ArticleBritish journal of cancer2007
Cellular adaptations to hypoxia and acidosis during somatic evolution of breast cancer.
Article in British journal of cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 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
172 citing papers in PubMed, 343 citations in OpenAlex.
- Quinazoline-sulfonamide hybrids as multitarget anticancer agents: inhibition of carbonic anhydrase IX/XII isoforms and VEGFR-2 with in vitro and in silico validation.Molecular diversity · 2026Article
- 3D bioprinted in vitro models in cancer metabolism research.Magyar onkologia · 2026Review
- Modeling VEGF and GLUT1 Expression as Coadapted Foraging Strategies in Cancer.bioRxiv : the preprint server for biology · 2026Article
- Matters of life and death in computational cell biology.NPJ systems biology and applications · 2026Review
- Role of the NHE1 exchanger in the antitumor effects of copper(II) complexes and phenanthroline derivatives.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Article
- Article
- Article
- In vivo imaging of the spatial heterogeneity of intratumoral acidosis (pH) as a marker of the metastatic phenotype in breast cancer.Breast cancer research : BCR · 2025Article
- Evolutionary rescue model informs strategies for driving cancer cell populations to extinction.bioRxiv : the preprint server for biology · 2025Article
- Assessment of Hypoxia in Breast Cancer: Emerging Functional MR Imaging and Spectroscopy Techniques and Clinical Applications.Journal of magnetic resonance imaging : JMRI · 2025Review
- Targeting Hypoxia-Inducible Factor-1α in Pancreatic Cancer: siRNA Delivery Using Hyaluronic Acid-Displaying Nanoparticles.Pharmaceutics · 2024Article
- How Does Cancer Occur? How Should It Be Treated? Treatment from the Perspective of Alkalization Therapy Based on Science-Based Medicine.Biomedicines · 2024Review
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- Review
- Metabolic factors associated with the prognosis of oligometastatic patients treated with stereotactic body radiotherapy.Cancer metastasis reviews · 2023Review
- Desipramine induces eryptosis in human erythrocytes, an effect blunted by nitric oxide donor sodium nitroprusside and N-acetyl-L-cysteine but enhanced by Calcium depletion.Cell cycle (Georgetown, Tex.) · 2023Article
- Voltage-Gated Sodium Channel NaCancers · 2023Article
- NF-κB mediated regulation of tumor cell proliferation in hypoxic microenvironment.Frontiers in pharmacology · 2023Review
- Review
- Molecular signatures of in situ to invasive progression for basal-like breast cancers: An integrated mouse model and human DCIS study.NPJ breast cancer · 2022Article
112 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
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conceptual models of carcinogenesis typically consist of an evolutionary sequence of heritable changes in genes controlling proliferation, apoptosis, and senescence. We propose that these steps are necessary but not sufficient to produce invasive breast cancer because intraductal tumour growth is also constrained by hypoxia and acidosis that develop as cells proliferate into the lumen and away from the underlying vessels. This requires evolution of glycolytic and acid-resistant phenotypes that, we hypothesise, is critical for emergence of invasive cancer. Mathematical models demonstrate severe hypoxia and acidosis in regions of intraductal tumours more than 100 microm from the basement membrane. Subsequent evolution of glycolytic and acid-resistant phenotypes leads to invasive proliferation. Multicellular spheroids recapitulating ductal carcinoma in situ (DCIS) microenvironmental conditions demonstrate upregulated glucose transporter 1 (GLUT1) as adaptation to hypoxia followed by growth into normoxic regions in qualitative agreement with model predictions. Clinical specimens of DCIS exhibit periluminal distribution of GLUT-1 and Na(+)/H(+) exchanger (NHE) indicating transcriptional activation by hypoxia and clusters of the same phenotype in the peripheral, presumably normoxic regions similar to the pattern predicted by the models and observed in spheroids. Upregulated GLUT-1 and NHE-1 were observed in microinvasive foci and adjacent intraductal cells. Adaptation to hypoxia and acidosis may represent key events in transition from in situ to invasive cancer.
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.