ArticleDevelopmental cell2018
Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia.
Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 54 citations in OpenAlex.
- Twist1 overexpression models an aggressive subtype of pancreatic ductal adenocarcinoma in vivo.Lab animal · 2026Article
- MyoRep: A Novel Reporter System to Detect Early Muscle Atrophy In Vitro and In Vivo.Journal of cachexia, sarcopenia and muscle · 2026Article
- Review
- The myoblast methylome: multiple types of associations with chromatin and transcription.Epigenetics · 2025Article
- Skeletal muscle endothelial dysfunction through the activin A-PGC1α axis drives progression of cancer cachexia.Nature cancer · 2025Article
- Metabolic regulation in adult and aging skeletal muscle stem cells.Genes & development · 2025Review
- Genetics and biology of pancreatic ductal adenocarcinoma.Genes & development · 2025Review
- Temporal dynamics of gene and protein signatures following volumetric muscle loss.Frontiers in cell and developmental biology · 2025Article
- Review
- Cancer cachexia: multilevel metabolic dysfunction.Nature metabolism · 2024Review
- Proteasome gene expression is controlled by coordinated functions of multiple transcription factors.The Journal of cell biology · 2024Article
- Optimization of a mouse model of pancreatic cancer to simulate the human phenotypes of metastasis and cachexia.BMC cancer · 2024Article
- Advancing cancer cachexia diagnosis with -omics technology and exercise as molecular medicine.Sports medicine and health science · 2024Review
- Oncometabolite D-2-hydroxyglutarate-dependent metabolic reprogramming induces skeletal muscle atrophy during cancer cachexia.Communications biology · 2023Article
- Molecular mechanisms of cancer cachexia-related loss of skeletal muscle mass: data analysis from preclinical and clinical studies.Journal of cachexia, sarcopenia and muscle · 2023Review
- TWIST2-mediated chromatin remodeling promotes fusion-negative rhabdomyosarcoma.Science advances · 2023Article
- Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer.The Journal of cell biology · 2023Article
- Identify potential driver genes for PAX-FOXO1 fusion-negative rhabdomyosarcoma through frequent gene co-expression network mining.Frontiers in oncology · 2023Article
- Impact of cancer cachexia on respiratory muscle function and the therapeutic potential of exercise.The Journal of physiology · 2022Review
- NF1 loss of function as an alternative initiating event in pancreatic ductal adenocarcinoma.Cell reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Cancer cachexia is characterized by extreme skeletal muscle loss that results in high morbidity and mortality. The incidence of cachexia varies among tumor types, being lowest in sarcomas, whereas 90% of pancreatic ductal adenocarcinoma (PDAC) patients experience severe weight loss. How these tumors trigger muscle depletion is still unfolding. Serendipitously, we found that overexpression of Twist1 in mouse muscle progenitor cells, either constitutively during development or inducibly in adult animals, caused severe muscle atrophy with features reminiscent of cachexia. Using several genetic mouse models of PDAC, we detected a marked increase in Twist1 expression in muscle undergoing cachexia. In cancer patients, elevated levels of Twist1 are associated with greater degrees of muscle wasting. Finally, both genetic and pharmacological inactivation of Twist1 in muscle progenitor cells afforded substantial protection against cancer-mediated cachexia, which translated into meaningful survival benefits, implicating Twist1 as a possible target for attenuating muscle cachexia in cancer patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.