ArticlePloS one2012
Feedback within the inter-cellular communication and tumorigenesis in carcinomas.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 20 citations in OpenAlex.
- Prolyl hydroxylase 2 inhibits glycolytic activity in colorectal cancer via the NF‑κB signaling pathway.International journal of oncology · 2024Article
- Tunneling Nanotubes and Tumor Microtubes in Cancer.Cancers · 2020Review
- A role for RASSF1A in tunneling nanotube formation between cells through GEFH1/Rab11 pathway control.Cell communication and signaling : CCS · 2018Article
- Lost in translation: applying 2D intercellular communication via tunneling nanotubes in cell culture to physiologically relevant 3D microenvironments.The FEBS journal · 2017Review
- Intercellular Conduits in Tumors: The New Social Network.Trends in cancer · 2016Article
- Towards a molecular basis of oligometastatic disease: potential role of micro-RNAs.Clinical & experimental metastasis · 2014Review
- Intercellular communication in malignant pleural mesothelioma: properties of tunneling nanotubes.Frontiers in physiology · 2014Article
- Molecular mechanism of the "feedback loop" model of carcinogenesis.Communicative & integrative biology · 2012Article
- Even stressed cells are individuals: second messengers of free radicals in pathophysiology of cancer.Croatian medical journal · 2012Article
- Cancer conundrum.Journal of oral and maxillofacial pathology : JOMFPArticle
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The classical somatic mutation theory (SMT) of carcinogenesis and metastasis postulates that malignant transformation occurs in cells that accumulate a sufficient amount of mutations in the appropriate oncogenes and/or tumor suppressor genes. These mutations result in cell-autonomous activation of the mutated cell and a growth advantage relative to neighboring cells. However, the SMT cannot completely explain many characteristics of carcinomas. Contrary to the cell-centered view of the SMT with respect to carcinogenesis, recent research has revealed evidence that the tumor microenvironment plays a role in carcinogenesis as well. In this review, we present a new model that accommodates the role of the tumor microenvironment in carcinogenesis and complements the classical SMT. Our "feedback" model emphasizes the role of an altered spatiotemporal communication between epithelial and stromal cells during carcinogenesis: a dysfunctional intracellular signaling in tumorigenic epithelial cells leads to inappropriate cellular responses to stimuli from associated stromal or inflammatory cells. Thus, a positive feedback loop of the information flow between parenchymal and stromal cells results. This constant communication between the stromal cells and the tumor cells causes a perpetually activated state of tumor cells analogous to resonance disaster.
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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.