ReviewCell cycle (Georgetown, Tex.)2006
Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy.
Review in Cell cycle (Georgetown, Tex.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 92 citations in OpenAlex.
- Combined Analysis of Bulk and Single-Cell Transcriptomic Data Reveals Dormancy-Associated Genes in Colorectal Cancer.International journal of molecular sciences · 2026Article
- NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer.Nature communications · 2026Article
- Collagen hydroxylation couples NAD+/NADH dynamics to tumor dormancy and reactivation.Research square · 2025Article
- Active fraction of ground cherry (Biomedical reports · 2024Article
- Advancements in Understanding the Hide-and-Seek Strategy of Hibernating Breast Cancer Cells and Their Implications in Oncology from a Broader Perspective: A Comprehensive Overview.Current issues in molecular biology · 2024Review
- Intercellular Molecular Transfer Mediated by Extracellular Vesicles in Cancer.Results and problems in cell differentiation · 2024Review
- Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors.Experientia supplementum (2012) · 2022Article
- Ribociclib Induces Broad Chemotherapy Resistance and EGFR Dependency in ESR1 Wildtype and Mutant Breast Cancer.Cancers · 2021Article
- MAGI1 inhibits the AMOTL2/p38 stress pathway and prevents luminal breast tumorigenesis.Scientific reports · 2021Article
- Article
- Epithelial-Mesenchymal Transition Programs and Cancer Stem Cell Phenotypes: Mediators of Breast Cancer Therapy Resistance.Molecular cancer research : MCR · 2020Review
- The Role of the ECM in Lung Cancer Dormancy and Outgrowth.Frontiers in oncology · 2020Review
- Bone secreted factors induce cellular quiescence in prostate cancer cells.Scientific reports · 2019Article
- Review
- Silencing ofFrontiers in cell and developmental biology · 2019Article
- Bioengineered models to study tumor dormancy.Journal of biological engineering · 2019Review
- Dormant tumour cells, their niches and the influence of immunity.Nature cell biology · 2018Review
- Osteoblast-Secreted Factors Mediate Dormancy of Metastatic Prostate Cancer in the Bone via Activation of the TGFβRIII-p38MAPK-pS249/T252RB Pathway.Cancer research · 2018Article
- Modeling treatment-dependent glioma growth including a dormant tumor cell subpopulation.BMC cancer · 2018Article
- EngineeredJournal of biological engineering · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cancer dormancy is a poorly understood stage of cancer progression. However, the ability to control this step of the disease offers novel therapeutic opportunities. Here we summarize recent findings that implicate the extracellular matrix and adhesion receptor signaling in the escape or induction of tumor dormancy. We further review evidence suggesting that imbalances in the activity ratio of ERK to p38 signaling may determine the fate (i.e., tumorigenicity vs. dormancy) of different carcinoma cells. Special attention is placed on the mechanisms that p38 signaling regulates during the induction of dormancy and how modulation of these pathways may offer a therapeutic opportunity. We also review evidence for a novel drug-resistance mechanism in dormant tumor cells that when blocked may enable killing of dormant tumor cells. Finally, we explore the notion that dormancy of tumor cells may be the result of a selective adaptive response that allows disseminated tumor cells to pause their growth and cope with stress signaling imposed by dissemination and/or treatment until growth can be restored.
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.