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559 results for “Cancer metabolism”
Suplementary data, results and scripts: "Reconstruction of Cell-specific Models Capturing the Influence of Metabolism on DNA methylation in Cancer"
<p>This repository contains supplementary data, models and scripts associated with "Reconstruction of Cell-specific Models Capturing the Influence of Metabolism on DNA methylation in Cancer".</p><p>Folders content:</p><p>'data_results_matlabscripts': data, result files and scripts (original python scripts and adapted MATLAB scripts)</p><p>'supplementary_figures': supplementary figures</p><p>'supplementary_tables': supplementary tables</p>
Lipogenesis mediated by OGR1 regulates metabolic adaptation to acid stress in cancer cells via autophagy
<p>Malignant tumors exhibit altered metabolism resulting in a highly acidic extracellular microenvironment. Here we show that cytoplasmic lipid droplet (LD) accumulation, indicative of a lipogenic phenotype is a cellular adaption to extracellular acidity. LD marker PLIN2, is strongly associated with poor overall survival in breast cancer patients. Acid-induced LD accumulation is triggered by activation of the acid-sensing GPCR, OGR1 expressed highly in breast tumors. OGR1 depletion inhibited acid induced lipid accumulation while activation by synthetic agonist triggered LD formation. Inhibition of OGR1 downstream signaling abrogated the lipogenic phenotype which could be rescued with OGR1 ectopic expression. OGR1 depleted cells showed growth inhibition under acidic growth conditions in vitro and tumor formation in vivo. Isotope tracing showed that the source of lipid precursors is primarily autophagy-derived ketogenic amino acids. OGR1 depleted cells were defective in endoplasmic reticulum stress response and autophagy, hence failed to accumulate LDs affecting survival under acidic stress.</p>
Feasibility and metabolic outcomes of a well-formulated ketogenic diet as an adjuvant therapeutic intervention for women with stage IV metastatic breast cancer: The Keto-CARE trial
<p><em>Purpose:</em></p> <p>Ketogenic diets may positively influence cancer through pleiotropic mechanisms, but only a few small and short-term studies have addressed feasibility and efficacy in cancer patients. The primary goals of this study were to evaluate the feasibility and the sustained metabolic effects of a personalized well-formulated ketogenic diet (WFKD) designed to achieve consistent blood beta-hydroxybutyrate (<span>β</span>HB) >0.5 mM in women diagnosed with stage IV metastatic breast cancer (MBC) undergoing chemotherapy.</p> <p><em>Methods: </em></p> <p>Women (n = 20) were enrolled in a six-month two-phase, single-arm WFKD intervention (NCT03535701). Phase I was a highly-supervised, ad libitum, personalized WFKD, where women were provided with ketogenic-appropriate food daily for three-months. Phase II transitioned women to a self-administered WFKD with ongoing coaching for an additional three-months. Fasting capillary <span>β</span>HB and glucose were collected daily; weight, body composition, plasma insulin, and insulin resistance were collected at baseline, three- and six-months. </p> <p><em>Results:</em></p> <p>Capillary <span>β</span>HB indicated women achieved nutritional ketosis (Phase I mean: 0.8 mM (n = 15); Phase II mean: 0.7 mM (n = 9)). Body weight decreased 10% after three-months, primarily from body fat. Fasting plasma glucose, plasma insulin, and insulin resistance also decreased significantly after three-months (p < 0.01), an effect that persisted at six-months.</p> <p><em>Conclusions</em>:</p> <p>Women diagnosed with MBC undergoing chemotherapy can safely achieve and maintain nutritional ketosis, while improving body composition and insulin resistance, out to six-months.</p>
Time series transcriptomes resolve metabolic pathways underlying crocin's anti-cancer activity | Dataset: sequencing reads (2,6,12,24 hr crocin treatments)
<p><span>Natural products like saffron show promise in treating hepatocellular carcinoma (HCC), but their mechanisms remain unclear. Here, we used time-series transcriptomics to elucidate crocin's anti-cancer mechanisms in HCC cells. We treated HepG2 cells with 1 and 2 mM crocin for 2, 6, 12, and 24 hours and analyzed transcriptomic profiles at each timepoint. The strongest transcriptional response occurred at 2 hours with 1 mM crocin, with diminishing effects at later timepoints. We observed upregulation of metabolic-, adhesion-, and endocytosis-related genes across all timepoints. Pathway analysis revealed activation of DNA damage checkpoints and senescence while proliferation pathways were suppressed. Notably, 52 genes involved in non-alcoholic fatty liver disease were downregulated at 24 hours (FDR p = 8 × 10⁻⁸), suggesting reversal of carcinogenic pathways. Strikingly, crocin consistently downregulated spliceosomal machinery genes across all timepoints while upregulating senescence and autophagy pathways. This spliceosome targeting represents a clinically relevant mechanism, as aberrant splicing drives oncogenesis in more than 90% of cancers. The transcription factor PAX5 was significantly upregulated while oncogenic ELK1 targets were downregulated. Our findings show that crocin treatment is accompanied by HCC cell senescence induction through coordinated spliceosome disruption and metabolic reprogramming, providing novel therapeutic targets for hepatocellular carcinoma.</span></p> <p><strong><span>Keywords: </span></strong><span>Hepatocellular carcinoma (HCC), crocin, transcriptomics, spliceosome, senescence, natural anti-cancer compounds</span></p>
