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Isidro Machado

Fundación Instituto Valenciano de Oncología

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Antonio Llombart‐Bosch

Universitat de València

Katia Scotlandi

Istituto Ortopedico Rizzoli

José Antonio López‐Guerrero

Universidad de Granada

Antonio Llombart-Bosch

Universitat de València

Hamid Band

University of Nebraska Medical Center

Bhopal Mohapatra

University of Nebraska Medical Center

Donald W. Coulter

University of Nebraska Medical Center

Sameer Mirza

University of Nebraska Medical Center

Gargi Ghosal

University of Nebraska Medical Center

Vimla Band

University of Nebraska Medical Center

Cooperative Institutions

Fundación Instituto Valenciano de Oncología

Centro de Investigación Biomédica en Red de Cáncer

Universitat de València

Instituto de Salud Carlos III

Hospital Universitari i Politècnic La Fe

Hospital Clínico Universitario de Valencia

Universidad Autónoma de Madrid

Memorial Sloan Kettering Cancer Center

Hospital Clínic de Barcelona

Universitat de Barcelona

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415 A Nude-mice Xenotrnotransplant Model for Studying the Early Stages of Tumor Angiogenesis of Human Osteosarcomas

European Journal of Cancer (2012)

José Antonio López‐Guerrero Francisco Giner Isidro Machado Zaida García‐Casado A. Peydo-Olaya

Nude mouse

10.1016/s0959-8049(12)71097-3

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Molecular Diagnosis of Ewing Sarcoma Family of Tumors

Diagnostic Molecular Pathology (2009)

Isidro Machado Rosa Noguera Antonio Pellı́n José Antonio López‐Guerrero Marta Piqueras

To compare the sensitivity and specificity of fluorescence in situ hybridization (FISH) with reverse transcription polymerase chain reaction (RT-PCR) in the diagnosis of Ewing sarcoma family of tumors (ESFTs) and other small round-cell tumors (SRCTs) in formalin-fixed paraffin-embedded tissue assembled in tissue microarrays (TMAs). The second objective is to confirm the value of molecular methods and immunohistochemical (IHC) assays, to perform a differential diagnosis between ESFTs and SRCTs with similar or overlapping morphology.A total of 560 cases were selected for the present study out the 806 cases collected from the PROgnosis and THerapeutic Targets in the Ewing's Family of TumorS project. Case selection bias included only the cases with enough material to enable the TMA construction, as FISH analysis and the majority of IHC studies were performed in TMAs. Histopathologic, IHC, and molecular assays were carried out.Of the 560 total cases, 411 (73.4%) were considered informative (with results by FISH and/or RT-PCR assays). From the informative cases, 382 (92.9%) were diagnosed as ESFT, 23 cases (5.6%) as non-ESFT but with specific diagnosis for another established entity, and 6 cases (1.5%) as small round cell tumors not otherwise specified. Sensitivity and specificity for the FISH assays was 96.3% and 95.2%, respectively, whereas RT-PCR presented a sensitivity of 97.5% and specificity of 92.9%. In concordant cases, both methods showed a sensitivity and specificity of 99.2% and 100%, respectively. Twenty-nine cases (7.1%) initially interpreted at morphologic level as atypical ESFTs were finally reclassified, with the support of molecular methods and IHC, as either non-ESFT with another specific histologic type or as small round cell tumors not otherwise specified.FISH and RT-PCR are ancillary techniques possessing high sensitivity in the diagnosis of ESFT; nevertheless, FISH is more specific than RT-PCR in the diagnosis of formalin-fixed paraffin-embedded tissue. Both methods in combination displayed the highest sensitivity and specificity. The combination of histopathologic, IHC, and molecular findings is the method of choice for the diagnosis of ESFT, as well as for the differential diagnosis with other SRCTs.

Ewing's sarcoma

10.1097/pdm.0b013e3181a06f66

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The utility of SATB2 immunohistochemical expression in distinguishing between osteosarcomas and their malignant bone tumor mimickers, such as Ewing sarcomas and chondrosarcomas

Pathology - Research and Practice (2016)

Isidro Machado Samuel Navarro Piero Picci Antonio Llombart‐Bosch

CD99

Osteoid

Ewing's sarcoma

10.1016/j.prp.2016.06.012

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Figure S4 from USP1 expression driven by EWS::FLI1 transcription factor stabilizes Survivin and mitigates replication stress in Ewing sarcoma

Halle J. Mallard Shibiao Wan Prakriti Nidhi Yvan D. Hanscom-Trofy Bhopal Mohapatra

<p>Figure S4 shows Identification of novel potential USP1 substrates.</p>

Survivin

FLI1

Ewing's sarcoma

Replication

Transcription

10.1158/1541-7786.27035452

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Data from USP1 expression driven by EWS::FLI1 transcription factor stabilizes Survivin and mitigates replication stress in Ewing sarcoma

Halle J. Mallard Shibiao Wan Prakriti Nidhi Yvan D. Hanscom-Trofy Bhopal Mohapatra

<div>Abstract<p>In this study, we identify USP1 as a transcriptional target of EWS::FLI1 and demonstrate the requisite function of USP1 in Ewing sarcoma (EWS) cell survival in response to endogenous replication stress. EWS::FLI1 oncogenic transcription factor drives most Ewing sarcomas, a pediatric bone cancer. EWS cells display elevated levels of R-loops and replication stress. The mechanism by which EWS cells override activation of apoptosis or cellular senescence in response to increased replication stress is not known. We show that USP1 is overexpressed in EWS and EWS::FLI1 regulates USP1 transcript levels. USP1 knockdown or inhibition arrests EWS cell growth and induces cell death by apoptosis. Mechanistically, USP1 regulates Survivin (BIRC5/API4) protein stability and the activation of caspase-9 and caspase-3/7 in response to endogenous replication stress. Notably, USP1 inhibition sensitizes cells to doxorubicin and etoposide treatment. Together, our study demonstrates that USP1 is regulated by EWS::FLI1, the USP1-Survivin axis promotes EWS cell survival, and USP1 inhibition sensitizes cells to standard of care chemotherapy. Implications: High USP1 and replication stress levels driven by EWS::FLI1 transcription factor in Ewing sarcoma are vulnerabilities that can be exploited to improve existing treatment avenues and overcome drug resistance.</p></div>

