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  1. 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

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    Zs.A 3139: Show issues Location:
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  2. Article: Metabolic Response to Everolimus in Patient-Derived Triple-Negative Breast Cancer Xenografts

    Euceda, Leslie R / Hill Deborah K / Stokke Endre / Hatem Rana / El Botty Rania / Bièche Ivan / Marangoni Elisabetta / Bathen Tone F / Moestue Siver A

    Journal of Proteome Research. 2017 May 05, v. 16, no. 5

    2017  

    Abstract: Patients with triple-negative breast cancer (TNBC) are unresponsive to endocrine and anti-HER2 pharmacotherapy, limiting their therapeutic options to chemotherapy. TNBC is frequently associated with abnormalities in the PI3K/AKT/mTOR signaling pathway; ... ...

    Abstract Patients with triple-negative breast cancer (TNBC) are unresponsive to endocrine and anti-HER2 pharmacotherapy, limiting their therapeutic options to chemotherapy. TNBC is frequently associated with abnormalities in the PI3K/AKT/mTOR signaling pathway; drugs targeting this pathway are currently being evaluated in these patients. However, the response is variable, partly due to heterogeneity within TNBC, conferring a need to identify biomarkers predicting response and resistance to targeted therapy. In this study, we used a metabolomics approach to assess response to the mTOR inhibitor everolimus in a panel of TNBC patient-derived xenografts (PDX) (n = 103 animals). Tumor metabolic profiles were acquired using high-resolution magic angle spinning magnetic resonance spectroscopy. Partial least-squares-discriminant analysis on relative metabolite concentrations discriminated treated xenografts from untreated controls with an accuracy of 67% (p = 0.003). Multilevel linear mixed-effects models (LMM) indicated reduced glycolytic lactate production and glutaminolysis after treatment, consistent with PI3K/AKT/mTOR pathway inhibition. Although inherent metabolic heterogeneity between different PDX models seemed to hinder prediction of treatment response, the metabolic effects following treatment were more pronounced in responding xenografts compared to nonresponders. Additionally, the metabolic information predicted p53 mutation status, which may provide complementary insight into the interplay between PI3K signaling and other drivers of disease progression.
    Keywords animals ; biochemical pathways ; biomarkers ; breast neoplasms ; disease course ; drug therapy ; drugs ; glycolysis ; lactic acid ; magnetism ; metabolites ; metabolomics ; models ; mutation ; patients ; phosphatidylinositol 3-kinase ; prediction ; proteome ; signal transduction ; spectroscopy
    Language English
    Dates of publication 2017-0505
    Size p. 1868-1879.
    Publishing place American Chemical Society
    Document type Article
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021%2Facs.jproteome.6b00918
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Rare overexpression of anaplastic lymphoma kinase gene in inflammatory and non-inflammatory breast cancer.

    Lerebours, Florence / Callens, Céline / Vacher, Sophie / Hatem, Rana / Guinebretière, Jean-Marc / Bièche, Ivan

    European journal of cancer (Oxford, England : 1990)

    2013  Volume 49, Issue 12, Page(s) 2774–2776

    MeSH term(s) Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Inflammatory Breast Neoplasms/enzymology ; Inflammatory Breast Neoplasms/genetics ; Inflammatory Breast Neoplasms/pathology ; Receptor Protein-Tyrosine Kinases/genetics ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; anaplastic lymphoma kinase (EC 2.7.10.1)
    Language English
    Publishing date 2013-08
    Publishing country England
    Document type Letter
    ZDB-ID 82061-1
    ISSN 1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
    ISSN (online) 1879-0852
    ISSN 0277-5379 ; 0959-8049 ; 0964-1947
    DOI 10.1016/j.ejca.2013.04.010
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  4. Article ; Online: Metabolic Response to Everolimus in Patient-Derived Triple-Negative Breast Cancer Xenografts.

    Euceda, Leslie R / Hill, Deborah K / Stokke, Endre / Hatem, Rana / El Botty, Rania / Bièche, Ivan / Marangoni, Elisabetta / Bathen, Tone F / Moestue, Siver A

    Journal of proteome research

    2017  Volume 16, Issue 5, Page(s) 1868–1879

    Abstract: Patients with triple-negative breast cancer (TNBC) are unresponsive to endocrine and anti-HER2 pharmacotherapy, limiting their therapeutic options to chemotherapy. TNBC is frequently associated with abnormalities in the PI3K/AKT/mTOR signaling pathway; ... ...

