tumor growth phenotype
Evidence from:
primary |
all sources
Related entities (2)
| Subject | Relation | Object | p-value | Evidence |
|---|---|---|---|---|
| astrocytes | risk_factor_for | tumor growth | — | 1 |
| Ctbp2 | regulates | tumor growth | — | 1 |
Mentioned in (38)
Papers in which this entity is mentioned.
- Extrachromosomal DNA-Driven Oncogene Spatial Heterogeneity and Evolution in Glioblastoma. (2025)
- FET fusion oncoproteins disrupt physiologic DNA repair and create a targetable opportunity for ATR inhibitor therapy. (2025)
- Tumor-informed deep sequencing of ctDNA detects minimal residual disease and predicts relapse in osteosarcoma. (2024)
- ENPP1 Immunobiology as a Therapeutic Target. (2023)
- Desmoplastic stromal signatures predict patient outcomes in pancreatic ductal adenocarcinoma. (2023)
- Osteoclasts in Osteosarcoma: Mechanisms, Interactions, and Therapeutic Prospects. (2023)
- Towards understandings of serine/arginine-rich splicing factors. (2023)
- RNA splicing dysregulation and the hallmarks of cancer. (2023)
- Construction and validation of a novel gene signature for predicting the prognosis of osteosarcoma. (2022)
- Macrophage Polarization States in the Tumor Microenvironment. (2021)
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer. (2020)
- Single-cell RNA landscape of intratumoral heterogeneity and immunosuppressive microenvironment in advanced osteosarcoma. (2020)
- Astrocyte Reactivity: Subtypes, States, and Functions in CNS Innate Immunity. (2020)
- Single-Cell RNA-Seq Reveals AML Hierarchies Relevant to Disease Progression and Immunity. (2019)
- Whole-exome sequencing of cervical carcinomas identifies activating ERBB2 and PIK3CA mutations as targets for combination therapy. (2019)
- Genome-Informed Targeted Therapy for Osteosarcoma. (2019)
- Positively selected enhancer elements endow osteosarcoma cells with metastatic competence. (2018)
- Sexual Dimorphism of miRNAs Secreted by Bovine -produced Embryos. (2017)
- B lymphocytes and cancer: a love-hate relationship. (2016)
- Inhibition of Mammary Cancer Progression in Fetal Alcohol Exposed Rats by β-Endorphin Neurons. (2016)
- Evolutionary Insights into RNA trans-Splicing in Vertebrates. (2016)
- CtBP2 is an independent prognostic marker that promotes GLI1 induced epithelial-mesenchymal transition in hepatocellular carcinoma. (2015)
- Endocannabinoids are conserved inhibitors of the Hedgehog pathway. (2015)
- Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing. (2015)
- Activation of the FGFR-STAT3 pathway in breast cancer cells induces a hyaluronan-rich microenvironment that licenses tumor formation. (2014)
- CDK9-mediated transcription elongation is required for MYC addiction in hepatocellular carcinoma. (2014)
- PVT1 dependence in cancer with MYC copy-number increase. (2014)
- Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis. (2014)
- Mitogen-activated protein kinase modulates ethanol inhibition of cell adhesion mediated by the L1 neural cell adhesion molecule. (2013)
- Large-scale genotyping identifies 41 new loci associated with breast cancer risk. (2013)
- Differential expression profiles of glycosphingolipids in human breast cancer stem cells vs. cancer non-stem cells. (2013)
- Myeloid cells in tumor inflammation. (2012)
- Chronic shift-lag alters the circadian clock of NK cells and promotes lung cancer growth in rats. (2012)
- Regulation of cancer progression by β-endorphin neuron. (2012)
- Cellular metabolic stress: considering how cells respond to nutrient excess. (2010)
- Adrenomedullin signaling is necessary for murine lymphatic vascular development. (2008)
- Competing interactions between micro-RNAs determine neural progenitor survival and proliferation after ethanol exposure: evidence from an ex vivo model of the fetal cerebral cortical neuroepithelium. (2007)
- Perlecan, a candidate gene for the CAPB locus, regulates prostate cancer cell growth via the Sonic Hedgehog pathway. (2006)
Merged raw entities (1)
All extracted name/type variants the normalize job merged into this entity. Use this to spot wrong merges, or aliases that should be split off.
| Raw name | Type | Papers | Mentions |
|---|---|---|---|
| tumor growth | phenotype | 38 | 77 |