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3 results on '"Nuciforo PG"'

1. Targeted multiplex proteomics for molecular prescreening and biomarker discovery in metastatic colorectal cancer

Author

Roberta Fasani, Stefania Landolfi, Sheeno Thyparambil, Fiorella Ruiz-Pace, Fabiola Cecchi, Paolo Nuciforo, Garazi Serna, Elena Elez, José Antonio Jiménez, Rodrigo Dienstmann, Josep Tabernero, Todd Hembrough, Ana Vivancos, [Garazi S, Fasani R, Jimenez J, Nuciforo PG] Grup d’Oncologia Molecular, Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain. [Ruiz-Pace F, Dienstmann R] Grup d’Oncology Data Science (ODysSey), Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain. [Cecchi F, Thyparambil S] NantOmics, LLC, Rockville, MD, USA. [Landolfi S] Servei d’Anatomia Patològica, Vall d'Hebron Hospital Universitari, Barcelona, Spain. Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Madrid, Spain. [Elez E, Tabernero J] Servei de Medicina Oncològica, Vall d'Hebron Hospital Universitari, Barcelona, Spain. [Vivancos, A] Grup de Genòmica del Càncer, Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain, Hospital Universitari Vall d'Hebron, and Vall d'Hebron Barcelona Hospital Campus

Subjects
Male, Proteomics, 0301 basic medicine, Colorectal cancer, Digestive System Diseases::Digestive System Neoplasms::Gastrointestinal Neoplasms::Intestinal Neoplasms::Digestive System Diseases::Digestive System Diseases::Digestive System Diseases::Digestive System Diseases::Colorectal Neoplasms [DISEASES], factores biológicos::biomarcadores::marcadores tumorales [COMPUESTOS QUÍMICOS Y DROGAS], lcsh:Medicine, medicine.disease_cause, Neuroendocrine differentiation, 0302 clinical medicine, Other subheadings::/diagnosis [Other subheadings], Neoplasm Metastasis, Biomarker discovery, lcsh:Science, Multidisciplinary, Molecular medicine, biology, Middle Aged, Prognosis, Phenotype, Colon cancer, Gene Expression Regulation, Neoplastic, Mesothelin, Female, Enfermedades del Sistema Digestivo::Neoplasias del Sistema Digestivo::Neoplasias Gastrointestinales::Neoplasias Intestinales::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Neoplasias Colorrectales [ENFERMEDADES], KRAS, Colorectal Neoplasms, Adult, Otros calificadores::/diagnóstico [Otros calificadores], GPI-Linked Proteins, Predictive markers, Article, Proto-Oncogene Proteins p21(ras), 03 medical and health sciences, medicine, Humans, Biological Factors::Biomarkers::Biomarkers, Tumor [CHEMICALS AND DRUGS], enfermedades del sistema digestivo::neoplasias del sistema digestivo::neoplasias gastrointestinales::neoplasias intestinales::enfermedades del sistema digestivo::enfermedades del sistema digestivo::enfermedades del sistema digestivo::enfermedades del sistema digestivo::neoplasias colorrectales [ENFERMEDADES], Aged, business.industry, Marcadors tumorals, lcsh:R, PTEN Phosphohydrolase, Cancer, medicine.disease, Survival Analysis, 030104 developmental biology, Mutation, biology.protein, Cancer research, Còlon - Càncer - Diagnòstic, lcsh:Q, business, Biomarkers, 030217 neurology & neurosurgery
Abstract

