Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Postoperative Exercise Training in Patients With Colorectal Liver Metastases Undergoing Surgery (ELMA)

ABSTRACT: Surgery is a primary treatment modality in the intended curative treatment of colorectal liver metastases (CRLM). However, surgery elicits a cascade of potentially detrimental stress responses that may drive the onset of long-term disease progression. Exercise training is emerging as an adjunct treatment in surgical oncology and holds potential to modify the surgical stress response. Against this background, we designed the present randomized controlled trial to evaluate the therapeutic role of pre- and postoperative exercise training in patients with CRLM undergoing open liver resection.

DISEASE(S): Colorectal Liver Metastasis,Neoplasm Metastasis,Liver Neoplasms,Cancer

PROVIDER: 2367157 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Tissue-specific immunosuppressive and proliferating macrophages fuel early metastatic progression of human colorectal cancer to liver

Project description:Early synchronous colorectal liver metastasis (CRLM) represents a clinical condition characterized by the simultaneous presence of primary colorectal cancer (CRC) and metastatic liver lesions (CRLM). The present study characterizes the tissues-specific transcriptomes, phenotypes, and functional relevance of tumor associated macrophages (TAMs) within the tumor microenvironment (TME) of CRC and CRLM specimens in patients who underwent simultaneous surgical removals of these malignancies. The high-throughput single-cell transcriptional analysis revealed an inverse ratio of inflammatory and immunoregulatory TAMs in CRC and CRLM TMEs, along with significant heterogeneity in both tumoral tissues. Importantly, we found that inflammatory TAMs in CRC express inhibitory ligands that might support the tumor immune escape, thus favoring liver metastatic progression. In contrast, CRLM lesions possess a highly immunosuppressive milieu characterized by large proliferative CTLA4pos immunoregulatory TAMs and by the presence of IL7Rpos cytotoxic TAMs. Higher frequencies of these specific TAM subsets in CRLM are associated with a shorter disease-free survival and worse patient prognosis. The identification and characterization of immunoregulatory TAMs preferentially enriched in CRLM is key for the development of novel immune-therapeutic strategies aimed at boosting anti-cancer immune responses within TME.

2025-08-11 | GSE298084 | GEO

Preoperative exercise induces anti-tumor Kupffer cells to prevent surgical stress-promoted colorectal cancer liver metastasis

Project description:We have employed single-cell RNA sequencing using the 10x Genomics platform to investigate the immune cell distribution in the liver of Sedentary (Sed) and preoperative exercise (PEx) mice following surgical stress-promoted colorectal cancer liver metastasis model. The liver immune microenvironment plays a critical role in tumor progression and response to PEx. This study provides a comprehensive immune landscape at single-cell resolution, offering novel insights into how PEx modulates hepatic immune cell populations to mitigate surgical stress-induced tumor progression.

2025-02-27 | GSE290055 | GEO

Differential regulation of extracellular matrix proteins in three recurrent liver metastases of a single patient with colorectal cancer

Project description:Colorectal cancer (CRC) patients suffer from the second highest mortality among all cancer entities. In half of all CRC patients, colorectal cancer liver metastases (CRLM) can be observed. Metastatic colorectal cancer is associated with poor overall survival and limited treatment options. Even after successful surgical resection of the primary tumor, metachronous liver metastases occur in one out of eight cases. The only available curative intended treatment is hepatic resection, but metachronous CRLM frequently recur after approximately one year. In this study, we performed a proteome analysis of three recurrent liver metastases of a single CRC patient by mass spectrometry. Despite surgical resection of the primary CRC and adjuvant chemotherapy plus cetuximab treatment, the patient developed three metachronous CRLM which occurred consecutively after 9, 21 and 31 months. We identified a set of 1,132 proteins expressed in the three metachronous CRLM, of which 481 were differentially regulated, including 81 proteins that were associated with the extracellular matrix (ECM). 56 ECM associated proteins were identified as upregulated in the third metastasis, 26 (46%) of which were previously described as negative prognostic markers in CRC, including tenascin C, nidogen 1, fibulin1 and vinculin. These data may reflect an ascending trend of malignancy from the first to the third metachronous colorectal cancer liver metastasis. Additionally, the results indicate different ECM phenotypes for recurrent metachronous metastasis, associated with different grades of malignancy and highlights the importance of individual analysis of molecular features in different, consecutive metastatic events in a single patient.