Survivin

Replication

FLI1

Transcription

10.1158/1541-7786.c.6792154.v3

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Incidence and patterns of phospho insulin growth factor receptor-1 (pIGF-1R) and matrilysin (MMP7) expression in metastatic colorectal cancer (mCRC), and correlation with KRAS status: A prospective evaluation in the PULSE trial—A GEMCAD study.

Journal of Clinical Oncology (2012)

Vicente Alonso Carlos Fernández-Martos Marta Martín Antonieta Salud José Carlos Méndez

e14041 Background: MMP7 can activate IGF-1R by IGF release due to IGFBP degradation. Activation of IGF-1R can contribute to EGFR resistance by transactivation. We previously described that concomitant expression of p-IGF-1R and MMP7 (Double positive; DP), correlates with poor prognosis, in KRAS WT patients (pts) treated with anti-EGFR compounds (Horndler el al, 2011). Therefore we designed a prospective clinical trial to validate DP as a marker of resistance in KRAS WT pts treated in first-line therapy with FOLFOX-6 plus panitumumab. Methods: mCRC pts in the ongoing prospective PULSE trial (NCT0128833) were prospectively evaluated for p-IGF-1R (p-1316), MMP7 expression and KRAS mutational status. Pts defined as DP should express MMP7 (++ or +++ intensity in >66% of tumor cells) and p-IGF-1R (++ or +++ intensity in >66% of tumor cells). KRAS pts with mutations at exon 2 were excluded. The study was designed to include 40 pts in the two groups (DP vs non-DP) to detect a Hazard ratio difference in PFS of <0.5 (DP vs non-DP) with 80% power. Results: From November 2010 to December 2011, 113 consecutive pts were screened from 24 Spanish Institutions. 54 KRAS WT (40 pts non-DP and 14 DP) have been included. The non-DP arm has being recently closed for inclusion, due to pre-planned complete accrual. Among DP pts, 27% were KRAS WT and 30% KRAS mutant; p=0.63. 48% of cases were positive for p-IGF-1R. Phospho-IGF-1R positive cases had different patterns of staining: peri-nuclear in 76%, 11% nuclear and only 13% membrane-apical staining. These patterns do not differ between KRAS WT; (n=70) and KRAS mutant pts (n=43) (p=0.60). Tumors with positive p-IGF-1R expression, independently of the pattern, have higher MMP7 co-expression (59%) compared with negative cases (13%) (p<0.0001). Conclusions: MMP7 contributes to activate IGF-1R pathway in pts with mCRC. Internalization of the activated IGF-1R, could explain in part, the lack of efficacy of IGF-1R inhibitors in mCRC clinical trials.

Panitumumab

Predictive marker

10.1200/jco.2012.30.15_suppl.e14041

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Models of Biobanking and Tissue Preservation: RNA Quality in Archival Samples in Pathology Laboratories and “In VivoBiobanking” by Tumor Xenografts in Nude Mice—Two Models of Quality Assurance in Pathology

Biopreservation and Biobanking (2011)

Giorgio Stanta Serena Bonin Isidro Machado Antonio Llombart‐Bosch

Tissue banks represent essential resources and platforms for biomedical research serving basic, translational, and clinical research projects. In this article, we describe 2 models of biobanking and tissue preservation with different approaches and aims. Archive tissue biobanking is described here as a resource of residual pathology tissues for translational research, which represents the huge clinical heterogeneity. In this context, managing of tissues and RNA quality in archive tissue are discussed. The other model of tissue biobanking is referred to as xenograft tissue banking, which represents an alternative method for obtaining large amounts of tissue, over an indefinite period, in so far as the tumor can be transferred in vivo over generations, maintaining the histological and genetic particularities. A description of the method and examples of the application are given with particular emphasis on sarcomas (Ewing's sarcoma/primitive neuroectodermal sarcoma, synovial sarcomas, and rhabdomyosarcomas) and early stages of tumor angiogenesis in sarcomas.

Tissue bank

Translational Research

Synovial Sarcoma

10.1089/bio.2011.0010

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Figure S4 from USP1 Expression Driven by EWS::FLI1 Transcription Factor Stabilizes Survivin and Mitigates Replication Stress in Ewing Sarcoma

Halle J. Mallard Shibiao Wan Prakriti Nidhi Yvan D. Hanscom-Trofy Bhopal Mohapatra

<p>Figure S4 shows Identification of novel potential USP1 substrates.</p>

Survivin

Replication

Transcription

FLI1

10.1158/1541-7786.24473974.v1

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[Gastric cancer in Venezuela].

M Matos L Anderson M Aparcero Bravo Conde F Rosa María Izu Belloso

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Supplementary Figure Legends from Suppression of Deacetylase SIRT1 Mediates Tumor-Suppressive NOTCH Response and Offers a Novel Treatment Option in Metastatic Ewing Sarcoma

Jozef Ban Dave N.T. Aryee Argyro Fourtouna Wietske van der Ent Max Kauer

<p>Supplementary Figure Legends. Legend for Supplementary Figures S1-S5.</p>

Legend

Ewing's sarcoma

10.1158/0008-5472.22404545

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