Tarek Hallal
A5011422737- Cancer, Lipids, and Metabolism
- Diet and metabolism studies
- Cancer, Hypoxia, and Metabolism
- Metabolomics and Mass Spectrometry Studies
- Prostate Cancer Treatment and Research
- Cancer Genomics and Diagnostics
- Cell Adhesion Molecules Research
- Cancer Research and Treatments
- Bone health and treatments
- Cancer-related molecular mechanisms research
- RNA Research and Splicing
- Gut microbiota and health
McGill University Health Centre
2021-2024
McGill University
2021-2024
Abstract c-MYC (MYC) is a major driver of prostate cancer tumorigenesis and progression. Although MYC overexpressed in both early metastatic disease associated with poor survival, its impact on transcriptional reprogramming remains elusive. We demonstrate that overexpression significantly diminishes the androgen receptor (AR) program (the set genes directly targeted by AR protein) luminal cells without altering expression. Analyses clinical specimens reveal concurrent low high programs...
The gut microbiota modulates response to hormonal treatments in prostate cancer (PCa) patients, but whether it influences PCa progression remains unknown. Here, we show a reduction fecal alpha-diversity correlating with increase tumour burden two distinct groups of hormonotherapy naïve patients and three murine models. Fecal transplantation (FMT) from high volume is sufficient stimulate the growth mouse revealing existence microbiome-cancer crosstalk. Analysis microbial-related pathways mice...
Abstract Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation metabolites that reprogram tumor microenvironment (TME) and drive cancer could facilitate development precision nutrition approaches. Using Hi-MYC prostate mouse model, we demonstrated an obesogenic high-fat diet (HFD) rich in saturated fats accelerates c-MYC–driven invasive through...
<p>Supplementary Figure S7 shows the output of mouse-based deconvolution models ImmuCC and mMCP.</p>
<p>Supplementary Figure S2 shows the effect of obesogenic HFD on AP and VP lobes, cell proliferation rate in MYC-transformed DLP, WT prostate lobes.</p>
<p>Supplementary Figure S1 shows the systemic effects of HFD.</p>
<p>Supplementary Figure S2 shows the effect of obesogenic HFD on AP and VP lobes, cell proliferation rate in MYC-transformed DLP, WT prostate lobes.</p>
<p>Supplementary Figure S6 includes scRNA-seq data showing that Luminal (high Ly6d) cells in MYC-transformed DLP display glycolytic features.</p>
<p>Supplementary Figure S5 shows the output of ESTIMATE and PUREE methods to assess tumor purity.</p>
<p>Supplementary Figure S4 shows the effect of obesogenic high-fat diet on glycolytic enzymes and HIF-1 alpha in vivo.</p>
<div>Abstract<p>Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation metabolites that reprogram tumor microenvironment (TME) and drive cancer could facilitate development precision nutrition approaches. Using Hi-MYC prostate mouse model, we demonstrated an obesogenic high-fat diet (HFD) rich in saturated fats accelerates c-MYC–driven...
<p>Supplementary Figure S3 shows a graphical representation of key metabolic pathways altered by MYC alone or obesogenic HFD in WT and MYC-transformed DLP.</p>
<p>Supplementary Figure S10 shows the output of human-based deconvolution model QuanTIseq.</p>
<p>Supplementary Figure S1 shows the systemic effects of HFD.</p>
<p>Supplementary Figure S6 includes scRNA-seq data showing that Luminal (high Ly6d) cells in MYC-transformed DLP display glycolytic features.</p>
<p>Supplementary Figure S10 shows the output of human-based deconvolution model QuanTIseq.</p>
<p>Supplementary Figure S8 shows migration assays of MYC-CaP cells treated with lactate or LDHA inhibitor FX11.</p>
<p>Supplementary Figure S3 shows a graphical representation of key metabolic pathways altered by MYC alone or obesogenic HFD in WT and MYC-transformed DLP.</p>
<div>Abstract<p>Cancer cells exhibit metabolic plasticity to meet oncogene-driven dependencies while coping with nutrient availability. A better understanding of how systemic metabolism impacts the accumulation metabolites that reprogram tumor microenvironment (TME) and drive cancer could facilitate development precision nutrition approaches. Using Hi-MYC prostate mouse model, we demonstrated an obesogenic high-fat diet (HFD) rich in saturated fats accelerates c-MYC–driven...
<p>Supplementary Figure S7 shows the output of mouse-based deconvolution models ImmuCC and mMCP.</p>
<p>Supplementary Figure S9 shows GSEA_Hallmark results in human PCa</p>
<p>Supplementary Figure S9 shows GSEA_Hallmark results in human PCa</p>
<p>Supplementary Figure S8 shows migration assays of MYC-CaP cells treated with lactate or LDHA inhibitor FX11.</p>