Central obesity, body mass index, metabolic syndrome and mortality in Mediterranean breast cancer patients
<p>Importance: Obesity and metabolic disorders have been associated with an increased risk of cancer and with poorer outcomes in many cohorts of breast cancer (BC) patients, with poor evidence from Mediterranean cohorts. <br> Objective: To investigate the prognostic potential of anthropometric variables, namely body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), as well as Metabolic Syndrome (MetS) and its components, in early BC patients living in a Southern Mediterranean region of Italy.<br> Design: Prospective cohort study enrolling consecutive early BC patients who were treated between January 2009 and December 2013 in Southern Italy. Median follow-up was 11.8 years and ended on June 15th 2022. Physicians who measured the study variables were blinded to patient groupings.<br> Setting: Multicenter study enrolling consecutive, early BC patients referred to specialized cancer centers.<br> Participants: A total of 955 early BC patients consecutively treated at the Istituto Nazionale dei Tumori, “G. Pascale” and at the Policlinico University Hospital “Federico II”, Naples, Italy, were enrolled. All study subjects provided written informed consent to participate. <br> Intervention(s) (for clinical trials) and exposure (for observational studies): Anthropometric measurements and indices (BMI, hip circumference and WC) were collected. MetS was defined according to NCEP-ATP III criteria. MetS components were categorized as 0, 1-2 or ≥3. <br> Main Outcomes and Measures: Overall survival and BC-specific survival. <br> Results: Mean age was 55.3 years (±12.5 years); 61% of patients were post-menopausal. At the end of follow-up, 208 (22%) patients had died, 131 (14%) of whom from BC. Obesity (BMI≥30 kg/m2) was found in 29% of enrolled patients (14% in pre- and 38% in post-menopause); 24% of patients met the criteria for a diagnosis of MetS (7% in pre- and 36% in post-menopause), whereas 1-2 MetS criteria were found in 53% of patients<br> High WC or WHR were associated with a moderately increased risk of all-cause mortality (WC ≥ 88 cm, HR=1.39, 95%CI: 1.00-1.94; WHR > 0.85, HR=1.62, 95%CI: 1.12-2.37). Furthermore, an increased risk of all-cause mortality was observed with the presence of MetS (HR=1.61, 95%CI: 1.12-2.32). An increased BC-specific mortality risk was found in obese patients (BMI≥30 kg/m2, HR=1.72, 95%CI: 1.06-2.78) and in those with WC ≥88 (HR=1.71, 95%CI: 1.12-2.61). High WHR was also associated with increased risk of BC-specific mortality, both when evaluated as a categorical variable (WHR>0.85, HR=1.80, 95%CI: 1.13-2.86) and as a continuous variable (for each 0.1-U increase in WHR, HR=1.33, 95%CI: 1.08-1.63). The presence of MetS was associated with an 81% increased risk of BC-specific mortality (HR=1.81, 95%CI: 1.51-2.85). <br> These associations varied according to menopausal status. In particular, in pre-menopausal patients higher BMI was associated with an increased risk of both all-cause and BC-specific mortality (HR=1.43 and HR=1.58, respectively). In post-menopausal women an increased risk of all-cause mortality was found only in the presence of ≥3 MetS components (HR=2.77, 95%CI: 1.09-7.06). The associations among anthropometric variables and all-cause and BC-specific mortality also varied according to BC subtype. Triple negative BC was the only disease subtype that wasn’t independently associated with BMI, WC, WHR or MetS or all-cause and BC-specific mortality.<br> Conclusions and Relevance: Central obesity and metabolic disorders result in a highly increased risk of BC death. The magnitude of this effect suggests that obesity may nullify the benefit of effective BC therapies. Active lifestyle interventions to maintain optimal body weight and to prevent MetS should be recommended for several expected beneficial effects, including a potential reduction in BC-specific mortality.</p>
Study to Investigate the Absorption, Metabolism, and Excretion of [14C]-Pamiparib in Participants With Advanced Cancer
ClinicalTrials.gov study NCT03991494. IPD Sharing: YES. Countries: 1. Publications: 1.