    Abstract Patients with triple-negative breast cancer (TNBC) are unresponsive to endocrine and anti-HER2 pharmacotherapy, limiting their therapeutic options to chemotherapy. TNBC is frequently associated with abnormalities in the PI3K/AKT/mTOR signaling pathway; drugs targeting this pathway are currently being evaluated in these patients. However, the response is variable, partly due to heterogeneity within TNBC, conferring a need to identify biomarkers predicting response and resistance to targeted therapy. In this study, we used a metabolomics approach to assess response to the mTOR inhibitor everolimus in a panel of TNBC patient-derived xenografts (PDX) (n = 103 animals). Tumor metabolic profiles were acquired using high-resolution magic angle spinning magnetic resonance spectroscopy. Partial least-squares-discriminant analysis on relative metabolite concentrations discriminated treated xenografts from untreated controls with an accuracy of 67% (p = 0.003). Multilevel linear mixed-effects models (LMM) indicated reduced glycolytic lactate production and glutaminolysis after treatment, consistent with PI3K/AKT/mTOR pathway inhibition. Although inherent metabolic heterogeneity between different PDX models seemed to hinder prediction of treatment response, the metabolic effects following treatment were more pronounced in responding xenografts compared to nonresponders. Additionally, the metabolic information predicted p53 mutation status, which may provide complementary insight into the interplay between PI3K signaling and other drivers of disease progression.
    Language English
    Publishing date 2017-05-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021/acs.jproteome.6b00918
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Inhibition of mTOR downregulates expression of DNA repair proteins and is highly efficient against BRCA2-mutated breast cancer in combination to PARP inhibition.

    El Botty, Rania / Coussy, Florence / Hatem, Rana / Assayag, Franck / Chateau-Joubert, Sophie / Servely, Jean-Luc / Leboucher, Sophie / Fouillade, Charles / Vacher, Sophie / Ouine, Bérengère / Cartier, Aurélie / de Koning, Leanne / Cottu, Paul / Bièche, Ivan / Marangoni, Elisabetta

    Oncotarget

    2018  Volume 9, Issue 51, Page(s) 29587–29600

    Abstract: Breast cancer is a complex disease in which each patient could present several genetic alterations that are therapeutically relevant in cancers. Here we explored the therapeutic benefit of combining PARP and mTOR inhibitors in a context of DNA repair ... ...

    Abstract Breast cancer is a complex disease in which each patient could present several genetic alterations that are therapeutically relevant in cancers. Here we explored the therapeutic benefit of combining PARP and mTOR inhibitors in a context of DNA repair deficiency and PI3K pathway activation. The combination of everolimus and olaparib was tested in BRCA2-mutated patient-derived xenografts (PDX) carrying alterations in the PI3K/AKT/mTOR pathway. An RPPA analysis of different signalling pathways was performed in untreated and treated xenografts. Everolimus and olaparib showed marked anti-tumor activities in the monotherapy setting and high efficacy when given in combination with 100% of mice showing tumor regressions. The fraction of P-H2AX positive cells was increased in both monotherapy arms and strongly increased in the combination setting. Everolimus given as monotherapy resulted in downregulation of different proteins involved in DNA damage repair, including FANCD2, RAD50 and SUV39H1. In the combination setting, expression of these proteins was almost completely abolished, suggesting convergence of PARP and mTOR in downregulation of DNA damage repair components. In conclusion, our results suggest that combining mTOR and DNA repair inhibition could be a successful strategy to treat a subset of breast cancer with BRCA2 mutation and alterations in the PI3K/AKT/mTOR pathway.
    Language English
    Publishing date 2018-07-03
    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.25640
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Prognostic value of a newly identified MALAT1 alternatively spliced transcript in breast cancer.

    Meseure, Didier / Vacher, Sophie / Lallemand, François / Alsibai, Kinan Drak / Hatem, Rana / Chemlali, Walid / Nicolas, Andre / De Koning, Leanne / Pasmant, Eric / Callens, Celine / Lidereau, Rosette / Morillon, Antonin / Bieche, Ivan

    British journal of cancer

    2016  Volume 114, Issue 12, Page(s) 1395–1404

    Abstract: Background: Epigenetic deregulation is considered as a new hallmark of cancer. The long non-coding RNA MALAT1 has been implicated in several cancers; however, its role in breast cancer is still little known.: Methods: We used RT-PCR, in situ ... ...