2021-09-09 | PXD020109 | Pride

Loss of skeletal muscle Bmal1 +/- Exercise Training [Mouse liver, heart, inguinal white adipose and lung tissues

Project description:Investigate the effects loss of skeletal muscle Bmal1 has on systemic transcriptomes +/- exercise training. Mouse liver, heart, white adipose and lung tissues were collected 47 hours post their last exercise bout, with or without 6-weeks of daily treadmill training. +/- Skeletal muscle Bmal1

2024-07-02 | GSE253735 | GEO

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.

2014-05-23 | GSE57880 | GEO

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks

Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays

2014-05-23 | E-GEOD-57880 | biostudies-arrayexpress

Nuclear Prohibitin 1 Protects Against Alcohol-Associated Liver Injury and Sensitization to Colon Cancer Liver Metastasis [Spatial Transcriptomics]

Project description:Alcohol-associated liver disease (ALD) is associated with higher incidence of colorectal liver metastasis (CRLM); prohibitin 1 (PHB1) defends against CRLM yet its role in ALD and ALD-CRLM is unknown and was investigated here. In human, murine, and in vitro ALD models, cytosolic and nuclear PHB1 were depleted, whereas mitochondrial PHB1 was preserved. Nuclear PHB1 loss was driven by CRM1-mediated export, and blocking this interaction with a PHB1 nuclear export signal (NES) peptide retained nuclear PHB1, ameliorating both ALD and ALD-CRLM. PHB1 NES prevented depletion of nuclear methionine adenosyltransferase α1, oxidative stress, and induction of matrix metalloproteinase 7 (MMP-7) and multiple oncogenes. Single-nucleus RNA sequencing of NIAAA diet-fed mouse livers revealed that PHB1 NES treatment mitigated alcohol-induced metabolic and oncogenic stress, attenuated pro-inflammation and pro-fibrogenic responses, and contributed to overall hepatoprotection. These findings identify nuclear PHB1 depletion as a driver and a promising therapeutic target in ALD and ALD-CRLM.

2026-09-14 | GSE338350 | GEO

Nuclear Prohibitin 1 Protects Against Alcohol-Associated Liver Injury and Sensitization to Colon Cancer Liver Metastasis [snRNA-seq]

2026-09-14 | GSE316359 | GEO

Role of aerobic exercise in ameliorating NASH

Project description:To investigate the effect of aerobic exercise on liver injury in nonalcoholic steatohepatitis (NASH), we established a NASH model induced by atherosclerotic (Ath) diet and intervened with aerobic exercise training.

2023-01-11 | GSE217155 | GEO

Gene expression profiling of neoadjuvant ABFOLFOX treatment in patients with unresectable colorectal cancer with liver metastases

Project description:To characterize the impact of neoadjuvant ABFOLFOX (Atezolizumab, Bevacizumab, and FOLFOX) therapy on the tumor microenvironment of colorectal liver metastases (CRLM), we performed a comprehensive molecular analysis using bulk RNA-seq. The study comprised two distinct cohorts: a cross-sectional cohort (Cohort A, n=60) and a prospective longitudinal cohort (Cohort B, n=20). Cohort A included patients who underwent hepatic surgery, categorized into three groups (n=20 each): those who underwent upfront surgery (G1 group); those treated with neoadjuvant chemotherapy (NAC; FOLFOX or FOLFIRI) (G2 group); and those treated with NAC plus bevacizumab (G3 group). In Cohort B, CRLM specimens were analyzed at three serial time points: T0 (baseline liver biopsy), T1 (biopsy after atezolizumab monotherapy), and T2 (surgical or biopsied specimen after ABFOLFOX). Our findings suggest a progressive increase in immunogenicity within the CRLM tumor ecosystem following treatment. In particular, the monocyte lineage and SP140 regulon appear to serve as potential mediators of the observed therapeutic benefits. This submission presents the transcriptomic data supporting the interplay between systemic therapy and the immune landscape in CRLM.

2026-05-21 | GSE330465 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data