Jean‐Philippe Theurillat

ORCID: 0000-0003-0111-5937
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About
Contact & Profiles
Research Areas
  • Prostate Cancer Treatment and Research
  • Ubiquitin and proteasome pathways
  • Protein Degradation and Inhibitors
  • Melanoma and MAPK Pathways
  • Cancer Genomics and Diagnostics
  • Monoclonal and Polyclonal Antibodies Research
  • Cancer, Hypoxia, and Metabolism
  • RNA Interference and Gene Delivery
  • Computational Drug Discovery Methods
  • Cancer-related gene regulation
  • Cancer, Lipids, and Metabolism
  • Immunotherapy and Immune Responses
  • Prostate Cancer Diagnosis and Treatment
  • Growth Hormone and Insulin-like Growth Factors
  • interferon and immune responses
  • Cancer-related Molecular Pathways
  • Metabolism, Diabetes, and Cancer
  • RNA and protein synthesis mechanisms
  • CAR-T cell therapy research
  • Radiopharmaceutical Chemistry and Applications
  • Epigenetics and DNA Methylation
  • Molecular Biology Techniques and Applications
  • Cell death mechanisms and regulation
  • Autophagy in Disease and Therapy
  • HER2/EGFR in Cancer Research

Institute of Oncology Research
2015-2025

Università della Svizzera italiana
2020-2025

University Hospital of Lausanne
2016-2017

University of Lausanne
2016-2017

Broad Institute
2012-2016

ETH Zurich
2011-2016

Dana-Farber Cancer Institute
2013-2014

Harvard University
2013-2014

Brigham and Women's Hospital
2013

University of Duisburg-Essen
2013

RAF inhibitors such as vemurafenib and dabrafenib block BRAF-mediated cell proliferation achieve meaningful clinical benefit in the vast majority of patients with BRAF(V600E)-mutant melanoma. However, some do not respond to this regimen, nearly all progress therapeutic resistance. We used a pooled RNA interference screen targeting more than 16,500 genes discover loss-of-function events that could drive resistance inhibition. The highest ranking gene was NF1, which encodes neurofibromin,...

10.1158/2159-8290.cd-12-0470 article EN Cancer Discovery 2013-01-04

Mutant protein in tumors hits the DEK Cancer genome sequencing projects have uncovered a multitude of mutations human tumors. Understanding whether and how these contribute to tumor development progression could ultimately lead new therapies. Theurillat et al. studied product gene that is recurrently mutated prostate cancer. Normally this helps attach biochemical tag cellular proteins marks them for degradation. The work shows tumor-associated mutant loses tagging ability, which results...

10.1126/science.1250255 article EN Science 2014-10-02

Microbes hijack prostate cancer therapy Androgens such as testosterone and dihydrotestosterone are essential for male reproduction sexual function. can also influence the growth of tumor cells, androgen deprivation (ADT) either by surgical means (castration) or pharmacological approaches (hormone suppression), is cornerstone current treatments. Pernigoni et al . found that when body was deprived androgens during ADT, gut microbiome could produce from precursors (see Perspective McCulloch...

10.1126/science.abf8403 article EN Science 2021-10-08

Abstract Therapy resistance and metastatic processes in prostate cancer (PCa) remain undefined, due to lack of experimental models that mimic different disease stages. We describe an androgen-dependent PCa patient-derived xenograft (PDX) model from treatment-naïve, soft tissue metastasis (PNPCa). RNA whole-exome sequencing the PDX organoids confirmed transcriptomic genomic similarity primary tumor. PNPCa harbors BRCA2 CHD1 somatic mutations, shows SPOP/FOXA1 -like signature microsatellite...

10.1038/s41467-021-21300-6 article EN cc-by Nature Communications 2021-02-18

Abstract Comprehensive genomic studies have delineated key driver mutations linked to disease progression for most cancers. However, corresponding transcriptional changes remain largely elusive because of the bias associated with cross-study analysis. Here, we overcome these hurdles and generate a comprehensive prostate cancer transcriptome atlas that describes roadmap tumor in qualitative quantitative manner. Most cancers follow uniform trajectory characterized by upregulation...

