Evidence map›Paper›PMID 30224860›Full record

ReviewCancer informatics2018

An Introduction to the Mathematical Modeling in the Study of Cancer Systems Biology.

Abdallah K Alameddine, Frederick Conlin, Brian Binnall

Open access · goldAbstract readReview
In one paragraph

Review in Cancer informatics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 36% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

3 authors at 2 institutions in 1 country.

Abdallah K AlameddineDivision of Cardiac Surgery, Baystate Medical Center, Springfield, MA, USA.
Frederick ConlinDepartment of Anesthesiology, Baystate Medical Center, Springfield, MA, USA.
Brian BinnallDivision of Cardiac Surgery, Baystate Medical Center, Springfield, MA, USA.
Baystate Medical Center · USUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFrequently occurring in cancer are the aberrant alterations of regulatory onco-metabolites, various oncogenes/epigenetic stochasticity, and suppressor genes, as well as the deficient mismatch repair mechanism, chronic inflammation, or those deviations belonging to the other cancer characteristics. How these aberrations that evolve overtime determine the global phenotype of malignant tumors remains to be completely understood. Dynamic analysis may have potential to reveal the mechanism of carcinogenesis and can offer new therapeutic intervention.

aimsWe introduce simplified mathematical tools to model serial quantitative data of cancer biomarkers. We also highlight an introductory overview of mathematical tools and models as they apply from the viewpoint of known cancer features.

methodsMathematical modeling of potentially actionable genomic products and how they proceed overtime during tumorigenesis are explored. This report is intended to be instinctive without being overly technical.

resultsTo date, many mathematical models of the common features of cancer have been developed. However, the dynamic of integrated heterogeneous processes and their cross talks related to carcinogenesis remains to be resolved.

conclusionsIn cancer research, outlining mathematical modeling of experimentally obtained data snapshots of molecular species may provide insights into a better understanding of the multiple biochemical circuits. Recent discoveries have provided support for the existence of complex cancer progression in dynamics that span from a simple 1-dimensional deterministic system to a stochastic (ie, probabilistic) or to an oscillatory and multistable networks. Further research in mathematical modeling of cancer progression, based on the evolving molecular kinetics (time series), could inform a specific and a predictive behavior about the global systems biology of vulnerable tumor cells in their earlier stages of oncogenesis. On this footing, new preventive measures and anticancer therapy could then be constructed.

Indexed as

biomarkerscancer biologymathematical modelingsystems biologytime series snapshots

Identifiers

PMID30224860
PMCPMC6136108
OpenAlexW2890062104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.