ArticleProceedings of the National Academy of Sciences of the United States of America2014
Tissue factor expression provokes escape from tumor dormancy and leads to genomic alterations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
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- Conversion of anti-tissue factor antibody sequences to chimeric antigen receptor and bi-specific T-cell engager format.Cancer immunology, immunotherapy : CII · 2024Article
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- Integrin regulation by tissue factor promotes cancer stemness and metastatic dissemination in breast cancer.Oncogene · 2022Article
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- The immunoregulation effect of tumor microenvironment in pancreatic ductal adenocarcinoma.Frontiers in oncology · 2022Review
- Tissue factor potentiates adherence of breast cancer cells to human umbilical vein endothelial cells under static and flow conditions.Cell adhesion & migration · 2021Article
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- Genomic profiling identifies somatic mutations predicting thromboembolic risk in patients with solid tumors.Blood · 2021Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
The coagulation system links immediate (hemostatic) and late (inflammatory, angiogenic) tissue responses to injury, a continuum that often is subverted in cancer. Here we provide evidence that tumor dormancy is influenced by tissue factor (TF), the cancer cell-associated initiator of the coagulation system and a signaling receptor. Thus, indolent human glioma cells deficient for TF remain viable but permanently dormant at the injection site for nearly a year, whereas the expression of TF leads to a step-wise transition to latent and overt tumor growth phases, a process that is preceded by recruitment of vascular (CD105(+)) and myeloid (CD11b(+) and F4/80(+)) cells. Importantly, the microenvironment orchestrated by TF expression drives permanent changes in the phenotype, gene-expression profile, DNA copy number, and DNA methylation state of the tumor cells that escape from dormancy. We postulate that procoagulant events in the tissue microenvironment (niche) may affect the fate of occult tumor cells, including their biological and genetic progression to initiate a full-blown malignancy.
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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.