Evidence map›Paper›PMID 27977008›Full record

ReviewNature reviews. Cancer2017

The recurrent architecture of tumour initiation, progression and drug sensitivity.

Andrea Califano, Mariano J Alvarez

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05719428 (A Phase II Trial of Neural Network-based Treatment Decision Support Tool in Patients With Refractory Solid Organ Malignancies), which is not on this map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

NCT05719428 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

A Phase II Trial of Neural Network-based Treatment Decision Support Tool in Patients With Refractory Solid Organ Malignancies

TypeinterventionalSponsorNational University Hospital, SingaporeRan2023 to 2026Enrolled37ConditionsSolid Organ MalignanciesArmsDRUID AI Program
3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Distinct gene expression characteristics in epithelial cell-International journal of medical sciences · 2019
    Pooled it
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  12. Review
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Andrea CalifanoDepartment of Systems Biology, Columbia University, and the Departments of Biomedical Informatics, Biochemistry and Molecular Biophysics, JP Sulzberger Columbia Genome Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York 10032, USA.
Mariano J AlvarezDarwinHealth, Inc., 3960 Broadway, Suite 540, New York, New York 10032, USA.

Funding

Predicting Cancer Cell Response to Endogenous and Exogenous Perturbations at the Single Cell LevelR35CA197745 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ANDREA CALIFANO · 2015 to 2026
$11.5M
Systematic pharmacological targeting of the core mechanisms responsible for maintaining cancer cell stateU54CA209997 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CALIFANO, ANDREA, HONIG, BARRY H · 2016 to 2021
$10.9M
Systems Biology of Tumor Progression and Drug ResistanceU01CA168426 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CALIFANO, ANDREA · 2012 to 2016
$6.5M
High-performance compute cluster for biomedical computingS10OD012351 · OD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CALIFANO, ANDREA · 2012 to 2012
$2.0M
Storage System for High Performance ComputingS10OD021764 · OD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CALIFANO, ANDREA · 2016 to 2016
$600k
NCI NIH HHS R35 CA197745NCI NIH HHS U01 CA168426NCI NIH HHS U54 CA209997NIH HHS S10 OD012351NIH HHS S10 OD021764
6 · The paper itself

Abstract

Recent studies across multiple tumour types are starting to reveal a recurrent regulatory architecture in which genomic alterations cluster upstream of functional master regulator (MR) proteins, the aberrant activity of which is both necessary and sufficient to maintain tumour cell state. These proteins form small, hyperconnected and autoregulated modules (termed tumour checkpoints) that are increasingly emerging as optimal biomarkers and therapeutic targets. Crucially, as their activity is mostly dysregulated in a post-translational manner, rather than by mutations in their corresponding genes or by differential expression, the identification of MR proteins by conventional methods is challenging. In this Opinion article, we discuss novel methods for the systematic analysis of MR proteins and of the modular regulatory architecture they implement, including their use as a valuable reductionist framework to study the genetic heterogeneity of human disease and to drive key translational applications.

Indexed as

AnimalsCCAAT-Enhancer-Binding Protein-betaCell Transformation, NeoplasticDisease ProgressionDrug Resistance, NeoplasmGlucocorticoidsHomeostasisHumansNeoplasmsOncogenesSystems BiologyCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanGlucocorticoids

Identifiers

PMID27977008
PMCPMC5541669

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

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 Socratic graph.