Magnesium Treatment on Vitamin D Metabolism in Participants Completed Personalized Prevention of Colorectal Cancer Trial
ClinicalTrials.gov study NCT03265483. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Aborption and Metabolism of Lyophilized Black Raspberry Food Products in Men With Prostate Cancer Undergoing Surgery
ClinicalTrials.gov study NCT01823562. IPD Sharing: Not stated. Countries: 1. Publications: 0.
A Multi-omics-based Metabolic Typing Study of Gastric Cancer
ClinicalTrials.gov study NCT06134011. IPD Sharing: NO. Countries: 1. Publications: 3.
Patient-derived organotypic tissue cultures as a platform to evaluate metabolic reprogramming in breast cancer patients
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Feasibility and metabolic outcomes of a well-formulated ketogenic diet as an adjuvant therapeutic intervention for women with stage IV metastatic breast cancer: The Keto-CARE trial
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Datasets: Carbon sources and pathways for citrate secreted by human prostate cancer cells determined by NMR tracing and metabolic modeling
<p>Zipped NMR datasets:</p> <p>data1 LNCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate</p> <p>data2 LNCaP medium with [1,6-<sup>13</sup>C<sub>2</sub>]glucose</p> <p>data3 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data4 VCaP medium with [1,6-<sup>13</sup>C<sub>2</sub>]glucose</p> <p>data5 VCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data6 VCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data7 VCaP medium with [2-<sup>13</sup>C]pyruvate -glucose +aspartate</p> <p>data8 VCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data9 VCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data10 VCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data11 LNCaP and VCaP medium with and without zinc(II)</p> <p>data12 LNCaP and VCaP medium with and without zinc(II)</p> <p>data13 LNCaP and VCaP medium with and without zinc(II)</p> <p>data14 LNCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data15 LNCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data16 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data17 LNCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data18 VCaP medium with [1,6-<sup>13</sup>C<sub>2</sub>]glucose</p> <p>data19 VCaP medium with [1,6-<sup>13</sup>C<sub>2</sub>]glucose</p> <p>data20 VCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data21 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data22 LNCaP medium with [2-<sup>13</sup>C]pyruvate +citr. Spiking</p> <p>data23 LNCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data24 LNCaP medium with [5-<sup>13</sup>C]glutamine</p> <p>data25 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data26 VCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data27 VCaP medium with [2-<sup>13</sup>C]pyruvate -glucose +aspartate</p> <p>data28 VCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data29 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data30 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data31 LNCaP medium with [2-<sup>13</sup>C]pyruvate</p> <p>data32 VCaP medium with [2-<sup>13</sup>C]pyruvate -glucose +aspartate</p> <p>data33 VCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data34 VCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data35 LNCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate</p> <p>data36 VCaP medium with [U-<sup>13</sup>C<sub>4</sub>]aspartate -glucose +pyruvate</p> <p>data37 LNCaP medium with [5-<sup>13</sup>C]glutamine + citr. spiking</p>
raw data Figure 1 of the paper entitled "Plasma metabolic signature predictive of developing cancer in patients with Lynch syndrome "
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Genomic Alterations of the Metabolic Pathways Across 32 Cancer Types and Their Clinical Significance
<p>Supplementary Information for the thesis chapter: Genomic Alterations of the Metabolic Pathways Across 32 Cancer Types and Their Clinical Significance </p>
Source data sets_Figure 1, 2, 6_Salmonella cancer therapy metabolically disrupts tumours at the collateral cost of T cell immunity