10.1038/s41467-021-26840-5 article EN cc-by Nature Communications 2021-12-02

Abstract Aim: The unexpected identification of myoglobin (MB) in breast cancer prompted us to evaluate the clinico‐pathological value MB, haemoglobin (HB) and cytoglobin (CYGB) human carcinoma cases. We further screened for presence neuroglobin (NGB) CYGB tumours diverse origin, assessed O 2 ‐response HB, MB mRNAs cell lines, better elicit links between this ectopic globin expression tumour hypoxia. Methods: Breast were analysed by immunohistochemistry correlated with parameters. Screening...

10.1111/j.1748-1716.2010.02205.x article EN Acta Physiologica 2010-10-19

Prostate cancer (PCa) has a broad spectrum of clinical behavior; hence, biomarkers are urgently needed for risk stratification. Here, we aim to find potential stratification, by utilizing gene co-expression network transcriptomics data in addition laser-microdissected proteomics from human and murine prostate FFPE samples. We show up-regulation oxidative phosphorylation (OXPHOS) PCa on the transcriptomic level TCA cycle/OXPHOS proteomic level, which is inversely correlated STAT3 expression....

10.15252/msb.20199247 article EN cc-by Molecular Systems Biology 2020-04-01

Abstract Background Prostate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated potential oncogenic drivers, molecular programs contributing to progression are not fully understood. Methods We analyzed expression clinical samples across different stages and investigated its functional role Pten -deficient mouse model. performed histopathological...

10.1186/s12943-024-02022-x article EN cc-by Molecular Cancer 2024-05-29

Members of the ETS transcription factor family have been implicated in several cancers, where they are often dysregulated by genomic derangement. variant 1 (ETV1) is an gene that undergoes chromosomal translocation prostate cancers and Ewing sarcomas, amplification melanomas, lineage dysregulation gastrointestinal stromal tumors. Pharmacologic perturbation ETV1 would be appealing these cancers; however, oncogenic factors deemed "undruggable" conventional methods. Here, we used small-molecule...

10.1158/1535-7163.mct-13-0689 article EN Molecular Cancer Therapeutics 2014-04-16

Extracellular vesicles (EVs) are relevant means for transferring signals across cells and facilitate propagation of oncogenic stimuli promoting disease evolution metastatic spread in cancer patients. Here, we investigated the release miR-424 circulating small EVs or exosomes from prostate patients assessed functional implications multiple experimental models. We found higher frequency positive with compared to primary tumors BPH. Release was enhanced cell lines (LNCaPabl), transgenic mice...

10.1038/s42003-020-01642-5 article EN cc-by Communications Biology 2021-01-26

Abstract Driver genes with a mutually exclusive mutation pattern across tumor genomes are thought to have overlapping roles in tumorigenesis. In contrast, we show here that prostate cancer driver alterations involving the ERG transcription factor and ubiquitin ligase adaptor SPOP synthetic sick. At molecular level, incompatible pathways driven by opposing functions SPOP. upregulates wild type dampen androgen receptor (AR) signaling sustain activity through degradation of bromodomain histone...

10.1038/s41467-020-20820-x article EN cc-by Nature Communications 2021-02-02

243 Background: Alterations in AVPC-TSG (TP53, RB1, PTEN) are related with androgen insensitivity and aggressive disease. However, their role mHSPC prognosis treatment guidance is unclear. This retrospective study assesses the value of alterations refining predicting ARPI benefit mHSPC. Methods: We included 158 patients available genomic tumor sequencing analysis undergoing between 2013 2023. compared AVPC-TSGalt tumors (defined by ≥1 TP53 gene, RB1 or PTEN/PI3K/AKT pathway genes) to those...

10.1200/jco.2025.43.5_suppl.243 article EN Journal of Clinical Oncology 2025-02-10
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