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  1. Article ; Online: Using Machine Learning to Predict TP53 Mutation Status and Aggressiveness of Prostate Cancer from Routine Histology Images.

    Bordeleau, François

    Cancer research

    2023  Volume 83, Issue 17, Page(s) 2809–2810

    Abstract: Despite years of progress, we still lack reliable tools to predict the aggressiveness of tumors, including in the case of prostate cancer. Biomarkers have been developed, but they often suffer from poor accuracy if used alone due to tumor heterogeneity. ... ...

    Abstract Despite years of progress, we still lack reliable tools to predict the aggressiveness of tumors, including in the case of prostate cancer. Biomarkers have been developed, but they often suffer from poor accuracy if used alone due to tumor heterogeneity. Nevertheless, some mutations, notably TP53 mutations, are highly correlated with progression. In their work in this issue of Cancer Research, Pizurica and colleagues implemented a machine learning-based model applied to routine histology and trained with prior information on TP53 mutation status. Their model output provides a quantitative prediction of TP53 mutation status while having a strong correlation with aggressiveness, showing promise as a prognostic in silico biomarker. See related article by Pizurica et al., p. 2970.
    MeSH term(s) Male ; Humans ; Tumor Suppressor Protein p53/genetics ; Prognosis ; Disease-Free Survival ; Mutation ; Phenotype ; Prostatic Neoplasms/genetics
    Chemical Substances Tumor Suppressor Protein p53 ; TP53 protein, human
    Language English
    Publishing date 2023-08-31
    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-23-1856
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Recreating heterogeneity of bladder cancer microenvironment to study its recurrences and progression.

    Bordeleau, François / Brownell, David / Chabaud, Stephane / Huot, Marc-Etienne / Bolduc, Stephane

    Stem cell investigation

    2023  Volume 10, Page(s) 5

    Language English
    Publishing date 2023-03-07
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2884645-X
    ISSN 2313-0792 ; 2306-9759
    ISSN (online) 2313-0792
    ISSN 2306-9759
    DOI 10.21037/sci-2023-004
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  3. Article: The Extracellular Matrix Stiffening: A Trigger of Prostate Cancer Progression and Castration Resistance?

    Luthold, Carole / Hallal, Tarek / Labbé, David P / Bordeleau, François

    Cancers

    2022  Volume 14, Issue 12

    Abstract: Despite advancements made in diagnosis and treatment, prostate cancer remains the second most diagnosed cancer among men worldwide in 2020, and the first in North America and Europe. Patients with localized disease usually respond well to first-line ... ...

    Abstract Despite advancements made in diagnosis and treatment, prostate cancer remains the second most diagnosed cancer among men worldwide in 2020, and the first in North America and Europe. Patients with localized disease usually respond well to first-line treatments, however, up to 30% develop castration-resistant prostate cancer (CRPC), which is often metastatic, making this stage of the disease incurable and ultimately fatal. Over the last years, interest has grown into the extracellular matrix (ECM) stiffening as an important mediator of diseases, including cancers. While this process is increasingly well-characterized in breast cancer, a similar in-depth look at ECM stiffening remains lacking for prostate cancer. In this review, we scrutinize the current state of literature regarding ECM stiffening in prostate cancer and its potential association with disease progression and castration resistance.
    Language English
    Publishing date 2022-06-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14122887
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  4. Article ; Online: Use of Electronic Medical Record Data to Create a Dashboard on Access to Primary Care.

    Breton, Mylaine / Gaboury, Isabelle / Bordeleau, François / Lamoureux-Lamarche, Catherine / Martin, Élisabeth / Deslauriers, Véronique / Deville-Stoetzel, Jean-Benoît

    Healthcare policy = Politiques de sante

    2023  Volume 18, Issue 4, Page(s) 72–88

    Abstract: Objective: This study aims to present a proof of concept of a dashboard on a set of indicators of access to primary healthcare (PHC) based on electronic medical records (EMRs).: Methods: This research builds on a multi-method design study including ( ... ...

