Evidence map›Paper›PMID 25338553›Full record

ArticleBulletin of mathematical biology2014

Fastest time to cancer by loss of tumor suppressor genes.

Cynthia Sanchez-Tapia, Frederic Y M Wan

Abstract read
In one paragraph

Article in Bulletin of mathematical biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Optimal Proliferation and Differentiation ofStudies in applied mathematics (Cambridge, Mass.) · 2017
    Article
  5. Evolution of genetic instability in heterogeneous tumors.Journal of theoretical biology · 2016
    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

2 authors at 1 institution in 1 country.

Cynthia Sanchez-TapiaDepartment of Mathematics, University of California, Irvine, Irvine, CA , 92697-3875, USA, hixacyn@gmail.com.
Frederic Y M Wan
University of California, Irvine · US

Funding

Uncover Strategies Used By Biological SystemsP50GM076516 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI LANDER, ARTHUR D · 2007 to 2016
$25.1M
Principles of Robust Developmental PatterningR01GM067247 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI LANDER, ARTHUR D, NIE, QING · 2002 to 2014
$4.7M
NIGMS NIH HHS P50 GM076516NIGMS NIH HHS P50-GM076516NIGMS NIH HHS R01 GM067247NIGMS NIH HHS R01-GM067247
6 · The paper itself

Abstract

Genetic instability promotes cancer progression (by increasing the probability of cancerous mutations) as well as hinders it (by imposing a higher cell death rate for cells susceptible to cancerous mutation). With the loss of tumor suppressor gene function known to be responsible for a high percentage of breast and colorectal cancer (and a good fraction of lung cancer and other types as well), it is important to understand how genetic instability can be orchestrated toward carcinogenesis. In this context, this paper gives a complete characterization of the optimal (time-varying) cell mutation rate for the fastest time to a target cancerous cell population through the loss of both copies of a tumor suppressor gene. Similar to the (one-step) oncogene activation model previously analyzed, the optimal mutation rate of the present two-step model changes qualitatively with the convexity of the (mutation rate-dependent) cell death rate. However, the structure of the Hamiltonian for the new model differs significantly and intrinsically from that of the one-step model, and a completely new approach is needed for the solution of the present two-step problem. Considerable insight into the biology of optimal switching (between corner controls) is extracted from numerical results for cases with nonconvex death rates.

Indexed as

Genes, Tumor SuppressorCarcinogenesisGenomic InstabilityHumansMathematical ConceptsModels, GeneticNeoplasmsTime Factors

Identifiers

PMID25338553
PMCPMC4282520
OpenAlexW2070399509

What OpenQuestion holds

Textmetadata
LicenceTDM
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.