    Abstract Background: Epigenetic deregulation is considered as a new hallmark of cancer. The long non-coding RNA MALAT1 has been implicated in several cancers; however, its role in breast cancer is still little known.
    Methods: We used RT-PCR, in situ hybridisation, and RPPA methods to quantify (i) the full-length (FL) and an alternatively spliced variant (Δsv) of MALAT1, and (ii) a panel of transcripts and proteins involved in MALAT1 pathways, in a large series of breast tumours from patients with known clinical/pathological status and long-term outcome.
    Results: MALAT1 was overexpressed in 14% (63/446) of the breast tumours. MALAT1-overexpressed tumour epithelial cells showed marked diffuse nuclear signals and numerous huge nuclear speckles. Screening of the dbEST database led to the identification of Δsv-MALAT1, a major alternatively spliced MALAT1 transcript, with a very different expression pattern compared with FL-MALAT1. This alternative Δsv-MALAT1 transcript was mainly underexpressed (18.8%) in our breast tumour series. Multivariate analysis showed that alternative Δsv-MALAT1 transcript is an independent prognostic factor. Δsv-MALAT1 expression was associated with alterations of the pre-mRNAs alternative splicing machinery, and of the Drosha-DGCR8 complex required for non-coding RNA biogenesis. Alternative Δsv-MALAT1 transcript expression was associated to YAP protein status and with an activation of the PI3K-AKT pathway.
    Conclusions: Our results reveal a complex expression pattern of various MALAT1 transcript variants in breast tumours, and suggest that this pattern of expressions should be taken into account to evaluate MALAT1 as predictive biomarker and therapeutic target.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Alternative Splicing ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Proliferation/genetics ; Epigenomics ; Female ; Humans ; Middle Aged ; Prognosis ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
    Chemical Substances CDKN2B antisense RNA, human ; HOTAIR long untranslated RNA, human ; MALAT1 long non-coding RNA, human ; RNA, Long Noncoding ; RNA, Messenger
    Language English
    Publishing date 2016-05-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/bjc.2016.123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Vandetanib as a potential new treatment for estrogen receptor-negative breast cancers.

    Hatem, Rana / Labiod, Dalila / Château-Joubert, Sophie / de Plater, Ludmilla / El Botty, Rania / Vacher, Sophie / Bonin, Florian / Servely, Jean-Luc / Dieras, Véronique / Bièche, Ivan / Marangoni, Elisabetta

    International journal of cancer

    2016  Volume 138, Issue 10, Page(s) 2510–2521

    Abstract: The receptor tyrosine kinase RET is implicated in the progression of luminal breast cancers (BC) but its role in estrogen receptor (ER) negative tumors is unknown. Here we investigated the expression of RET in breast cancer patients tumors and patient- ... ...

    Abstract The receptor tyrosine kinase RET is implicated in the progression of luminal breast cancers (BC) but its role in estrogen receptor (ER) negative tumors is unknown. Here we investigated the expression of RET in breast cancer patients tumors and patient-derived xenografts (PDX) and evaluated the therapeutic potential of Vandetanib, a tyrosin kinase inhibitor with strong activity against RET, EGFR and VEGFR2, in ER negative breast cancer PDX. The RT-PCR analysis of RET expression in breast tumors of 446 patients and 57 PDX, showed elevated levels of RET in ER+ and HER2+ subtypes and in a small subgroup of triple-negative breast cancers (TNBC). The activity of Vandetanib was tested in vivo in three PDX models of TNBC and one model of HER2+ BC with different expression levels of RET and EGFR. Vandetanib induced tumor regression in PDX models with high expression of RET or EGFR. The effect was associated with inhibition of RET/EGFR phosphorylation and MAP kinase pathway and increased necrosis. In a PDX model with no expression of RET nor EGFR, Vandetanib slowed tumor growth without inducing tumor regression. In addition, treatment by Vandetanib decreased expression of murine Vegf receptors and the endothelial marker Cd31 in the four PDX models tested, suggesting inhibition of tumor vascularization. In summary, these preclinical results suggest that Vandetanib treatment could be useful for patients with ER negative breast cancers overexpressing Vandetanib's main targets.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Disease Models, Animal ; Female ; Gene Expression ; Humans ; MAP Kinase Signaling System/drug effects ; Mice ; Middle Aged ; Molecular Targeted Therapy ; Neoplasm Grading ; Neoplasm Metastasis ; Neovascularization, Pathologic/drug therapy ; Phosphorylation/drug effects ; Piperidines/pharmacology ; Piperidines/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins c-ret/genetics ; Proto-Oncogene Proteins c-ret/metabolism ; Quinazolines/pharmacology ; Quinazolines/therapeutic use ; RNA, Messenger/genetics ; Receptors, Estrogen/deficiency ; Receptors, Estrogen/metabolism ; Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors ; Receptors, Vascular Endothelial Growth Factor/genetics ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Tumor Burden/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor ; Piperidines ; Protein Kinase Inhibitors ; Quinazolines ; RNA, Messenger ; Receptors, Estrogen ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1) ; vandetanib (YO460OQ37K)
    Language English
    Publishing date 2016-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.29974
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 576: Show issues

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  8. Article ; Online: Targeting mTOR pathway inhibits tumor growth in different molecular subtypes of triple-negative breast cancers.

