ArticleCancer research2015
Gain of glucose-independent growth upon metastasis of breast cancer cells to the brain.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 189 citations in OpenAlex.
- Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.Biomarker research · 2026Review
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Targeting MET in non-small cell lung cancer brain metastases: from molecular mechanism to precision therapy.Journal of translational medicine · 2026Review
- The evolving landscape of brain metastasis: volume II.Trends in cancer · 2026Review
- Breast cancer brain metastasis: mechanisms, emerging biomarkers, and therapeutic opportunities.American journal of cancer research · 2026Review
- Targeting the metabolic niche: vulnerabilities and opportunities in brain metastases.Oxford open neuroscience · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Breast cancer brain metastasis: from molecular insights to therapeutic innovation.Frontiers in immunology · 2026Review
- GlycoRNA in cancer immune regulation and progression: biological mechanisms and translational therapeutic prospects.Frontiers in immunology · 2026Review
- The role and research progress of FGF21 in breast cancer: a review.Frontiers in oncology · 2026Review
- Multi-omics investigation reveals molecular determinants of cancer cell evolution on soft extracellular matrix.bioRxiv : the preprint server for biology · 2025Article
- Metabolic adaptations of brain metastasis.Nature reviews. Cancer · 2025Review
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Review
- Metabolic reprogramming in glioblastoma: a rare case of recurrence to scalp metastasis.BJC reports · 2025Article
- Cancer metastasis: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2025Review
- Metabolic interplays between the tumour and the host shape the tumour macroenvironment.Nature reviews. Cancer · 2025Review
- Mucin 5AC Promotes Breast Cancer Brain Metastasis through cMET/CD44v6.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- MicroRNAs in Lung Cancer Brain Metastasis.International journal of molecular sciences · 2024Review
- Glucose metabolism in B cell malignancies: a focus on glycolysis branching pathways.Molecular oncology · 2024Review
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer brain metastasis is resistant to therapy and a particularly poor prognostic feature in patient survival. Altered metabolism is a common feature of cancer cells, but little is known as to what metabolic changes benefit breast cancer brain metastases. We found that brain metastatic breast cancer cells evolved the ability to survive and proliferate independent of glucose due to enhanced gluconeogenesis and oxidations of glutamine and branched chain amino acids, which together sustain the nonoxidative pentose pathway for purine synthesis. Silencing expression of fructose-1,6-bisphosphatases (FBP) in brain metastatic cells reduced their viability and improved the survival of metastasis-bearing immunocompetent hosts. Clinically, we showed that brain metastases from human breast cancer patients expressed higher levels of FBP and glycogen than the corresponding primary tumors. Together, our findings identify a critical metabolic condition required to sustain brain metastasis and suggest that targeting gluconeogenesis may help eradicate this deadly feature in advanced breast 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.