Animal studyMechanismReported positivePreclinical onlyTier 2 · animal
Trends in pharmacological sciences · Nov 2025 · commentary/review of a study
glioblastomabrain neoplasms
This article discusses a study in glioblastoma showing that tumor cells took up more serine. It also reports that limiting serine uptake made chemoradiation work better in preclinical models. The abstract is mainly a commentary on emerging research rather than a full original trial report.
Studied with: chemoradiation.
Key findings
- Tumor metabolism in glioblastoma patients showed increased import of serine.
- Limiting serine uptake enhanced the effectiveness of chemoradiation in preclinical models of glioblastoma.
Limitations: This is not a full original study report; it is a commentary/review-style article.; The abstract does not provide methods, sample size, or quantitative results.; The sensitization finding is preclinical, so human clinical benefit is unproven..
Discusses a metabolic vulnerability in glioblastoma and preclinical chemoradiation sensitization.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
Cell · Jan 2025 · preclinical experimental study using retrograde tracing and genetic ablation in glioblastoma models
glioblastomabrain neoplasms
This study used rabies-virus-based retrograde tracing to map neurons connected to glioblastoma in experimental models. The authors found that glioblastoma formed widespread connections with neurons, and that cholinergic neurons promoted invasion. They also reported that radiotherapy increased neuron-tumor connectivity, while blocking neuronal activity together with radiotherapy had greater effects, and that genetic ablation of tumor-connected neurons halted glioblastoma progression in their models.
Studied with: radiotherapy.
Key findings
- Glioblastoma integrated into neural circuits across the brain and showed widespread functional communication.
- Cholinergic neurons were reported to drive glioblastoma invasion.
- Radiotherapy increased neuron-tumor connectivity by increasing neuronal activity.
- Simultaneous neuronal activity inhibition and radiotherapy showed increased therapeutic effects in the models.
- Rabies-mediated genetic ablation of tumor-connected neurons halted glioblastoma progression in the study models.
Limitations: Preclinical animal/model-system study; no human clinical outcomes reported.; The abstract does not provide sample size, effect sizes, or statistical details.; Use of rabies-virus-based tracing and genetic ablation is experimental and not a standard clinical intervention.; Findings are based on glioblastoma models, so generalizability to patients is uncertain..
The study focuses on glioblastoma biology and experimental targeting of neuron-tumor networks, not on a repurposed drug or natural compound.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab
Redox biology · Oct 2022 · cell culture mechanistic study
This laboratory study looked at TRIM7 in human glioblastoma cells. The authors found that lowering TRIM7 reduced cell growth and increased cell death, while increasing TRIM7 had the opposite effect. They also reported that TRIM7 reduced NCOA4-related ferritinophagy and ferroptosis, and that removing TRIM7 made the cells more sensitive to temozolomide.
Studied with: temozolomide.
Key findings
- TRIM7 expression was elevated in human glioblastoma cells and tissues.
- TRIM7 silence suppressed growth and induced death, while TRIM7 overexpression facilitated growth and inhibited death of human glioblastoma cells.
- TRIM7-silenced cells exhibited increased iron accumulation, lipid peroxidation and ferroptosis, which were significantly reduced by TRIM7 overexpression.
- TRIM7 directly bound to and ubiquitinated NCOA4 using K48-linked chains, thereby reducing NCOA4-mediated ferritinophagy and ferroptosis.
- TRIM7 deletion sensitized human glioblastoma cells to temozolomide therapy.
Limitations: In vitro cell-line study only; no animal or human outcomes.; Mechanistic findings are based on engineered TRIM7 knockdown/overexpression models.; No quantitative effect sizes, sample size, or dose information were reported in the abstract.; Clinical relevance is uncertain because the study did not test patient outcomes..