<p>Flow cytometry data files associated with Copland <em>et al., </em><strong><em><span>Salmonella </span></em></strong><strong><span>cancer therapy metabolically disrupts tumours at the collateral cost of T cell immunity.</span></strong></p> <p><span>Data associated to Figures 1, 2 and 6. <br></span></p>
Time series transcriptomes resolve metabolic pathways underlying crocin's anti-cancer activity: Control FASTQ sequencing reads
<p><span>Natural products like saffron show promise in treating hepatocellular carcinoma (HCC), but their mechanisms remain unclear. Here, we used time-series transcriptomics to elucidate crocin's anti-cancer mechanisms in HCC cells. We treated HepG2 cells with 1 and 2 mM crocin for 2, 6, 12, and 24 hours and analyzed transcriptomic profiles at each timepoint. The strongest transcriptional response occurred at 2 hours with 1 mM crocin, with diminishing effects at later timepoints. We observed upregulation of metabolic-, adhesion-, and endocytosis-related genes across all timepoints. Pathway analysis revealed activation of DNA damage checkpoints and senescence while proliferation pathways were suppressed. Notably, 52 genes involved in non-alcoholic fatty liver disease were downregulated at 24 hours (FDR p = 8 × 10⁻⁸), suggesting reversal of carcinogenic pathways. Strikingly, crocin consistently downregulated spliceosomal machinery genes across all timepoints while upregulating senescence and autophagy pathways. This spliceosome targeting represents a clinically relevant mechanism, as aberrant splicing drives oncogenesis in more than 90% of cancers. The transcription factor PAX5 was significantly upregulated while oncogenic ELK1 targets were downregulated. Our findings show that crocin treatment is accompanied by HCC cell senescence induction through coordinated spliceosome disruption and metabolic reprogramming, providing novel therapeutic targets for hepatocellular carcinoma.</span></p> <p><strong><span>Keywords: </span></strong><span>Hepatocellular carcinoma (HCC), crocin, transcriptomics, spliceosome, senescence, natural anti-cancer compounds</span></p>
Lipidomic and fatty acid metabolism changes in pancreatic cancer upon ELOVL6 inhibition
<p>LC-MS data for the analysis of lipidomic and fatty acid metabolism changes in pancreatic cancer upon ELOVL6 inhibition and MYC deletion or overexpression</p>
Data for: Link between glucose metabolism and EMT drives triple negative breast cancer migratory heterogeneity
<p>Intracellular and environmental cues result in heterogeneous cancer cell populations with different metabolic and migratory behaviors. While glucose metabolism and EMT have previously been linked, we aim to understand how this relationship fuels cancer cell migration. We show that while glycolysis drives single-cell migration in confining microtracks, fast and slow cells display different migratory sensitivities to glycolysis and oxidative phosphorylation inhibition. Phenotypic sorting of highly and weakly migratory subpopulations (MDA<sup>+</sup>, MDA<sup>-</sup>) reveals that more mesenchymal, highly migratory MDA<sup>+</sup> preferentially use glycolysis while more epithelial, weakly migratory MDA<sup>-</sup> utilize mitochondrial respiration. These phenotypes are plastic and MDA<sup>+</sup> can be made less glycolytic, mesenchymal, and migratory and MDA<sup>-</sup> can be made more glycolytic, mesenchymal, and migratory via modulation of glucose metabolism or EMT. These findings reveal an intrinsic link between EMT and glucose metabolism that controls migration. Identifying mechanisms fueling phenotypic heterogeneity is essential to develop targeted metastatic therapeutics.</p>
Profiling single cancer cell metabolism via high-content SRS imaging with chemical sparsity
<p>Raw data for Profiling single cancer cell metabolism via high-content SRS imaging with chemical sparsity </p>
A Metabolomics-based Study to Explore the Mechanism of Remission of Metabolic Syndrome Radical Resection of Colorectal Cancer
ClinicalTrials.gov study NCT06710314. IPD Sharing: UNDECIDED. Countries: 1. Publications: 5.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.