ArticleCancer discovery2012
Identification of luminal breast cancers that establish a tumor-supportive macroenvironment defined by proangiogenic platelets and bone marrow-derived cells.
Article in Cancer discovery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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
97 citing papers in PubMed, 167 citations in OpenAlex.
- Tumor-platelet cross talk in cancer: mechanisms, thrombotic risk, and translational opportunities.Blood advances · 2026Review
- Tumor-Associated Platelets Suppress T-cell Function and Promote Immune Evasion in TNBC via the P-selectin/P-selectin Glycoprotein Ligand 1 Pathway.Cancer research communications · 2026Article
- Nano-biosensors for circulating tumor markers: advancing liquid biopsy toward precision cancer diagnostics.Journal of cancer research and clinical oncology · 2026Review
- HMGB1-Platelet Interactions: Mechanisms and Targeted Therapy Strategies.Thrombosis and haemostasis · 2026Review
- Upregulated lncRNA AK058003 in Tumor-Educated Platelets and Plasma as Liquid Biopsy Biomarkers for Esophageal Cancer.Cancer management and research · 2026Article
- Platelet‑circulating tumor cell crosstalk: A pivotal target in cancer diagnosis and therapy (Review).Oncology reports · 2026Review
- Tumor-mediated remote regulation of peripheral blood platelets.Cell biology and toxicology · 2025Review
- Network Controllability Reveals Key Mitigation Points for Tumor-Promoting Signaling in Tumor-Educated Platelets.International journal of molecular sciences · 2025Article
- Fibrin as the mediator of tumor cell interaction with platelets.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Ginsenoside Rb prevents the metastasis of hepatocarcinoma by blocking the platelet-tumor cell interaction.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Development of an accurate breast cancer detection classifier based on platelet RNA.Scientific reports · 2024Article
- Review
- Review
- Platelet Contributions to the (Pre)metastatic Tumor Microenvironment.Seminars in thrombosis and hemostasis · 2024Review
- TEP RNA: a new frontier for early diagnosis of NSCLC.Journal of cancer research and clinical oncology · 2024Review
- A novel platelets-related gene signature for predicting prognosis, immune features and drug sensitivity in gastric cancer.Frontiers in immunology · 2024Article
- Plateletcrit is predictive of clinical outcome and prognosis for early-stage breast cancer: A retrospective cohort study based on propensity score matching.Cancer medicine · 2024Article
- The dynamic role of platelets in cancer progression and their therapeutic implications.Nature reviews. Cancer · 2024Review
- The prospects of microphysiological systems in modeling platelet pathophysiology in cancer.Platelets · 2023Review
- Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
unlabelledBreast cancer recurrence rates vary following treatment, suggesting that tumor cells disseminate early from primary sites but remain indolent indefinitely before progressing to symptomatic disease. The reasons why some indolent disseminated tumors erupt into overt disease are unknown. We discovered a novel process by which certain luminal breast cancer (LBC) cells and patient tumor specimens (LBC "instigators") establish a systemic macroenvironment that supports outgrowth of otherwise-indolent disseminated tumors ("responders"). Instigating LBCs secrete cytokines that are absorbed by platelets, which are recruited to responding tumor sites where they aid vessel formation. Instigator-activated bone marrow cells enrich responding tumor cell expression of CD24, an adhesion molecule for platelets, and provide a source of VEGF receptor 2(+) tumor vessel cells. This cascade results in growth of responder adenocarcinomas and is abolished when platelet activation is inhibited by aspirin. These findings highlight the macroenvironment as an important component of disease progression that can be exploited therapeutically. SIGNIFICANCE: Currently, processes that mediate progression of otherwise indolent tumors are not well understood, making it difficult to accurately predict which cancer patients are likely to relapse. Our findings highlight the macroenvironment as an important component of disease progression that can be exploited to more accurately identify patients who would benefit from adjuvant therapy.
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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.