The study examines a molecular mechanism in glioblastoma cells and how TRIM7 affects cell growth, ferroptosis, and temozolomide sensitivity.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismMixed resultsLimited evidenceTier 1 · lab
International journal of molecular sciences · Aug 2021 · review
breast cancercolon cancerprostate cancerendometrial cancerthyroid cancerbladder cancerglioblastomaadrenocortical carcinomaovarian epithelial carcinoma
This review discusses nucleobindin-2/nesfatin-1 (NUCB2/NESF-1) as a cancer-related molecule. It summarizes reports that higher expression is linked with poorer outcomes and with increased cancer cell proliferation, migration, and invasion in several cancers, while other reports suggest it may inhibit growth in some cancer cell types. The article does not present new experimental data.
Key findings
- High NUCB2/NESF-1 expression has been associated with poor outcomes in several cancers.
- Reported effects include increased cell proliferation, migration, and invasion in breast, colon, prostate, endometrial, thyroid, and bladder cancers, and glioblastoma.
- The review also notes conflicting findings where nesfatin-1 inhibited proliferation in human adrenocortical carcinoma and ovarian epithelial carcinoma cells.
- The authors propose NUCB2/NESF-1 as a prognostic and predictive marker in cancers.
Limitations: Review article; no original experimental or clinical data.; The abstract summarizes heterogeneous prior studies with conflicting findings.; No quantitative effect estimates are reported in the abstract.; No details on study quality, sample sizes, or methods of the cited studies are provided..
This is a review of a molecule reported to be associated with cancer progression and prognosis, not a primary intervention study.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMixed resultsLimited evidenceTier 4 · clinical
Therapeutics and clinical risk management · Dec 2015 · review
This review discusses bevacizumab for glioblastoma and summarizes prior findings. It says bevacizumab can promote tumor regression and reduce cerebral edema, and that adding it to standard chemoradiotherapy with temozolomide prolonged progression-free survival and improved performance status in newly diagnosed glioblastoma. However, it did not extend overall survival, and the review emphasizes balancing benefits and risks.
Studied with: temozolomide, chemoradiotherapy.
Key findings
- Bevacizumab was described as promoting tumor regression and improving cerebral edema.
- The review states that adding bevacizumab to standard chemoradiotherapy with temozolomide prolonged progression-free survival and improved performance status.
- The review states that overall survival was not extended.
- The review notes adverse events, especially hypertension and proteinuria, and that many other adverse events overlap with glioblastoma complications.
Limitations: This is a narrative review, not a primary study.; No new patient data or original analyses are presented in the abstract.; Quantitative effect sizes are not reported in the abstract.; The abstract does not specify the underlying studies' sample sizes or follow-up durations..
Review of bevacizumab use in glioblastoma, focusing on efficacy, safety, and clinical challenges.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveLimited evidenceTier 4 · clinical
Future oncology (London, England) · Dec 2014 · Review
gastric cancerglioblastoma multiformehepatocellular carcinomabladder cancerlung cancercolon cancerovarian cancerleukemiabreast cancerhead and neck cancerrhabdomyosarcomaneuroblastoma
This is a narrative review summarizing published reports about the adaptor protein CRKL in cancer. The authors report that CRKL is overexpressed in many tumor types and appears to promote aggressive or malignant behaviors, and they suggest CRKL has potential as a diagnostic/prognostic biomarker.
Key findings
- CRKL is a member of the CRK family and functions as an adaptor protein in intracellular signal transduction.
- CRKL has been reported overexpressed in a variety of cancers.
- CRKL appears to play a tumor-promotion role in multiple cancers, including those listed in the abstract.
- The review summarizes associations between CRKL and malignant tumor behaviors and potential mechanisms of action.
- The authors state CRKL has potential to be used as a biomarker for diagnosis, treatment and prognosis of certain tumors.
Limitations: This is a review article and does not present new primary experimental data.; Abstract provides no information on search strategy, inclusion criteria, or quality assessment of included studies.; Heterogeneity across many cancer types and study designs likely limits generalizability of conclusions.; The abstract does not report quantitative synthesis or effect sizes..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed