ArticleBlood2009
Toward a stem cell gene therapy for breast cancer.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Engineered artificial antigen-presenting cells for tumor immunotherapy: Design strategies, clinical applications, and translational challenges.Materials today. Bio · 2026Review
- Relaxin-2-secreting CAR-T cells exhibit enhanced efficacy in stromal-rich xenograft tumors.Frontiers in immunology · 2025Article
- Role of Relaxin Signaling in Cancer: A Review.Biochemical pharmacology · 2024Review
- The diverse influences of relaxin-like peptide family on tumor progression: Potential opportunities and emerging challenges.Heliyon · 2024Review
- Programmed Death-Ligand (PD-L1), Epidermal Growth Factor (EGF), Relaxin, and Matrix Metalloproteinase-3 (MMP3): Potential Biomarkers of Malignancy in Canine Mammary Neoplasia.International journal of molecular sciences · 2024Article
- Applications of Innovation Technologies for Personalized Cancer Medicine: Stem Cells and Gene-Editing Tools.ACS pharmacology & translational science · 2023Review
- Relaxins enhance growth of spontaneous murine breast cancers as well as metastatic colonization of the brain.Clinical & experimental metastasis · 2014Article
- Penton-dodecahedral particles trigger opening of intercellular junctions and facilitate viral spread during adenovirus serotype 3 infection of epithelial cells.PLoS pathogens · 2013Article
- Activation of the sonic hedgehog signaling pathway occurs in the CD133 positive cells of mouse liver cancer Hepa 1-6 cells.OncoTargets and therapy · 2013Article
- High expression of Sonic Hedgehog signaling pathway genes indicates a risk of recurrence of breast carcinoma.OncoTargets and therapy · 2013Article
- Overcoming physical barriers in cancer therapy.Tissue barriers · 2013Article
- Strategies to increase drug penetration in solid tumors.Frontiers in oncology · 2013Article
- Induced transgene expression for the treatment of solid tumors by hematopoietic stem cell-based gene therapy.Cancer gene therapy · 2012Article
- Hematopoietic stem cells: transcriptional regulation, ex vivo expansion and clinical application.Current molecular medicine · 2012Review
- Epithelial junction opener JO-1 improves monoclonal antibody therapy of cancer.Cancer research · 2011Article
- Controlled extracellular matrix degradation in breast cancer tumors improves therapy by trastuzumab.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Immuno-therapy with anti-CTLA4 antibodies in tolerized and non-tolerized mouse tumor models.PloS one · 2011Article
- Desmoglein 2 is a receptor for adenovirus serotypes 3, 7, 11 and 14.Nature medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Current approaches for treatment of late-stage breast cancer rarely result in a long-term cure. In part this is due to tumor stroma that prevents access of systemically or intratumorally applied therapeutics. We propose a stem cell gene therapy approach for controlled tumor stroma degradation that uses the pathophysiologic process of recruitment of inflammatory cells into the tumor. This approach involves genetic modification of hematopoietic stem cells (HSCs) and their subsequent transplantation into tumor-bearing mice. We show that inducible, intratumoral expression of relaxin (Rlx) either by transplanting tumor cells that contained the Rlx gene or by transplantation of mouse HSCs transduced with an Rlx-expressing lentivirus vector delays tumor growth in a mouse model of breast cancer. The antitumor effect of Rlx was mediated through degradation of tumor stroma, which provided increased access of infiltrating antitumor immune cells to their target tumor cells. Furthermore, we have shown in a human/mouse chimeric model that genetically modified HSCs expressing a transgene can access the tumor site. Our findings are relevant for cancer gene therapy and immunotherapy.
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.