    Abstract Objective: This study aims to present a proof of concept of a dashboard on a set of indicators of access to primary healthcare (PHC) based on electronic medical records (EMRs).
    Methods: This research builds on a multi-method design study including (1) a systematic review, (2) a pilot phase and (3) the development of a dashboard.
    Results: Eight indicators were carefully selected and successfully extracted from EMRs obtained from 151 PHC providers. Indicators of access over time, as well as among providers and among clinics, have been enabled in the dashboard.
    Conclusion: EMR data enabled the development of a real-time dashboard on access, giving PHC providers a reliable portrait of their own practice, its evolution over time and how it compares with those of their peers.
    MeSH term(s) Humans ; Electronic Health Records ; Access to Primary Care ; Health Personnel ; Primary Health Care
    Language English
    Publishing date 2023-07-24
    Publishing country Canada
    Document type Systematic Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1715-6580
    ISSN (online) 1715-6580
    DOI 10.12927/hcpol.2023.27092
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  5. Article ; Online: Coordination of non-professional efferocytosis and actomyosin contractility during epithelial tissue morphogenesis.

    Tang, You Chi / Ponsin, Khoren / Graham-Paquin, Adda-Lee / Luthold, Carole / Homsy, Kevin / Schindler, Magdalena / Tran, Viviane / Côté, Jean-François / Bordeleau, François / Khadra, Anmar / Bouchard, Maxime

    Cell reports

    2023  Volume 42, Issue 3, Page(s) 112202

    Abstract: In developing embryos, specific cell populations are often removed to remodel tissue architecture for organogenesis. During urinary tract development, an epithelial duct called the common nephric duct (CND) gets shortened and eventually eliminated to ... ...

    Abstract In developing embryos, specific cell populations are often removed to remodel tissue architecture for organogenesis. During urinary tract development, an epithelial duct called the common nephric duct (CND) gets shortened and eventually eliminated to remodel the entry point of the ureter into the bladder. Here we show that non-professional efferocytosis (the process in which epithelial cells engulf apoptotic bodies) is the main mechanism that contributes to CND shortening. Combining biological metrics and computational modeling, we show that efferocytosis with actomyosin contractility are essential factors that drive the CND shortening without compromising the ureter-bladder structural connection. The disruption of either apoptosis, non-professional efferocytosis, or actomyosin results in contractile tension reduction and deficient CND shortening. Actomyosin activity helps to maintain tissue architecture while non-professional efferocytosis removes cellular volume. Together our results demonstrate that non-professional efferocytosis with actomyosin contractility are important morphogenetic factors controlling CND morphogenesis.
    MeSH term(s) Actomyosin ; Epithelial Cells ; Phagocytosis ; Epithelium ; Morphogenesis
    Chemical Substances Actomyosin (9013-26-7)
    Language English
    Publishing date 2023-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112202
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  6. Article ; Online: Coordination of non-professional efferocytosis and actomyosin contractility during epithelial tissue morphogenesis

    You Chi Tang / Khoren Ponsin / Adda-Lee Graham-Paquin / Carole Luthold / Kevin Homsy / Magdalena Schindler / Viviane Tran / Jean-François Côté / François Bordeleau / Anmar Khadra / Maxime Bouchard

    Cell Reports, Vol 42, Iss 3, Pp 112202- (2023)

    2023  

    Abstract: Summary: In developing embryos, specific cell populations are often removed to remodel tissue architecture for organogenesis. During urinary tract development, an epithelial duct called the common nephric duct (CND) gets shortened and eventually ... ...

    Abstract Summary: In developing embryos, specific cell populations are often removed to remodel tissue architecture for organogenesis. During urinary tract development, an epithelial duct called the common nephric duct (CND) gets shortened and eventually eliminated to remodel the entry point of the ureter into the bladder. Here we show that non-professional efferocytosis (the process in which epithelial cells engulf apoptotic bodies) is the main mechanism that contributes to CND shortening. Combining biological metrics and computational modeling, we show that efferocytosis with actomyosin contractility are essential factors that drive the CND shortening without compromising the ureter-bladder structural connection. The disruption of either apoptosis, non-professional efferocytosis, or actomyosin results in contractile tension reduction and deficient CND shortening. Actomyosin activity helps to maintain tissue architecture while non-professional efferocytosis removes cellular volume. Together our results demonstrate that non-professional efferocytosis with actomyosin contractility are important morphogenetic factors controlling CND morphogenesis.
    Keywords CP: Cell biology ; CP: Developmental biology ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: Cancer-Associated Fibroblasts in a 3D Engineered Tissue Model Induce Tumor-like Matrix Stiffening and EMT Transition.

