provide recent findings on the role of known ncRNAs relevant to EMT and cancer metastasis and discuss the role of the interaction between ncRNAs and TME as co-drivers of EMT. Developmental Dynamics 247:405-431, 2018. © 2017 Wiley Periodicals, Inc.
MeSH term(s)	Animals ; Disease Progression ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Neoplasm Metastasis ; Neoplasms/pathology ; RNA, Untranslated/physiology ; Tumor Microenvironment
Chemical Substances	RNA, Untranslated
Language	English
Publishing date	2017-09-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.24548
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ub I Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 64: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article: Expression, Localization and Prognosis Association of MEP50 in Breast Cancer.

Suresh, Samyuktha / Vinet, Mathilde / Dakroub, Rayan / Lesage, Laetitia / Ye, Mengliang / Fayyad-Kazan, Hussein / Nicolas, André / Meseure, Didier / Dubois, Thierry

Cancers

2022 Volume 14, Issue 19

Abstract: Breast cancer is composed of distinct subgroups, triple-negative breast cancer (TNBC), human epidermal growth factor receptor-2 (HER2), luminal A, and luminal B, which are associated with different prognosis. MEP50 is the main partner of the arginine ... ...

Abstract	Breast cancer is composed of distinct subgroups, triple-negative breast cancer (TNBC), human epidermal growth factor receptor-2 (HER2), luminal A, and luminal B, which are associated with different prognosis. MEP50 is the main partner of the arginine methyltransferase PRMT5 required for its enzymatic activity. Here, we examined
Language	English
Publishing date	2022-09-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14194766
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Deciphering the spatial landscape and plasticity of immunosuppressive fibroblasts in breast cancer.

Croizer, Hugo / Mhaidly, Rana / Kieffer, Yann / Gentric, Geraldine / Djerroudi, Lounes / Leclere, Renaud / Pelon, Floriane / Robley, Catherine / Bohec, Mylene / Meng, Arnaud / Meseure, Didier / Romano, Emanuela / Baulande, Sylvain / Peltier, Agathe / Vincent-Salomon, Anne / Mechta-Grigoriou, Fatima

Nature communications

2024 Volume 15, Issue 1, Page(s) 2806

Abstract: Although heterogeneity of FAP+ Cancer-Associated Fibroblasts (CAF) has been described in breast cancer, their plasticity and spatial distribution remain poorly understood. Here, we analyze trajectory inference, deconvolute spatial transcriptomics at ... ...

Abstract	Although heterogeneity of FAP+ Cancer-Associated Fibroblasts (CAF) has been described in breast cancer, their plasticity and spatial distribution remain poorly understood. Here, we analyze trajectory inference, deconvolute spatial transcriptomics at single-cell level and perform functional assays to generate a high-resolution integrated map of breast cancer (BC), with a focus on inflammatory and myofibroblastic (iCAF/myCAF) FAP+ CAF clusters. We identify 10 spatially-organized FAP+ CAF-related cellular niches, called EcoCellTypes, which are differentially localized within tumors. Consistent with their spatial organization, cancer cells drive the transition of detoxification-associated iCAF (Detox-iCAF) towards immunosuppressive extracellular matrix (ECM)-producing myCAF (ECM-myCAF) via a DPP4- and YAP-dependent mechanism. In turn, ECM-myCAF polarize TREM2+ macrophages, regulatory NK and T cells to induce immunosuppressive EcoCellTypes, while Detox-iCAF are associated with FOLR2+ macrophages in an immuno-protective EcoCellType. FAP+ CAF subpopulations accumulate differently according to the invasive BC status and predict invasive recurrence of ductal carcinoma in situ (DCIS), which could help in identifying low-risk DCIS patients eligible for therapeutic de-escalation.
MeSH term(s)	Humans ; Female ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Carcinoma, Intraductal, Noninfiltrating/pathology ; Fibroblasts/pathology ; Cancer-Associated Fibroblasts/pathology ; Extracellular Matrix/pathology ; Tumor Microenvironment ; Folate Receptor 2
Chemical Substances	FOLR2 protein, human ; Folate Receptor 2
Language	English
Publishing date	2024-04-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-47068-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A novel bioinformatic approach reveals cooperation between Cancer/Testis genes in basal-like breast tumors.

