Hugang Feng
A5077278945- Renal cell carcinoma treatment
- Cancer Genomics and Diagnostics
- Genomic variations and chromosomal abnormalities
- Chromosomal and Genetic Variations
- Chemical Reactions and Isotopes
- Cancer-related molecular mechanisms research
- Pancreatic function and diabetes
- Signaling Pathways in Disease
- Pancreatic and Hepatic Oncology Research
- Liver physiology and pathology
- Renal and related cancers
- Cancer, Hypoxia, and Metabolism
- Genetics and Neurodevelopmental Disorders
- Macrophage Migration Inhibitory Factor
- MicroRNA in disease regulation
- Peptidase Inhibition and Analysis
- Genomics and Chromatin Dynamics
- interferon and immune responses
- Ferroptosis and cancer prognosis
- Molecular Biology Techniques and Applications
- Prostate Cancer Treatment and Research
- Lipid metabolism and biosynthesis
- Chromatin Remodeling and Cancer
- Cancer Mechanisms and Therapy
The Francis Crick Institute
2023-2025
Institute of Cancer Research
2025
Institute of Cancer Research
2018-2022
Imperial College London
2017
TGF-β/Activin induces epithelial-to-mesenchymal transition and stemness in pancreatic ductal adenocarcinoma (PDAC). However, the microRNAs (miRNAs) regulated during this response have remained yet undetermined. Here, we show that TGF-β transcriptionally MIR100HG lncRNA, containing miR-100, miR-125b let-7a its intron, via SMAD2/3. Interestingly, find although pro-tumourigenic miR-100 accordingly increase, amount of anti-tumourigenic is unchanged, as also LIN28B inhibiting maturation. Notably,...
Abstract Although the key aspects of genetic evolution and their clinical implications in clear-cell renal cell carcinoma (ccRCC) are well documented, how features coevolve with phenotype tumor microenvironment (TME) remains elusive. Here, through joint genomic–transcriptomic analysis 243 samples from 79 patients recruited to TRACERx Renal study, we identify pervasive nongenetic intratumor heterogeneity, over 40% not attributable alterations. By integrating transcriptomes phylogenetic...
Abstract The specialised structure of the centromere is critical for effective chromosome segregation, but its repetitive nature makes it vulnerable to rearrangements. Centromere fragility can drive tumorigenesis, protective mechanisms preventing are still not fully understood. PBAF chromatin remodelling complex frequently misregulated in cancer, role cancer incompletely characterized. Here, we identify as a protector and pericentromere with profound consequences genome stability. A...
<p>Heterogeneity of the TME in ccRCC. <b>A,</b> Association cell abundance estimates from consensus and evolutionary trajectory tumor which sample is taken (in 171 primary samples). Comparisons are one against all using a linear mixed-effects model to control for inclusion multiple samples same patient. <i>P</i>-values corrected hypothesis testing by Benjamini–Hochberg (FDR). Significant associations (FDR < 0.05) highlighted with thicker borders. Negative...
<p>Evaluation of the potential to reconstruct TCR repertiore from bulk RNA-Sequencing data</p>
<p>Transcriptional evolution mirrors clonal structure and follows recurrent trends. <b>A,</b> Transcriptional distance between primary tumor samples other or adjacent normal kidney (12 patients with both available primary–primary primary–normal pairs). <b>B,</b> Proportion of genes significantly associated changes in expression normal–primary pairs using a gene-specific linear regression framework (see “Methods”). <b>C,</b> matched metastases (seven...
<p>Greater overall HERV expression, strongly associated with VHL loss of function, correlates longer progression-free survival in ccRCC. <b>A</b>, Distribution TRACERx Renal (<i>n</i> = 243 samples) the median expression across 615 transcripts overlapping annotated retroelements (HERVs and LTRs) by sample genotype. Boxes extend from lower to upper quartiles, line inside box representing median, whiskers indicating data within 1.5 times IQR quartiles....
<p>All Supplementary Figures are provided in PDF format with the corresponding legend after each figure. Figure 1. Genetic and clinical composition of TRACERx Renal cohort 2. Comparison between transcriptional inter intratumour heterogeneity 3. Representation I-TED to measure robustness analysis 4. Transcriptional ITH is not associated poorer outcomes ccRCC 5. Subclonal 9p loss subclonal somatic copy-number alteration greatest association 6. Variance explained by major clinico-genomic...
<p>Transcriptional inter- and intratumor heterogeneity is pervasive in TRACERx Renal. <b>A,</b> UMAP visualizing the transcriptional variation across 231 tumor samples (gray points). Samples from patients K390, K243, K153 are highlighted to illustrate varied levels of ITH distinct patients. For patient K153, we highlight phylogenetic tree branch containing clones observed adjacent sample points. <b>B,</b> Schematic representation calculation distance between two...
<div>Abstract<p>Although the key aspects of genetic evolution and their clinical implications in clear-cell renal cell carcinoma (ccRCC) are well documented, how features coevolve with phenotype tumor microenvironment (TME) remains elusive. Here, through joint genomic–transcriptomic analysis 243 samples from 79 patients recruited to TRACERx Renal study, we identify pervasive nongenetic intratumor heterogeneity, over 40% not attributable alterations. By integrating transcriptomes...
<p>Inputting information from previous TRACERx Renal studies</p>
<p>Spatial diversity of the TCR repertoire suggests heritable nature antigenic source in ccRCC. <b>A,</b> and BCR similarity between pairs samples across 60 TRACERx Renal patients with at least two regions sampled. Dark purple diamonds represent median (per-patient estimate TCR/BCR similarity). Pale squares minimum maximum similarities; blue points rest sample pairs, when available. Patients both plots are ordered by increasing similarity. <b>B,</b> Kaplan–Meier...
<p>Canonical ccRCC subclonal drivers and aneuploidy burden drive specific changes to the tumor transcriptome. <b>A,</b> Illustration of procedure analyze transcriptional association a copy number alteration without confounding effect patient-specific factors followed in this study. <b>B,</b> Association 50 different hallmark signatures with 9p 14q loss ccRCC. FDR was calculated by correcting <i>P</i>-values obtained via paired Wilcoxon tests...