    Millet, Martial / Bollmann, Enola / Ringuette Goulet, Cassandra / Bernard, Geneviève / Chabaud, Stéphane / Huot, Marc-Étienne / Pouliot, Frédéric / Bolduc, Stéphane / Bordeleau, François

    Cancers

    2022  Volume 14, Issue 15

    Abstract: A tumor microenvironment is characterized by its altered mechanical properties. However, most models remain unable to faithfully recreate the mechanical properties of a tumor. Engineered models based on the self-assembly method have the potential to ... ...

    Abstract A tumor microenvironment is characterized by its altered mechanical properties. However, most models remain unable to faithfully recreate the mechanical properties of a tumor. Engineered models based on the self-assembly method have the potential to better recapitulate the stroma architecture and composition. Here, we used the self-assembly method based on a bladder tissue model to engineer a tumor-like environment. The tissue-engineered tumor models were reconstituted from stroma-derived healthy primary fibroblasts (HFs) induced into cancer-associated fibroblast cells (iCAFs) along with an urothelium overlay. The iCAFs-derived extracellular matrix (ECM) composition was found to be stiffer, with increased ECM deposition and remodeling. The urothelial cells overlaid on the iCAFs-derived ECM were more contractile, as measured by quantitative polarization microscopy, and displayed increased YAP nuclear translocation. We further showed that the proliferation and expression of epithelial-to-mesenchymal transition (EMT) marker in the urothelial cells correlate with the increased stiffness of the iCAFs-derived ECM. Our data showed an increased expression of EMT markers within the urothelium on the iCAFs-derived ECM. Together, our results demonstrate that our tissue-engineered tumor model can achieve stiffness levels comparable to that of a bladder tumor, while triggering a tumor-like response from the urothelium.
    Language English
    Publishing date 2022-08-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14153810
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  8. Article ; Online: Matrix stiffness regulates tumor cell intravasation through expression and ESRP1-mediated alternative splicing of MENA.

    Wang, Wenjun / Taufalele, Paul V / Millet, Martial / Homsy, Kevin / Smart, Kyra / Berestesky, Emily D / Schunk, Curtis T / Rowe, Matthew M / Bordeleau, Francois / Reinhart-King, Cynthia A

    Cell reports

    2023  Volume 42, Issue 4, Page(s) 112338

    Abstract: During intravasation, cancer cells cross the endothelial barrier and enter the circulation. Extracellular matrix stiffening has been correlated with tumor metastatic potential; however, little is known about the effects of matrix stiffness on ... ...

    Abstract During intravasation, cancer cells cross the endothelial barrier and enter the circulation. Extracellular matrix stiffening has been correlated with tumor metastatic potential; however, little is known about the effects of matrix stiffness on intravasation. Here, we utilize in vitro systems, a mouse model, specimens from patients with breast cancer, and RNA expression profiles from The Cancer Genome Atlas Program (TCGA) to investigate the molecular mechanism by which matrix stiffening promotes tumor cell intravasation. Our data show that heightened matrix stiffness increases MENA expression, which promotes contractility and intravasation through focal adhesion kinase activity. Further, matrix stiffening decreases epithelial splicing regulatory protein 1 (ESRP1) expression, which triggers alternative splicing of MENA, decreases the expression of MENA
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Alternative Splicing/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; RNA-Binding Proteins/metabolism
    Chemical Substances ESRP1 protein, human ; ESRP1 protein, mouse ; RNA-Binding Proteins ; Enah protein, human ; Enah protein, mouse
    Language English
    Publishing date 2023-04-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112338
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  9. Article ; Online: Chaperone-Assisted Mitotic Actin Remodeling by BAG3 and HSPB8 Involves the Deacetylase HDAC6 and Its Substrate Cortactin

