Pierre Saintigny
A5065373099- Lung Cancer Treatments and Mutations
- Cancer Genomics and Diagnostics
- Uterine Myomas and Treatments
- Head and Neck Cancer Studies
- RNA modifications and cancer
- Cancer Immunotherapy and Biomarkers
- Lung Cancer Research Studies
- Pancreatic and Hepatic Oncology Research
- Axon Guidance and Neuronal Signaling
- Phagocytosis and Immune Regulation
- Ovarian cancer diagnosis and treatment
- Cancer-related molecular mechanisms research
- Ferroptosis and cancer prognosis
- Cancer Cells and Metastasis
- Cancer, Lipids, and Metabolism
- Hepatocellular Carcinoma Treatment and Prognosis
- Lung Cancer Diagnosis and Treatment
- Peptidase Inhibition and Analysis
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Radiomics and Machine Learning in Medical Imaging
- Cancer-related gene regulation
- Oral Health Pathology and Treatment
- Cancer Mechanisms and Therapy
- Genetic factors in colorectal cancer
- Molecular Biology Techniques and Applications
Centre Léon Bérard
2016-2025
Université Claude Bernard Lyon 1
2016-2025
Centre National de la Recherche Scientifique
2016-2025
Inserm
2016-2025
Centre de Recherche en Cancérologie de Lyon
2016-2025
The University of Texas MD Anderson Cancer Center
2009-2023
Université de Lyon
2023
Immunité et Cancer
2023
Communauté urbaine de Lyon
2021
UniCancer Group
2020
Epithelial-mesenchymal transition (EMT) has been associated with metastatic spread and EGF receptor (EGFR) inhibitor resistance. We developed validated a robust 76-gene EMT signature using gene expression profiles from four platforms non-small cell lung carcinoma (NSCLC) lines patients treated in the Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) study.We conducted an integrated expression, proteomic, drug response analysis tumors NSCLC. A was...
Abstract Small cell lung cancer (SCLC) is an aggressive malignancy distinct from non–small (NSCLC) in its metastatic potential and treatment response. Using integrative proteomic transcriptomic analysis, we investigated molecular differences contributing to the clinical behavior of SCLCs NSCLCs. showed lower levels several receptor tyrosine kinases decreased activation phosphoinositide 3-kinase (PI3K) Ras/mitogen-activated protein (MAP)/extracellular signal–regulated kinase (ERK) (MEK)...
Mutations in the v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) play a critical role cancer cell growth and resistance to therapy. Most mutations occur at codons 12 13. In colorectal cancer, presence of any mutant KRas amino acid substitution is negative predictor patient response targeted However, non–small lung (NSCLC), evidence that KRAS mutation predictive factor conflicting. We used data from molecularly clinical trial for 215 patients with tissues available out 268...
In a review of strategies for preventing oral cancer, an expert panel reports that the use tobacco (both smoking and smokeless), areca nut exposure, heavy alcohol consumption are major contributors to this illness.
Abstract The microRNA-200 (miR-200) family is part of a gene expression signature that predicts poor prognosis in lung cancer patients. In mouse model K-ras/p53-mutant adenocarcinoma, miR-200 levels are suppressed metastasis-prone tumor cells, and forced inhibits growth metastasis, but the target genes drive tumorigenesis have not been fully elucidated. Here, we scanned genome for putative binding sites found them 3′-untranslated region (3′-UTR) 35 amplified human cancer. Mining database...
No study has evaluated the predictive and prognostic role of CD8 PD-L1 coexpression in non-small-cell lung cancer (NSCLC).We analyzed RNA sequencing and/or immunohistochemistry staining NSCLC patients from The Cancer Genome Atlas (n = 1016), 34 metastatic samples not treated by immunotherapy as cohorts. As aspect PD-L1, we used 85 with anti-PD-1. Two validation cohorts were including 44 anti-PD-1 an external cohort different tumor types.In cohorts, high CD8A expression was associated longer...
CXCR2 in non-small cell lung cancer (NSCLC) has been studied mainly stromal cells and is known to increase tumor inflammation angiogenesis. Here, we examined the prognostic importance of NSCLC role its ligands cells. The effect expression on was using stable knockdown clones derived from a murine KRAS/p53-mutant adenocarcinoma line with high metastatic potential an orthotopic syngeneic mouse model vitro small-molecule antagonist (SB225002). protein analyzed 262 NSCLC. Gene profiles for...
Abstract HER2-positive breast cancer has long proven to be a clinically distinct class of cancers for which several targeted therapies are now available. However, resistance the treatment associated with specific gene expressions or mutations been observed, revealing underlying diversity these cancers. Therefore, understanding full extent disease heterogeneity still remains challenging. Here we carry out an in-depth genomic characterization 64 tumour genomes that exhibit four subgroups,...
Abstract Patients with oral premalignant lesion (OPL) have a high risk of developing cancer. Although certain factors, such as smoking status and histology, are known, our ability to predict cancer remains poor. The study objective was determine the value gene expression profiling in predicting development. Gene profile measured 86 162 OPL patients who were enrolled clinical chemoprevention trial that used incidence development prespecified endpoint. median follow-up time 6.08 years 35...
<h3>Importance</h3> Standard molecularly based strategies to predict and/or prevent oral cancer development in patients with premalignant lesions (OPLs) are lacking. <h3>Objective</h3> To test if the epidermal growth factor receptor inhibitor erlotinib would reduce high-risk OPLs defined by specific loss of heterozygosity (LOH) profiles. Secondary objectives included prospective determination LOH as a prognostic marker OPLs. <h3>Design</h3> The Erlotinib Prevention Oral Cancer (EPOC) study...
Abstract Leukoplakia is the most common premalignant lesion of oral cavity. Epidermal growth factor receptor (EGFR) abnormalities are associated with tumorigenesis and progression. We hypothesized that EGFR expression gene copy number changes predictors risk an (OPL) progressing to squamous cell carcinoma (OSCC). A formalin-fixed, paraffin-embedded OPL biopsy specimen was collected from each 162 patients in a randomized controlled clinical trial. assessed by immunohistochemistry two methods:...
Abstract Missense mutations in the polymerase epsilon (POLE) gene have been reported to generate proofreading defects resulting an ultramutated genome and sensitize tumors checkpoint blockade immunotherapy. However, many POLE-mutated do not respond such treatment. To better understand link between POLE mutation variants response immunotherapy, we prospectively assessed efficacy of nivolumab a multicenter clinical trial patients bearing advanced mismatch repair–proficient solid tumors. We...
Background Epigenetic silencing is a common mechanism to inactivate tumor suppressor genes during carcinogenesis. Enhancer of Zeste 2 (EZH2) the histone methyltransferase subunit in polycomb repressive complex which mediates transcriptional repression through methylation. EZH2 overexpression has been linked aggressive phenotypes certain cancers. However, that played promoting malignancy non-small cell lung cancer (NSCLC) remains unclear. In addition, correlation and prognosis NSCLC patients...
DNA promoter methylation of tumor suppressor genes and global hypomethylation are common features head neck cancers. Our goal was to identify early changes in oral premalignant lesions (OPL) that may serve as predictive markers developing squamous cell carcinoma (OSCC). Using high-throughput profiles 24 OPLs, we found the top 86 differentially methylated between patients who did or not develop OSCC were simultaneously hypermethylated, suggesting a CpG island phenotype occur during...
To report the clinical efficacy of sorafenib and to evaluate biomarkers associated with benefit in BATTLE (Biomarker-Integrated Approaches Targeted Therapy for Lung Cancer Elimination) program.