ArticleIntegrative biology : quantitative biosciences from nano to macro2012
Inter-cellular signaling network reveals a mechanistic transition in tumor microenvironment.
Article in Integrative biology : quantitative biosciences from nano to macro, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- The role of soluble mediators in the clinical course of EBV infection and B cell homeostasis after kidney transplantation.Scientific reports · 2020Trial
- Epigenetic changes in fibroblasts drive cancer metabolism and differentiation.Endocrine-related cancer · 2019Review
- Article
- Monocyte-derived macrophage assisted breast cancer cell invasion as a personalized, predictive metric to score metastatic risk.Scientific reports · 2015Article
- Metazoans evolved by taking domains from soluble proteins to expand intercellular communication network.Scientific reports · 2015Article
- Article
- Tumor-associated macrophage-derived IL-6 and IL-8 enhance invasive activity of LoVo cells induced by PRL-3 in a KCNN4 channel-dependent manner.BMC cancer · 2014Article
- Single-cell protein secretomic signatures as potential correlates to tumor cell lineage evolution and cell-cell interaction.Frontiers in oncology · 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
3 authors.
Funding
Abstract
We conducted inter-cellular cytokine correlation and network analysis based upon a stochastic population dynamics model that comprises five cell types and fifteen signaling molecules inter-connected through a large number of cell-cell communication pathways. We observed that the signaling molecules are tightly correlated even at very early stages (e.g. the first month) of human glioma, but such correlation rapidly diminishes when tumor grows to a size that can be clinically detected. Further analysis suggests that paracrine is shown to be the dominant force during tumor initiation and priming, while autocrine supersedes it and supports a robust tumor expansion. In correspondence, the cytokine correlation network evolves through an increasing to decreasing complexity. This study indicates a possible mechanistic transition from the microenvironment-controlled, paracrine-based regulatory mechanism to self-sustained rapid progression to fetal malignancy. It also reveals key nodes that are responsible for such transition and can be potentially harnessed for the design of new anti-cancer therapies.
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.