Evidence map›Paper›PMID 31350465›Full record

ArticleScientific reports2019

Stochastic modeling of phenotypic switching and chemoresistance in cancer cell populations.

Niraj Kumar, Gwendolyn M Cramer, Seyed Alireza Zamani Dahaj, Bala Sundaram, Jonathan P Celli, Rahul V Kulkarni

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

19 citing papers in PubMed, 4 citations in OpenAlex.

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  11. Threshold-awareness in adaptive cancer therapy.PLoS computational biology · 2024
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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

6 authors at 2 institutions in 1 country.

Niraj KumarDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA.
Gwendolyn M CramerDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA.
Seyed Alireza Zamani DahajDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA.
Bala SundaramDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA.
Jonathan P CelliDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA.
Rahul V KulkarniDepartment of Physics, University of Massachusetts Boston, Boston, MA, 02125, USA. rahul.kulkarni@umb.edu.
University of Massachusetts Boston · USGeorgia Institute of Technology · US

Funding

UMass Boston-DF/HCC U54 Partnership (2 of 2)U54CA156734 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI ADAN COLON-CARMONA, Jill A. Macoska · 2010 to 2026
$24.9M
Mechanism-based therapies for pancreatic cancer informed by stromal microrheologyR00CA155045 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CELLI, JONATHAN P · 2013 to 2015
$708k
NCI NIH HHS R00 CA155045NCI NIH HHS U54 CA156734
6 · The paper itself

Abstract

Phenotypic heterogeneity in cancer cells is widely observed and is often linked to drug resistance. In several cases, such heterogeneity in drug sensitivity of tumors is driven by stochastic and reversible acquisition of a drug tolerant phenotype by individual cells even in an isogenic population. Accumulating evidence further suggests that cell-fate transitions such as the epithelial to mesenchymal transition (EMT) are associated with drug resistance. In this study, we analyze stochastic models of phenotypic switching to provide a framework for analyzing cell-fate transitions such as EMT as a source of phenotypic variability in drug sensitivity. Motivated by our cell-culture based experimental observations connecting phenotypic switching in EMT and drug resistance, we analyze a coarse-grained model of phenotypic switching between two states in the presence of cytotoxic stress from chemotherapy. We derive analytical results for time-dependent probability distributions that provide insights into the rates of phenotypic switching and characterize initial phenotypic heterogeneity of cancer cells. The results obtained can also shed light on fundamental questions relating to adaptation and selection scenarios in tumor response to cytotoxic therapy.

Indexed as

Models, GeneticPhenotypeAntineoplastic AgentsCell Line, TumorDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansOxaliplatinPancreatic NeoplasmsTransforming Growth Factor betaTumor MicroenvironmentAntineoplastic AgentsOxaliplatinTransforming Growth Factor beta

Identifiers

PMID31350465
PMCPMC6659620
OpenAlexW2914115560

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.