ReviewNature reviews. Clinical oncology2010
Molecular circuits of solid tumors: prognostic and predictive tools for bedside use.
Review in Nature reviews. Clinical oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
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
50 citing papers in PubMed, 97 citations in OpenAlex.
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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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The explosion of knowledge in cancer biology in the past two decades has led to the identification of specific molecular circuits in solid tumors. These pathways reflect specific abnormalities thought to drive malignant progression. This knowledge has also generated a vast panel of cancer biomarkers although many of these biomarkers lack sufficient research and validation to be used in the clinic. This Review discusses relevant molecular prognostic and/or predictive biomarkers in the six leading tumors with the highest contribution to cancer mortality: breast, lung, colorectal, prostate, pancreatic and ovarian cancer. Each biomarker is described according to its associated clinicopathological presentation and specific associated molecular interactions. Despite only few biomarkers being currently implemented in clinical practice, a new generation of predictors is emerging that could modify the classic organ-based cancer classification (for example, defects in DNA repair, aberrant MAPK signaling and aberrant PI3K/Akt/mTOR signaling). The advent of high-throughput strategies will also probably substitute monobiomarker strategies.
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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.