    Hatem, Rana / El Botty, Rania / Chateau-Joubert, Sophie / Servely, Jean-Luc / Labiod, Dalila / de Plater, Ludmilla / Assayag, Franck / Coussy, Florence / Callens, Céline / Vacher, Sophie / Reyal, Fabien / Cosulich, Sabina / Diéras, Véronique / Bièche, Ivan / Marangoni, Elisabetta

    Oncotarget

    2016  Volume 7, Issue 30, Page(s) 48206–48219

    Abstract: Triple-negative breast cancers (TNBC) are characterized by frequent alterations in the PI3K/AKT/mTOR signaling pathway. In this study, we analyzed PI3K pathway activation in 67 patient-derived xenografts (PDX) of breast cancer and investigated the anti- ... ...

    Abstract Triple-negative breast cancers (TNBC) are characterized by frequent alterations in the PI3K/AKT/mTOR signaling pathway. In this study, we analyzed PI3K pathway activation in 67 patient-derived xenografts (PDX) of breast cancer and investigated the anti-tumor activity of the mTOR inhibitor everolimus in 15 TNBC PDX with different expression and mutational status of PI3K pathway markers. Expression of the tumor suppressors PTEN and INPP4B was lost in 55% and 76% of TNBC PDX, respectively, while mutations in PIK3CA and AKT1 genes were rare. In 7 PDX treatment with everolimus resulted in a tumor growth inhibition higher than 50%, while 8 models were classified as low responder or resistant. Basal-like, LAR (Luminal AR), mesenchymal and HER2-enriched tumors were present in both responder and resistant groups, suggesting that tumor response to everolimus is not restricted to a specific TNBC subtype. Analysis of treated tumors showed a correlation between tumor response and post-treatment phosphorylation of AKT, increased in responder PDX, while PI3K pathway markers at baseline were not sufficient to predict everolimus response. In conclusion, targeting mTOR decreased tumor growth in 7 out of 15 TNBC PDX tested. Response to everolimus occurred in different TNBC subtypes and was associated with post-treatment increase of P-AKT.
    Language English
    Publishing date 2016--26
    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.10195
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  9. Article ; Online: Vasculature analysis of patient derived tumor xenografts using species-specific PCR assays: evidence of tumor endothelial cells and atypical VEGFA-VEGFR1/2 signalings.

    Bieche, Ivan / Vacher, Sophie / Vallerand, David / Richon, Sophie / Hatem, Rana / De Plater, Ludmilla / Dahmani, Ahmed / Némati, Fariba / Angevin, Eric / Marangoni, Elisabetta / Roman-Roman, Sergio / Decaudin, Didier / Dangles-Marie, Virginie

    BMC cancer

    2014  Volume 14, Page(s) 178

    Abstract: Background: Tumor endothelial transdifferentiation and VEGFR1/2 expression by cancer cells have been reported in glioblastoma but remain poorly documented for many other cancer types.: Methods: To characterize vasculature of patient-derived tumor ... ...

