ArticleMolecular systems biology2017
Recurrent patterns of DNA copy number alterations in tumors reflect metabolic selection pressures.
Article in Molecular systems biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 85 citations in OpenAlex.
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Aneuploidy promotes transient stress adaptation and metabolic flexibility in the human fungal pathogen Aspergillus fumigatus.Current biology : CB · 2026Article
- NAD+/SIRT1 pathway regulates glycolysis to promote oxaliplatin resistance in colorectal cancer.World journal of gastroenterology · 2025Article
- Genetic Screen in a Preclinical Model of Sarcoma Development Defines Drivers and Therapeutic Vulnerabilities.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Metabolic adaptations in prostate cancer.British journal of cancer · 2024Review
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
- Ancestral aneuploidy and stable chromosomal duplication resulting in differential genome structure and gene expression control in trypanosomatid parasites.Genome research · 2024Article
- Evolutionary determinants of curability in cancer.Nature ecology & evolution · 2023Review
- Convergent TP53 loss and evolvability in cancer.BMC ecology and evolution · 2023Review
- GATA2 co-opts TGFβ1/SMAD4 oncogenic signaling and inherited variants at 6q22 to modulate prostate cancer progression.Journal of experimental & clinical cancer research : CR · 2023Article
- A fitness trade-off explains the early fate of yeast aneuploids with chromosome gains.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Unique Metabolic Contexts Sensitize Cancer Cells and Discriminate between Glycolytic Tumor Types.Cancers · 2023Article
- Chromosomal Instability, Selection and Competition: Factors That Shape the Level of Karyotype Intra-Tumor Heterogeneity.Cancers · 2022Review
- CONET: copy number event tree model of evolutionary tumor history for single-cell data.Genome biology · 2022Article
- Article
- Aneuploidy tolerance caused by BRG1 loss allows chromosome gains and recovery of fitness.Nature communications · 2022Article
- Tipping Cancer Cells Over the Edge: The Context-Dependent Cost of High Ploidy.Cancer research · 2022Article
- Article
- Loss of hexokinase 1 sensitizes ovarian cancer to high-dose metformin.Cancer & metabolism · 2021Article
- Molecular characterization of ulcerative colitis-associated colorectal carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 7 institutions in 3 countries.
Funding
Abstract
Copy number alteration (CNA) profiling of human tumors has revealed recurrent patterns of DNA amplifications and deletions across diverse cancer types. These patterns are suggestive of conserved selection pressures during tumor evolution but cannot be fully explained by known oncogenes and tumor suppressor genes. Using a pan-cancer analysis of CNA data from patient tumors and experimental systems, here we show that principal component analysis-defined CNA signatures are predictive of glycolytic phenotypes, including
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.