Biomarcadores del cáncer; Cáncer metástico colorrectal; Terapias experimentales Cancer biomarkers; Colorectal metastatic cancer; Experimental therapies Biomarcadors del càncer; Càncer metastàtic colorrectal; Teràpies experimentals Protein biomarkers are widely used in cancer diagnosis, prognosis, and prediction of treatment response. Here we introduce the use of targeted multiplex proteomics (TMP) as a tool to simultaneously measure a panel of 54 proteins involved in oncogenic, tumour suppression, drug metabolism and resistance, in patients with metastatic colorectal cancer (mCRC). TMP provided valuable diagnostic information by unmasking an occult neuroendocrine differentiation and identifying a misclassified case based on abnormal proteins phenotype. No significant differences in protein levels between unpaired primary and metastatic samples were observed. Four proteins were found differentially expressed in KRAS-mutant as compared to wild-type tumours (overexpressed in mutant: KRAS, EGFR; overexpressed in wild-type: TOPO1, TOP2A). Survival analyses revealed the association between mesothelin expression and poor overall survival, whereas lack of PTEN protein expression associated with lower progression-free survival with anti-EGFR-based therapy in the first-line setting for patients with RAS wild-type tumour. Finally, outlier analysis identified putative targetable proteins in 65% of patients lacking a targetable genomic alteration. Our data show that TMP constitutes a promising, novel molecular prescreening tool in mCRC to identify protein expression alterations that may impact on patient outcomes and more precisely guide patient eligibility to clinical trials with novel targeted experimental therapies.

Published
2019
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2. Targeted multiplex proteomics for molecular prescreening and biomarker discovery in metastatic colorectal cancer

Author

[Garazi S, Fasani R, Jimenez J, Nuciforo PG] Grup d’Oncologia Molecular, Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain. [Ruiz-Pace F, Dienstmann R] Grup d’Oncology Data Science (ODysSey), Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain. [Cecchi F, Thyparambil S] NantOmics, LLC, Rockville, MD, USA. [Landolfi S] Servei d’Anatomia Patològica, Vall d'Hebron Hospital Universitari, Barcelona, Spain. Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Madrid, Spain. [Elez E, Tabernero J] Servei de Medicina Oncològica, Vall d'Hebron Hospital Universitari, Barcelona, Spain. [Vivancos, A] Grup de Genòmica del Càncer, Vall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain and Hospital Universitari Vall d'Hebron

Subjects
Marcadors tumorals, Digestive System Diseases::Digestive System Neoplasms::Gastrointestinal Neoplasms::Intestinal Neoplasms::Digestive System Diseases::Digestive System Diseases::Digestive System Diseases::Digestive System Diseases::Colorectal Neoplasms [DISEASES], Còlon - Càncer - Diagnòstic, Other subheadings::/diagnosis [Other subheadings], Otros calificadores::/diagnóstico [Otros calificadores], factores biológicos::biomarcadores::marcadores tumorales [COMPUESTOS QUÍMICOS Y DROGAS], Enfermedades del Sistema Digestivo::Neoplasias del Sistema Digestivo::Neoplasias Gastrointestinales::Neoplasias Intestinales::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Enfermedades del Sistema Digestivo::Neoplasias Colorrectales [ENFERMEDADES], Biological Factors::Biomarkers::Biomarkers, Tumor [CHEMICALS AND DRUGS]
Published
2021

3. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication.

Author

Di Micco R, Fumagalli M, Cicalese A, Piccinin S, Gasparini P, Luise C, Schurra C, Garre' M, Nuciforo PG, Bensimon A, Maestro R, Pelicci PG, and d'Adda di Fagagna F

Subjects
Animals, Cell Proliferation, Cell Transformation, Neoplastic genetics, Cells, Cultured, Genetic Markers, Humans, Mice, Cellular Senescence genetics, DNA Replication, Genes, ras
Abstract

Early tumorigenesis is associated with the engagement of the DNA-damage checkpoint response (DDR). Cell proliferation and transformation induced by oncogene activation are restrained by cellular senescence. It is unclear whether DDR activation and oncogene-induced senescence (OIS) are causally linked. Here we show that senescence, triggered by the expression of an activated oncogene (H-RasV12) in normal human cells, is a consequence of the activation of a robust DDR. Experimental inactivation of DDR abrogates OIS and promotes cell transformation. DDR and OIS are established after a hyper-replicative phase occurring immediately after oncogene expression. Senescent cells arrest with partly replicated DNA and with DNA replication origins having fired multiple times. In vivo DNA labelling and molecular DNA combing reveal that oncogene activation leads to augmented numbers of active replicons and to alterations in DNA replication fork progression. We also show that oncogene expression does not trigger a DDR in the absence of DNA replication. Last, we show that oncogene activation is associated with DDR activation in a mouse model in vivo. We propose that OIS results from the enforcement of a DDR triggered by oncogene-induced DNA hyper-replication.

Published
2006
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