    Abstract Background: Tumor endothelial transdifferentiation and VEGFR1/2 expression by cancer cells have been reported in glioblastoma but remain poorly documented for many other cancer types.
    Methods: To characterize vasculature of patient-derived tumor xenografts (PDXs), largely used in preclinical anti-angiogenic assays, we designed here species-specific real-time quantitative RT-PCR assays. Human and mouse PECAM1/CD31, ENG/CD105, FLT1/VEGFR1, KDR/VEGFR2 and VEGFA transcripts were analyzed in a large series of 150 PDXs established from 8 different tumor types (53 colorectal, 14 ovarian, 39 breast and 15 renal cell cancers, 6 small cell and 5 non small cell lung carcinomas, 13 cutaneous melanomas and 5 glioblastomas) and in two bevacizumab-treated non small cell lung carcinomas xenografts.
    Results: As expected, mouse cell proportion in PDXs -evaluated by quantifying expression of the housekeeping gene TBP- correlated with all mouse endothelial markers and human VEGFA RNA levels. More interestingly, we observed human PECAM1/CD31 and ENG/CD105 expression in all tumor types, with higher rate in glioblastoma and renal cancer xenografts. Human VEGFR expression profile varied widely depending on tumor types with particularly high levels of human FLT1/VEGFR1 transcripts in colon cancers and non small cell lung carcinomas, and upper levels of human KDR/VEGFR2 transcripts in non small cell lung carcinomas. Bevacizumab treatment induced significant low expression of mouse Pecam1/Cd31, Eng/Cd105, Flt1/Vegfr1 and Kdr/Vefr2 while the human PECAM1/CD31 and VEGFA were upregulated.
    Conclusions: Taken together, our results strongly suggest existence of human tumor endothelial cells in all tumor types tested and of both stromal and tumoral autocrine VEGFA-VEGFR1/2 signalings. These findings should be considered when evaluating molecular mechanisms of preclinical response and resistance to tumor anti-angiogenic strategies.
    MeSH term(s) Angiogenesis Inhibitors/pharmacology ; Animals ; Antibodies, Monoclonal, Humanized/pharmacology ; Bevacizumab ; Biomarkers, Tumor/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Neoplasms, Experimental/genetics ; Receptors, Vascular Endothelial Growth Factor/genetics ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Xenograft Model Antitumor Assays
    Chemical Substances Angiogenesis Inhibitors ; Antibodies, Monoclonal, Humanized ; Biomarkers, Tumor ; Vascular Endothelial Growth Factor A ; Bevacizumab (2S9ZZM9Q9V) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2014-03-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1471-2407
    ISSN (online) 1471-2407
    DOI 10.1186/1471-2407-14-178
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Acquired resistance to endocrine treatments is associated with tumor-specific molecular changes in patient-derived luminal breast cancer xenografts.

    Cottu, Paul / Bièche, Ivan / Assayag, Franck / El Botty, Rania / Chateau-Joubert, Sophie / Thuleau, Aurélie / Bagarre, Thomas / Albaud, Benoit / Rapinat, Audrey / Gentien, David / de la Grange, Pierre / Sibut, Vonick / Vacher, Sophie / Hatem, Rana / Servely, Jean-Luc / Fontaine, Jean-Jacques / Decaudin, Didier / Pierga, Jean-Yves / Roman-Roman, Sergio /
    Marangoni, Elisabetta

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2014  Volume 20, Issue 16, Page(s) 4314–4325

    Abstract: Purpose: Patients with luminal breast cancer (LBC) often become endocrine resistant over time. We investigated the molecular changes associated with acquired hormonoresistances in patient-derived xenografts of LBC.: Experimental design: Two LBC ... ...

    Abstract Purpose: Patients with luminal breast cancer (LBC) often become endocrine resistant over time. We investigated the molecular changes associated with acquired hormonoresistances in patient-derived xenografts of LBC.
    Experimental design: Two LBC xenografts (HBCx22 and HBCx34) were treated with different endocrine treatments (ET) to obtain xenografts with acquired resistances to tamoxifen (TamR) and ovariectomy (OvaR). PI3K pathway activation was analyzed by Western blot analysis and IHC and responses to ET combined to everolimus were investigated in vivo. Gene expression analyses were performed by RT-PCR and Affymetrix arrays.
    Results: HBCx22 TamR xenograft was cross-resistant to several hormonotherapies, whereas HBCx22 OvaR and HBCx34 TamR exhibited a treatment-specific resistance profile. PI3K pathway was similarly activated in parental and resistant xenografts but the addition of everolimus did not restore the response to tamoxifen in TamR xenografts. In contrast, the combination of fulvestrant and everolimus induced tumor regression in vivo in HBCx34 TamR, where we found a cross-talk between the estrogen receptor (ER) and PI3K pathways. Expression of several ER-controlled genes and ER coregulators was significantly changed in both TamR and OvaR tumors, indicating impaired ER transcriptional activity. Expression changes associated with hormonoresistance were both tumor and treatment specific and were enriched for genes involved in cell growth, cell death, and cell survival.
    Conclusions: PDX models of LBC with acquired resistance to endocrine therapies show a great diversity of resistance phenotype, associated with specific deregulations of ER-mediated gene transcription. These models offer a tool for developing anticancer therapies and to investigate the dynamics of resistance emerging during pharmacologic interventions. Clin Cancer Res; 20(16); 4314-25. ©2014 AACR.
    MeSH term(s) Animals ; Antineoplastic Agents, Hormonal/pharmacology ; Apoptosis/drug effects ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Blotting, Western ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Drug Resistance, Neoplasm ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Immunoenzyme Techniques ; Mice ; Mice, Nude ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tamoxifen/pharmacology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents, Hormonal ; Biomarkers, Tumor ; ESR1 protein, human ; Estrogen Receptor alpha ; RNA, Messenger ; Tamoxifen (094ZI81Y45) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2014-06-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-13-3230
    Database MEDical Literature Analysis and Retrieval System OnLINE

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