Laisné, Marthe / Rodgers, Brianna / Benlamara, Sarah / Wicinski, Julien / Nicolas, André / Djerroudi, Lounes / Gupta, Nikhil / Ferry, Laure / Kirsh, Olivier / Daher, Diana / Philippe, Claude / Okada, Yuki / Charafe-Jauffret, Emmanuelle / Cristofari, Gael / Meseure, Didier / Vincent-Salomon, Anne / Ginestier, Christophe / Defossez, Pierre-Antoine

Oncogene

2024

Abstract: Breast cancer is the most prevalent type of cancer in women worldwide. Within breast tumors, the basal-like subtype has the worst prognosis, prompting the need for new tools to understand, detect, and treat these tumors. Certain germline-restricted genes ...

Abstract	Breast cancer is the most prevalent type of cancer in women worldwide. Within breast tumors, the basal-like subtype has the worst prognosis, prompting the need for new tools to understand, detect, and treat these tumors. Certain germline-restricted genes show aberrant expression in tumors and are known as Cancer/Testis genes; their misexpression has diagnostic and therapeutic applications. Here we designed a new bioinformatic approach to examine Cancer/Testis gene misexpression in breast tumors. We identify several new markers in Luminal and HER-2 positive tumors, some of which predict response to chemotherapy. We then use machine learning to identify the two Cancer/Testis genes most associated with basal-like breast tumors: HORMAD1 and CT83. We show that these genes are expressed by tumor cells and not by the microenvironment, and that they are not expressed by normal breast progenitors; in other words, their activation occurs de novo. We find these genes are epigenetically repressed by DNA methylation, and that their activation upon DNA demethylation is irreversible, providing a memory of past epigenetic disturbances. Simultaneous expression of both genes in breast cells in vitro has a synergistic effect that increases stemness and activates a transcriptional profile also observed in double-positive tumors. Therefore, we reveal a functional cooperation between Cancer/Testis genes in basal breast tumors; these findings have consequences for the understanding, diagnosis, and therapy of the breast tumors with the worst outcomes.
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-024-03002-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2218: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Patient Derived Xenografts (PDX) Models as an Avatar to Assess Personalized Therapy Options in Uveal Melanoma: A Feasibility Study.

Current oncology (Toronto, Ont.)

2023 Volume 30, Issue 10, Page(s) 9090–9103

Abstract: Uveal melanoma is the most common primary intraocular malignancy in adults. Up to 50% of UM patients develop metastatic disease, usually in the liver. When metastatic, the prognosis is poor, and few treatment options exist. Here, we investigated the ... ...

Abstract	Uveal melanoma is the most common primary intraocular malignancy in adults. Up to 50% of UM patients develop metastatic disease, usually in the liver. When metastatic, the prognosis is poor, and few treatment options exist. Here, we investigated the feasibility of establishing patient-derived xenografts (PDXs) from a patient's tumor in order to screen for therapies that the patient could benefit from. Samples obtained from 29 primary tumors and liver metastases of uveal melanoma were grafted into SCID mice. PDX models were successfully established for 35% of primary patient tumors and 67% of liver metastases. The tumor take rate was proportional to the risk of metastases. PDXs showed the same morphology, the same GNAQ/11, BAP1, and SF3B1 mutations, and the same chromosome 3 and 8q status as the corresponding patient samples. Six PDX models were challenged with two compounds for 4 weeks. We show that, for 31% of patients with high or intermediate risk of metastasis, the timing to obtain efficacy results on PDX models derived from their primary tumors was compatible with the selection of the therapy to treat the patient after relapse. PDXs could thus be a valid tool ("avatar") to select the best personalized therapy for one third of patients that are most at risk of relapse.
MeSH term(s)	Adult ; Animals ; Mice ; Humans ; Feasibility Studies ; Heterografts ; Mice, SCID ; Neoplasm Recurrence, Local ; Liver Neoplasms/genetics ; Recurrence
Language	English
Publishing date	2023-10-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1236972-x
ISSN	1718-7729 ; 1198-0052
ISSN (online)	1718-7729
ISSN	1198-0052
DOI	10.3390/curroncol30100657
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4305: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: PRMT1 Regulates EGFR and Wnt Signaling Pathways and Is a Promising Target for Combinatorial Treatment of Breast Cancer.

