A5064410285- Lung Cancer Treatments and Mutations
- Prostate Cancer Treatment and Research
- Glioma Diagnosis and Treatment
- Cancer Genomics and Diagnostics
- Cancer-related Molecular Pathways
- interferon and immune responses
- Cell death mechanisms and regulation
- Acute Myeloid Leukemia Research
- PARP inhibition in cancer therapy
- Epigenetics and DNA Methylation
- Protein Degradation and Inhibitors
- Prostate Cancer Diagnosis and Treatment
- Cancer Immunotherapy and Biomarkers
- Boron Compounds in Chemistry
- Nanoplatforms for cancer theranostics
- Renal cell carcinoma treatment
- Gut microbiota and health
- Inflammatory Biomarkers in Disease Prognosis
- Cancer, Hypoxia, and Metabolism
- Advanced Nanomaterials in Catalysis
- Single-cell and spatial transcriptomics
- Molecular Biology Techniques and Applications
- Hormonal and reproductive studies
- CRISPR and Genetic Engineering
- Genomics and Chromatin Dynamics
Institute of Cancer Research
2021-2024
Royal Marsden Hospital
2024
Wellcome Sanger Institute
2022
Royal Marsden NHS Foundation Trust
2020-2022
Abstract Inflammation is a hallmark of cancer 1 . In patients with cancer, peripheral blood myeloid expansion, indicated by high neutrophil-to-lymphocyte ratio, associates shorter survival and treatment resistance across malignancies therapeutic modalities 2–5 Whether inflammation drives progression prostate in humans remain unclear. Here we show that inhibition chemotaxis can reduce tumour-elicited reverse therapy subset metastatic castration-resistant (CRPC). We higher ratio reflects...
B7-H3 is a cell surface immunomodulatory glycoprotein overexpressed in prostate cancers (PCs). Understanding its longitudinal expression at emergence of castration resistance and association with tumour genomics are critical to the development patient selection for targeted therapies.To characterise same-patient hormone-sensitive (HSPC) castration-resistant (CRPC) PC biopsies, associating this genomics, evaluate antitumour activity an anti-B7-H3 antibody-drug conjugate (ADC) human CRPC vitro...
Abstract Cancer evolution lays the groundwork for predictive oncology. Testing evolutionary metrics requires quantitative measurements in controlled clinical trials. We mapped genomic intratumor heterogeneity locally advanced prostate cancer using 642 samples from 114 individuals enrolled trials with a 12-year median follow-up. concomitantly assessed morphological deep learning 1,923 histological sections 250 individuals. Genetic and (Gleason) diversity were independent predictors of...
Clinical diagnostic sequencing of circulating tumour DNA (ctDNA) is well advanced for adult patients, but application to paediatric cancer patients lags behind.
Abstract The retinoblastoma tumor suppressor (RB) is a critical regulator of E2F-dependent transcription, controlling multitude protumorigenic networks including but not limited to cell-cycle control. Here, genome-wide assessment E2F1 function after RB loss in isogenic models prostate cancer revealed unexpected repositioning and cooperation with oncogenic transcription factors, the major driver disease progression, androgen receptor (AR). Further investigation that observed AR/E2F1 elicited...
Background/Aim: Better diagnostic and prognostic markers are required for a more accurate diagnosis an earlier detection of glioma progression suggesting better treatment strategies. This retrospective study aimed to identify actionable gene variants define potential clinical significance. Materials Methods: 56 glioblastomas (GBM) 44 grade 2-3 astrocytomas were profiled with next generation sequencing (NGS) as part routine workup bioinformatics analysis was used the identification variants....
BACKGROUND. Clinical trials have suggested antitumor activity from PARP inhibition beyond homologous recombination deficiency (HRD). RNASEH2B loss is unrelated to HRD and preclinically sensitizes inhibition. The current study reports on protein in advanced prostate cancer its association with RB1 loss, clinical outcome clonal dynamics during treatment a prospective trial.
Abstract Multivalent second-generation TRAIL-R2 agonists are currently in late preclinical development and early clinical trials. Herein, we use a representative agent, MEDI3039, to address two major challenges facing these agents: lack of predictive biomarkers enable patient selection emergence resistance. Genome-wide CRISPR knockout screens were notable for the resistance mechanisms beyond canonical pathway (caspase-8, FADD, BID) as well p53 BAX TP53 wild-type models, whereas activatory...
Supplementary Data from Functional Genomic Identification of Predictors Sensitivity and Mechanisms Resistance to Multivalent Second-Generation TRAIL-R2 Agonists
Supplementary Figure from Functional Genomic Identification of Predictors Sensitivity and Mechanisms Resistance to Multivalent Second-Generation TRAIL-R2 Agonists
<div>Abstract<p>Multivalent second-generation TRAIL-R2 agonists are currently in late preclinical development and early clinical trials. Herein, we use a representative agent, MEDI3039, to address two major challenges facing these agents: lack of predictive biomarkers enable patient selection emergence resistance. Genome-wide CRISPR knockout screens were notable for the resistance mechanisms beyond canonical pathway (caspase-8, FADD, BID) as well p53 BAX TP53 wild-type models,...
Supplementary Figure from Functional Genomic Identification of Predictors Sensitivity and Mechanisms Resistance to Multivalent Second-Generation TRAIL-R2 Agonists
Supplementary Data from Functional Genomic Identification of Predictors Sensitivity and Mechanisms Resistance to Multivalent Second-Generation TRAIL-R2 Agonists
<div>Abstract<p>Multivalent second-generation TRAIL-R2 agonists are currently in late preclinical development and early clinical trials. Herein, we use a representative agent, MEDI3039, to address two major challenges facing these agents: lack of predictive biomarkers enable patient selection emergence resistance. Genome-wide CRISPR knockout screens were notable for the resistance mechanisms beyond canonical pathway (caspase-8, FADD, BID) as well p53 BAX TP53 wild-type models,...
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<div>Abstract<p>The retinoblastoma tumor suppressor (RB) is a critical regulator of E2F-dependent transcription, controlling multitude protumorigenic networks including but not limited to cell-cycle control. Here, genome-wide assessment E2F1 function after RB loss in isogenic models prostate cancer revealed unexpected repositioning and cooperation with oncogenic transcription factors, the major driver disease progression, androgen receptor (AR). Further investigation that...
<div>Abstract<p>The retinoblastoma tumor suppressor (RB) is a critical regulator of E2F-dependent transcription, controlling multitude protumorigenic networks including but not limited to cell-cycle control. Here, genome-wide assessment E2F1 function after RB loss in isogenic models prostate cancer revealed unexpected repositioning and cooperation with oncogenic transcription factors, the major driver disease progression, androgen receptor (AR). Further investigation that...
<p>Supplemental Figure 1</p>