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UnknownCancer stem cell drugs target K-ras signaling in a stemness context.
Cancer stem cells (CSCs) are considered to be responsible for treatment relapse and have therefore become a major target in cancer research. Salinomycin is the most established CSC inhibitor. However, its primary mechanistic target is still unclear, impeding the discovery of compounds with similar a...
S-EPMC5057041 | biostudies-literature
ProteomicsMetabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target
The genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutations such as mutant KRAS. Here we used genetically engineered mouse models (GEMMs), and multimodal mass spectrometry-based metabolomics to study the impact of co...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Mus Musculus (ncbitaxon:10090) 
2023-07-18 | MSV000092468 | MassIVE
UnknownKRAS allelic imbalance drives tumour initiation yet suppresses metastasis in colorectal cancer in vivo.
Oncogenic KRAS mutations are well-described functionally and are known to drive tumorigenesis. Recent reports describe a significant prevalence of KRAS allelic imbalances or gene dosage changes in human cancers, including loss of the wild-type allele in KRAS mutant cancers. However, the role of wild...
S-EPMC10762264 | biostudies-literature
UnknownKRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition.
Pancreatic cancer is characterized by the prevalence of oncogenic mutations in KRAS. Previous studies have reported that altered KRAS gene dosage drives progression and metastasis in pancreatic cancer. Whereas the role of oncogenic KRAS mutations is well characterized, the relevance of the partnerin...
S-EPMC11733531 | biostudies-literature
MetabolomicsGNPS - Metabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target
The genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutations such as mutant KRAS. Here we used genetically engineered mouse models (GEMMs), and multimodal mass spectrometry-based metabolomics to study the impact of co...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Mus Musculus (ncbitaxon:10090) 
2023-07-18 | MSV000092468 | GNPS
UnknownA RAC-GEF network critical for early intestinal tumourigenesis.
RAC1 activity is critical for intestinal homeostasis, and is required for hyperproliferation driven by loss of the tumour suppressor gene Apc in the murine intestine. To avoid the impact of direct targeting upon homeostasis, we reasoned that indirect targeting of RAC1 via RAC-GEFs might be effective...
S-EPMC7782582 | biostudies-literature
UnknownDynamic and adaptive cancer stem cell population admixture in colorectal neoplasia.
Intestinal homeostasis is underpinned by LGR5+ve crypt-base columnar stem cells (CBCs), but following injury, dedifferentiation results in the emergence of LGR5-ve regenerative stem cell populations (RSCs), characterized by fetal transcriptional profiles. Neoplasia hijacks regenerative signaling, so...
S-EPMC9592560 | biostudies-literature
UnknownNOTUM from Apc-mutant cells biases clonal competition to initiate cancer.
The tumour suppressor APC is the most commonly mutated gene in colorectal cancer. Loss of Apc in intestinal stem cells drives the formation of adenomas in mice via increased WNT signalling1, but reduced secretion of WNT ligands increases the ability of Apc-mutant intestinal stem cells to ...
S-EPMC7615049 | biostudies-literature
UnknownMetabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target.
The genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutations such as mutant KRAS. Here we used genetically engineered mouse models, and multimodal mass spectrometry-based metabolomics to study the impact of common gen...
S-EPMC10447251 | biostudies-literature
UnknownHepatocellular senescence induces multi-organ senescence and dysfunction via TGFβ.
Cellular senescence is not only associated with ageing but also impacts physiological and pathological processes, such as embryonic development and wound healing. Factors secreted by senescent cells affect their microenvironment and can induce spreading of senescence locally. Acute severe liver dise...
S-EPMC11628396 | biostudies-literature
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