Suresh, Samyuktha / Huard, Solène / Brisson, Amélie / Némati, Fariba / Dakroub, Rayan / Poulard, Coralie / Ye, Mengliang / Martel, Elise / Reyes, Cécile / Silvestre, David C / Meseure, Didier / Nicolas, André / Gentien, David / Fayyad-Kazan, Hussein / Le Romancer, Muriel / Decaudin, Didier / Roman-Roman, Sergio / Dubois, Thierry

Cancers

2022 Volume 14, Issue 2

Abstract: Identifying new therapeutic strategies for triple-negative breast cancer (TNBC) patients is a priority as these patients are highly prone to relapse after chemotherapy. Here, we found that protein arginine methyltransferase 1 (PRMT1) is highly expressed ... ...

Abstract	Identifying new therapeutic strategies for triple-negative breast cancer (TNBC) patients is a priority as these patients are highly prone to relapse after chemotherapy. Here, we found that protein arginine methyltransferase 1 (PRMT1) is highly expressed in all breast cancer subtypes. PRMT1 depletion decreases cell survival by inducing DNA damage and apoptosis in various breast cancer cell lines. Transcriptomic analysis and chromatin immunoprecipitation revealed that PRMT1 regulates the epidermal growth factor receptor (EGFR) and the Wnt signaling pathways, reported to be activated in TNBC. PRMT1 enzymatic activity is also required to stimulate the canonical Wnt pathway. Type I PRMT inhibitors decrease breast cancer cell proliferation and show anti-tumor activity in a TNBC xenograft model. These inhibitors display synergistic interactions with some chemotherapies used to treat TNBC patients as well as erlotinib, an EGFR inhibitor. Therefore, targeting PRMT1 in combination with these chemotherapies may improve existing treatments for TNBC patients.
Language	English
Publishing date	2022-01-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14020306
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Altered Expression of Three EGFR Posttranslational Regulators MDGI, MIG6, and EIG121 in Invasive Breast Carcinomas.

Meseure, Didier / Drak Alsibai, Kinan / Vacher, Sophie / Hatem, Rana / Nicolas, Andre / Callens, Celine / Lerebours, Florence / Bieche, Ivan

Analytical cellular pathology (Amsterdam)

2020 Volume 2020, Page(s) 9268236

Abstract: Epidermal growth factor receptor (EGFR) signalling is a highly regulated process with a tight balance between receptor activation and inactivation in invasive breast carcinomas (IBCs) particularly in triple-negative carcinomas (TNC). Clinical trials ... ...

Abstract	Epidermal growth factor receptor (EGFR) signalling is a highly regulated process with a tight balance between receptor activation and inactivation in invasive breast carcinomas (IBCs) particularly in triple-negative carcinomas (TNC). Clinical trials using anti-EGFR therapies are actually performed although no activating alterations (mutations, amplifications, or rearrangements) of
MeSH term(s)	Adaptor Proteins, Signal Transducing/biosynthesis ; Adaptor Proteins, Signal Transducing/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; ErbB Receptors/metabolism ; Fatty Acid Binding Protein 3/biosynthesis ; Fatty Acid Binding Protein 3/genetics ; Female ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Membrane Proteins/biosynthesis ; Membrane Proteins/genetics ; Neoplasm Invasiveness/genetics ; RNA Processing, Post-Transcriptional ; Tumor Suppressor Proteins/biosynthesis ; Tumor Suppressor Proteins/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; ELAPOR1 protein, human ; ERRFI1 protein, human ; FABP3 protein, human ; Fatty Acid Binding Protein 3 ; Membrane Proteins ; Tumor Suppressor Proteins ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2020-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2583629-8
ISSN	2210-7185 ; 2210-7177
ISSN (online)	2210-7185
ISSN	2210-7177
DOI	10.1155/2020/9268236
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3139: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: AXL Controls Directed Migration of Mesenchymal Triple-Negative Breast Cancer Cells.

Zajac, Olivier / Leclere, Renaud / Nicolas, André / Meseure, Didier / Marchiò, Caterina / Vincent-Salomon, Anne / Roman-Roman, Sergio / Schoumacher, Marie / Dubois, Thierry

Cells

2020 Volume 9, Issue 1

Abstract: Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with high risk of relapse and metastasis. TNBC is a heterogeneous disease comprising different molecular subtypes including those with mesenchymal features. The tyrosine kinase ... ...