    Carole Luthold / Alice-Anaïs Varlet / Herman Lambert / François Bordeleau / Josée N. Lavoie

    International Journal of Molecular Sciences, Vol 22, Iss 142, p

    2021  Volume 142

    Abstract: The fidelity of actin dynamics relies on protein quality control, but the underlying molecular mechanisms are poorly defined. During mitosis, the cochaperone BCL2-associated athanogene 3 (BAG3) modulates cell rounding, cortex stability, spindle ... ...

    Abstract The fidelity of actin dynamics relies on protein quality control, but the underlying molecular mechanisms are poorly defined. During mitosis, the cochaperone BCL2-associated athanogene 3 (BAG3) modulates cell rounding, cortex stability, spindle orientation, and chromosome segregation. Mitotic BAG3 shows enhanced interactions with its preferred chaperone partner HSPB8, the autophagic adaptor p62/SQSTM1, and HDAC6, a deacetylase with cytoskeletal substrates. Here, we show that depletion of BAG3, HSPB8, or p62/SQSTM1 can recapitulate the same inhibition of mitotic cell rounding. Moreover, depletion of either of these proteins also interfered with the dynamic of the subcortical actin cloud that contributes to spindle positioning. These phenotypes were corrected by drugs that limit the Arp2/3 complex or HDAC6 activity, arguing for a role for BAG3 in tuning branched actin network assembly. Mechanistically, we found that cortactin acetylation/deacetylation is mitotically regulated and is correlated with a reduced association of cortactin with HDAC6 in situ. Remarkably, BAG3 depletion hindered the mitotic decrease in cortactin–HDAC6 association. Furthermore, expression of an acetyl-mimic cortactin mutant in BAG3-depleted cells normalized mitotic cell rounding and the subcortical actin cloud organization. Together, these results reinforce a BAG3′s function for accurate mitotic actin remodeling, via tuning cortactin and HDAC6 spatial dynamics.
    Keywords BAG3 1 ; HSPB8 2 ; p62/SQSTM1 3 ; HDAC6 4 ; Arp2/3 5 ; cortactin 6 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 612
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article: Coupling Microfluidic Platforms, Microfabrication, and Tissue Engineered Scaffolds to Investigate Tumor Cells Mechanobiology.

    Millet, Martial / Ben Messaoud, Raoua / Luthold, Carole / Bordeleau, Francois

    Micromachines

    2019  Volume 10, Issue 6

    Abstract: The tumor microenvironment (TME) is composed of dynamic and complex networks composed of matrix substrates, extracellular matrix (ECM), non-malignant cells, and tumor cells. The TME is in constant evolution during the disease progression, most notably ... ...

    Abstract The tumor microenvironment (TME) is composed of dynamic and complex networks composed of matrix substrates, extracellular matrix (ECM), non-malignant cells, and tumor cells. The TME is in constant evolution during the disease progression, most notably through gradual stiffening of the stroma. Within the tumor, increased ECM stiffness drives tumor growth and metastatic events. However, classic in vitro strategies to study the TME in cancer lack the complexity to fully replicate the TME. The quest to understand how the mechanical, geometrical, and biochemical environment of cells impacts their behavior and fate has been a major force driving the recent development of new technologies in cell biology research. Despite rapid advances in this field, many challenges remain in order to bridge the gap between the classical culture dish and the biological reality of actual tissue. Microfabrication coupled with microfluidic approaches aim to engineer the actual complexity of the TME. Moreover, TME bioengineering allows artificial modulations with single or multiple cues to study different phenomena occurring in vivo. Some innovative cutting-edge tools and new microfluidic approaches could have an important impact on the fields of biology and medicine by bringing deeper understanding of the TME, cell behavior, and drug effects.
    Language English
    Publishing date 2019-06-22
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2620864-7
    ISSN 2072-666X
    ISSN 2072-666X
    DOI 10.3390/mi10060418
    Database MEDical Literature Analysis and Retrieval System OnLINE

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