ArticleChemotherapy research and practice2012
Extracellular matrix proteins modulate antimigratory and apoptotic effects of Doxorubicin.
Article in Chemotherapy research and practice, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 29 citations in OpenAlex.
- Glypican 3 as target therapy to prevent cell migration and proliferation in rhabdomyosarcoma.Scientific reports · 2025Article
- Integrated bioinformatics analysis reveals upregulated extracellular matrix hub genes in pancreatic cancer: Implications for diagnosis, prognosis, immune infiltration, and therapeutic strategies.Cancer reports (Hoboken, N.J.) · 2024Article
- Imaging and quantification of the tumor microenvironment of triple negative breast cancer using TPEF and scanning laser optical tomography.Biomedical optics express · 2023Article
- GelMA, Click-Chemistry Gelatin and Bioprinted Polyethylene Glycol-Based Hydrogels as 3D Ex Vivo Drug Testing Platforms for Patient-Derived Breast Cancer Organoids.Pharmaceutics · 2023Article
- The Role of Extracellular Matrix Proteins in Breast Cancer.Journal of clinical medicine · 2022Review
- CAM-DR: Mechanisms, Roles and Clinical Application in Tumors.Frontiers in cell and developmental biology · 2021Review
- The matrix-dependent 3D spheroid model of the migration of non-small cell lung cancer: a step towards a rapid automated screening.Frontiers in molecular biosciences · 2021Article
- Expression of TIMPs and MMPs in Ovarian Tumors, Ascites, Ascites-Derived Cells, and Cancer Cell Lines: Characteristic Modulatory Response Before and After Chemotherapy Treatment.Frontiers in oncology · 2021Article
- Breast cancer models: Engineering the tumor microenvironment.Acta biomaterialia · 2020Review
- Commentary on, "Generation of Three-dimensional Human Neuronal Cultures: Application to Modeling CNS Viral Infections".Journal of infectiology · 2019Article
- Current diagnostics and treatment of fibrosarcoma -perspectives for future therapeutic targets and strategies.Oncotarget · 2017Review
- Glycosylation in Cancer: Interplay between Multidrug Resistance and Epithelial-to-Mesenchymal Transition?Frontiers in oncology · 2016Review
- Complement System Part II: Role in Immunity.Frontiers in immunology · 2015Review
- The impact of chemotherapy and radiation therapy on the remodeling of acellular dermal matrices in staged, prosthetic breast reconstruction.Plastic and reconstructive surgery · 2015Article
- Dynamic monitoring of mechano-sensing of cells by gold nanoslit surface plasmon resonance sensor.PloS one · 2014Article
- Effect of nano-zinc oxide on doxorubicin- induced oxidative stress and sperm disorders in adult male Wistar rats.Iranian journal of reproductive medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anticancer drug resistance is a multifactorial process that includes acquired and de novo drug resistances. Acquired resistance develops during treatment, while de novo resistance is the primary way for tumor cells to escape chemotherapy. Tumor microenvironment has been recently shown to be one of the important factors contributing to de novo resistance and called environment-mediated drug resistance (EMDR). Two forms of EMDR have been described: soluble factor-mediated drug resistance (SFM-DR) and cell adhesion-mediated drug resistance (CAM-DR). Anthracyclines, among the most potent chemotherapeutic agents, are widely used in clinics against hematopoietic and solid tumors. Their main mechanism of action relies on the inhibition of topoisomerase I and/or II and the induction of apoptosis. Beyond this well-known antitumor activity, it has been recently demonstrated that anthracyclines may display potent anti-invasive effects when used at subtoxic concentrations. In this paper, we will describe two particular modes of EMDR by which microenvironment may influence tumor-cell response to one of these anthracyclines, doxorubicin. The first one considers the influence of type I collagen on the antimigratory effect of doxorubicin (CAM-DR). The second considers the protection of tumor cells by thrombospondin-I against doxorubicin-induced apoptosis (SFM-DR).
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.