Abstract	Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with high risk of relapse and metastasis. TNBC is a heterogeneous disease comprising different molecular subtypes including those with mesenchymal features. The tyrosine kinase AXL is expressed in mesenchymal cells and plays a role in drug resistance, migration and metastasis. We confirm that AXL is more expressed in mesenchymal TNBC cells compared to luminal breast cancer cells, and that its invalidation impairs cell migration while having no or little effect on cell viability. Here, we found that AXL controls directed migration. We observed that AXL displays a polarized localization at the Golgi apparatus and the leading edge of migratory mesenchymal TNBC cells. AXL co-localizes with F-actin at the front of the cells. In migratory polarized cells, the specific AXL inhibitor R428 displaces AXL and F-actin from the leading edge to a lateral area localized between the front and the rear of the cells where both are enriched in protrusions. In addition, R428 treatment disrupts the polarized localization of the Golgi apparatus towards the leading edge in migratory cells. Immunohistochemical analysis of aggressive chemo-resistant TNBC samples obtained before treatment reveals inter- and intra-tumor heterogeneity of the percentage of AXL expressing tumor cells, and a preference of these cells to be in contact with the stroma. Taken together, our study demonstrates that AXL controls directed cell migration most likely by regulating cell polarity.
MeSH term(s)	Cell Line, Tumor ; Cell Movement ; Female ; Golgi Apparatus/metabolism ; Humans ; Mesoderm/pathology ; Polymerization ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism ; Stromal Cells/pathology ; Triple Negative Breast Neoplasms/enzymology ; Triple Negative Breast Neoplasms/pathology
Chemical Substances	Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1)
Language	English
Publishing date	2020-01-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9010247
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Pivotal role of pervasive neoplastic and stromal cells reprogramming in circulating tumor cells dissemination and metastatic colonization.

Meseure, Didier / Drak Alsibai, Kinan / Nicolas, Andre

Cancer microenvironment : official journal of the International Cancer Microenvironment Society

2014 Volume 7, Issue 3, Page(s) 95–115

Abstract: Reciprocal interactions between neoplastic cells and their microenvironment are crucial events in carcinogenesis and tumor progression. Pervasive stromal reprogramming and remodeling that transform a normal to a tumorigenic microenvironment modify ... ...

Abstract	Reciprocal interactions between neoplastic cells and their microenvironment are crucial events in carcinogenesis and tumor progression. Pervasive stromal reprogramming and remodeling that transform a normal to a tumorigenic microenvironment modify numerous stromal cells functions, status redox, oxidative stress, pH, ECM stiffness and energy metabolism. These environmental factors allow selection of more aggressive cancer cells that develop important adaptive strategies. Subpopulations of cancer cells acquire new properties associating plasticity, stem-like phenotype, unfolded protein response, metabolic reprogramming and autophagy, production of exosomes, survival to anoikis, invasion, immunosuppression and therapeutic resistance. Moreover, by inducing vascular transdifferentiation of cancer cells and recruiting endothelial cells and pericytes, the tumorigenic microenvironment induces development of tumor-associated vessels that allow invasive cells to gain access to the tumor vessels and to intravasate. Circulating cancer cells can survive in the blood stream by interacting with the intravascular microenvironment, extravasate through the microvasculature and interact with the metastatic microenvironment of target organs. In this review, we will focus on many recent paradigms involved in the field of tumor progression.
Language	English
Publishing date	2014-12-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2422345-1
ISSN	1875-2284 ; 1875-2292
ISSN (online)	1875-2284
ISSN	1875-2292
DOI	10.1007/s12307-014-0158-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

2021 Volume 12, Issue 8, Page(s) 859–872

Abstract: Significant rational is available for specific targeting of PI3K/AKT/mTOR pathway in the treatment of non-small cell lung cancer (NSCLC). However, almost all clinical trials that have evaluated Pi3K pathway-based monotherapies/combinations did not ... ...

Abstract	Significant rational is available for specific targeting of PI3K/AKT/mTOR pathway in the treatment of non-small cell lung cancer (NSCLC). However, almost all clinical trials that have evaluated Pi3K pathway-based monotherapies/combinations did not observe an improvement of patient's outcome. The aim of our study was therefore to define combination of treatment based on the determination of predictive markers of resistance to the mTORC1 inhibitor RAD001/Everolimus. An
Language	English
Publishing date	2021-04-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27930
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito