References of "Hubert, Pascale"
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See detailTreatment algorithm and prognostic factors for patients with stage I–III carcinoma of the anal canal: a 20-year multicenter study
Bruyère, Diane ULiege; Monnien, Franck; Colpart, Prudence et al

in Modern Pathology (in press)

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See detailTGFα Promotes Chemoresistance of Malignant Pleural Mesothelioma
Staumont, Bernard ULiege; Jamakhani, Majeed ULiege; Costa, Chrisostome et al

in Cancers (2020), 12(6), 1484

Background: There is no standard chemotherapy for refractory or relapsing malignant pleural mesothelioma (MPM). Our previous reports nevertheless indicated that a combination of an anthracycline ... [more ▼]

Background: There is no standard chemotherapy for refractory or relapsing malignant pleural mesothelioma (MPM). Our previous reports nevertheless indicated that a combination of an anthracycline (doxorubicin) and a lysine deacetylase inhibitor (valproic acid, VPA) synergize to induce the apoptosis of MPM cells and reduce tumor growth in mouse models. A Phase I/II clinical trial indicated that this regimen is a promising therapeutic option for a proportion of MPM patients. Methods: The transcriptomes of mesothelioma cells were compared after Illumina HiSeq 4000 sequencing. The expression of differentially expressed genes was inhibited by RNA interference. Apoptosis was determined by cell cycle analysis and Annexin V/7-AAD labeling. Protein expression was assessed by immunoblotting. Preclinical efficacy was evaluated in BALB/c and NOD-SCID mice. Results: To understand the mechanisms involved in chemoresistance, the transcriptomes of two MPM cell lines displaying different responses to VPA-doxorubicin were compared. Among the differentially expressed genes, transforming growth factor alpha (TGFα) was associated with resistance to this regimen. The silencing of TGFα by RNA interference correlated with a significant increase in apoptosis, whereas the overexpression of TGFα desensitized MPM cells to the apoptosis induced by VPA and doxorubicin. The multi-targeted inhibition of histone deacetylase (HDAC), HER2 and TGFα receptor (epidermal growth factor receptor/EGFR) improved treatment efficacy in vitro and reduced tumor growth in two MPM mouse models. Finally, TGFα expression but not EGFR correlated with patient survival. Conclusions: Our data show that TGFα but not its receptor EGFR is a key factor in resistance to MPM chemotherapy. This observation may contribute to casting light on the promising but still controversial role of EGFR signaling in MPM therapy. [less ▲]

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See detailMethylglyoxal stress contributes to immunosuppression in breast cancer
Wissocq, Tom ULiege; Hubert, Pascale ULiege; Caprasse, Maurine ULiege et al

Poster (2020, February 07)

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See detailDeciphering the radiosensitivity of HPV-positive tumors
Bruyère, Diane ULiege; Lebeau, Alizée ULiege; RONCARATI, Patrick ULiege et al

Poster (2018, May 30)

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be ... [more ▼]

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be elucidated. A few hypotheses have been suggested regarding this differential radiosensitivity like, for example, an altered microtumoral environment or virus-host protein interactions. In this study, we focused on interactions between DNA repair proteins and virus oncoproteins. A large panel of 147 proteins implicated in DNA repair pathways was tested for potential interaction with HPV16 E6 and/or E7 oncoproteins using the GPCA method (Gaussia Princeps Complementation Assay). The proteins highlighted by the screening were validated by co-IP. The functional experiments, realized on HPV negative head and neck cancer (UPCI-SCC-111, FaDu, UPCI-SCC-40), vulva cancer (C33a) and control keratinocytes (HaCaT) stably transduced with E6 and/or E7, are in progress. [less ▲]

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See detailDeciphering the radiosensitivity of HPV-positive tumors
Bruyère, Diane ULiege; Lebeau, Alizée ULiege; RONCARATI, Patrick ULiege et al

Poster (2018, May 28)

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be ... [more ▼]

The increased radiosensitivity of HPV positive tumors (compared to HPV negative ones) is widely known in clinical settings. However, the mechanisms by which this phenomenon occurs are still to be elucidated. A few hypotheses have been suggested regarding this differential radiosensitivity like, for example, an altered microtumoral environment or virus-host protein interactions. In this study, we focused on interactions between DNA repair proteins and virus oncoproteins. A large panel of 147 proteins implicated in DNA repair pathways was tested for potential interaction with HPV16 E6 and/or E7 oncoproteins using the GPCA method (Gaussia Princeps Complementation Assay). The proteins highlighted by the screening were validated by co-IP. The functional experiments, realized on HPV negative head and neck cancer (UPCI-SCC-111, FaDu, UPCI-SCC-40), vulva cancer (C33a) and control keratinocytes (HaCaT) stably transduced with E6 and/or E7, are in progress. [less ▲]

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See detailImmunity drives TET1 regulation in cancer through NF-kappaB.
Collignon, Evelyne; Canale, Annalisa ULiege; Al Wardi, Clemence et al

in Science Advances (2018), 4(6), 7309

Ten-eleven translocation enzymes (TET1, TET2, and TET3), which induce DNA demethylation and gene regulation by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), are often down-regulated ... [more ▼]

Ten-eleven translocation enzymes (TET1, TET2, and TET3), which induce DNA demethylation and gene regulation by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), are often down-regulated in cancer. We uncover, in basal-like breast cancer (BLBC), genome-wide 5hmC changes related to TET1 regulation. We further demonstrate that TET1 repression is associated with high expression of immune markers and high infiltration by immune cells. We identify in BLBC tissues an anticorrelation between TET1 expression and the major immunoregulator family nuclear factor kappaB (NF-kappaB). In vitro and in mice, TET1 is down-regulated in breast cancer cells upon NF-kappaB activation through binding of p65 to its consensus sequence in the TET1 promoter. We lastly show that these findings extend to other cancer types, including melanoma, lung, and thyroid cancers. Together, our data suggest a novel mode of regulation for TET1 in cancer and highlight a new paradigm in which the immune system can influence cancer cell epigenetics. [less ▲]

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See detailPromoting vaginal distribution of two active siRNA-complexed in liposomes for cervical cancer treatment
Lechanteur, Anna ULiege; Furst, Tania; Delvenne, Philippe ULiege et al

Conference (2017, December 07)

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See detailPromoting vaginal distribution of two active siRNA-complexed in liposomes for cervical cancer treatment
Lechanteur, Anna ULiege; Furst, Tania; Delvenne, Philippe ULiege et al

Conference (2017, December 05)

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See detailPromoting vaginal distribution of two active siRNA-complexed in liposomes for cervical cancer treatment
Lechanteur, Anna ULiege; Furst Tania; Evrard, Brigitte ULiege et al

Conference (2017, April 25)

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See detailPromoting vaginal distribution of E7 and MCL-1 siRNA-silencing nanoparticles for cervical cancer treatment
Lechanteur, Anna ULiege; Furst, Tania; Delvenne, Philippe ULiege et al

in Molecular Pharmaceutics (2017)

Detailed reference viewed: 35 (14 ULiège)