ArticleInternational journal of oncology2016
Lipoprotein(a) and vitamin C impair development of breast cancer tumors in Lp(a)+; Gulo-/- mice.
Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
What it found
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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.
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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.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Lipoprotein(a) and Prostate Cancer: A Systematic Review of Observational, Genetic and Mendelian Randomization Evidence.International journal of molecular sciences · 2026Pooled it
- Pooled it
- Lipid Profile, PCSK9, ANGPTL3 and Lipoprotein (a) Levels in Men Diagnosed With Localized High-Grade Prostate Cancer and Men At-Risk of Prostate Cancer.Cancer medicine · 2025Article
- The functions of apolipoproteins and lipoproteins in health and disease.Molecular biomedicine · 2024Review
- Lipoprotein(a) in patients with breast cancer after chemotherapy: exploring potential strategies for cardioprotection.Lipids in health and disease · 2023Review
- Role of Vitamin C in Selected Malignant Neoplasms in Women.Nutrients · 2022Review
- Dietary Vitamin C and Age-Induced Lipid and Hormonal Metabolic Changes in a Humanized Mouse Model Not Synthesizing Vitamin C and Producing Lipoprotein(a) [Gulo (-/-); Lp(a)+].Journal of nutrition and metabolism · 2021Article
- L-Ascorbic Acid Shapes BovineFrontiers in veterinary science · 2021Article
- Cellular Mechanisms of Circulating Tumor Cells During Breast Cancer Metastasis.International journal of molecular sciences · 2020Review
- High Lipoprotein(a) Level Is Independently Associated with Adverse Clinicopathological Features in Patients with Prostate Cancer.Disease markers · 2019Article
- Lipoprotein (a): a promising prognostic biomarker in patients with hepatocellular carcinoma after curative resection.OncoTargets and therapy · 2018Article
- Intravenous Vitamin C for Cancer Therapy - Identifying the Current Gaps in Our Knowledge.Frontiers in physiology · 2018Review
- Role of extracellular matrix in breast cancer development: a brief update.F1000Research · 2018Review
- Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies.Clinical research in cardiology supplements · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer progression is characterized by loss of extracellular matrix (ECM) integrity, which is a precondition for tumor growth and metastasis. In order to elucidate the precise mechanisms of ECM degradation in cancer we used a genetically modified mouse mimicking two distinct human metabolic features associated with carcinogenesis, the lack of endogenous vitamin C synthesis and the production of human Lp(a). Female Lp(a)+; Gulo(-/-) and control wild-type Balb/c mice without these two metabolic features were orthotopically inoculated with 4T1 breast cancer cells (5x105). The transgenic and control mice were divided into 4 different dietary groups in respect to dietary vitamin C intake: i) low ascorbate intake for 6 weeks; ii) high ascorbate intake for 6 weeks; iii) low ascorbate intake for 3 weeks followed by high ascorbate for 3 weeks; iv) high ascorbate intake for 3 weeks followed by low ascorbate for 3 weeks. After 6 weeks, all wild-type mice developed tumors. In contrast, Lp(a)+; Gulo(-/-) mice developed one third less primary tumors (low ascorbate diet) or no primary tumors at all (high ascorbate diet). Significantly, tumors from Lp(a)+; Gulo(-/-) mice immunostained positively for Lp(a) and their size was inversely proportional to Lp(a) serum levels. The results implicate that Lp(a) may play a role in controlling tumor growth and expansion. The most likely mechanism is the competitive inhibition of plasmin-induced ECM degradation due to the homology of Lp(a) components to plasminogen. The confirmation of this pathomechanism could lead to a universal therapeutic target for the prevention and treatment of cancer.
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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.