Evidence map›Paper›PMID 26248648›Full record

ReviewMolecular cancer research : MCR2016

Tumor-Derived Cell Lines as Molecular Models of Cancer Pharmacogenomics.

Andrew Goodspeed, Laura M Heiser, Joe W Gray, James C Costello

Registry-linked trialAbstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05177432 (Quadratic Phenotypic Optimisation Platform), which is not on this map. Cited by 164 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 2 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.

NCT05177432 phase1unknown statusnot on this mapstarted 2021, after this paper: background citation

Quadratic Phenotypic Optimisation Platform (QPOP) Utilisation to Enhance Selection of Patient Therapy Through Patient Derived Organoids in Breast Cancer

TypeinterventionalSponsorNational University Hospital, SingaporeRan2021 to 2025Enrolled26ConditionsBreast CancerArmsQPOP
3 · Its place in the literature

Who cites it

164 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Tissue specificity of in vitro drug sensitivity.Journal of the American Medical Informatics Association : JAMIA · 2018
    Pooled it
  3. Review
  4. Article
  5. Review
  6. Study of Cytotoxicity of Pyrrolo[3,4-International journal of molecular sciences · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Advances and challenges in human 3D solid tumor models.Advanced functional materials · 2025
    Article
  17. Article
  18. Study Models forMicroorganisms · 2025
    Review
  19. Article
  20. Article

104 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

4 authors.

Andrew GoodspeedDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Laura M HeiserDepartment of Biomedical Engineering, Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon.
Joe W GrayDepartment of Biomedical Engineering, Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon.
James C CostelloDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado. University of Colorado Comprehensive Cancer Center, University of Colorado Anschutz Medical Campus, Aurora, Colorado. james.costello@ucdenver.edu.

Funding

Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Systems-Based Predictions of Responses to Cancer TherapyU54CA112970 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI SPELLMAN, PAUL T. · 2004 to 2014
$27.1M
OutreachU54HG008100 · NHGRI · OREGON HEALTH & SCIENCE UNIVERSITY · PI GRAY, JOE W., HEISER, LAURA MADELINE · 2014 to 2019
$10.5M
PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1M
Intratumor heterogeneity underlying treatment resistance in HER2+ breast tumorsU01CA195469 · NCI · DANA-FARBER CANCER INST · PI GRAY, JOE W., MICHOR, FRANZISKA · 2015 to 2019
$3.3M
NCI NIH HHS 5P30CA069533-16NCI NIH HHS P30 CA069533NCI NIH HHS U01 CA195469NCI NIH HHS U54 CA112970NHGRI NIH HHS U54 HG008100NIGMS NIH HHS T32 GM007635
6 · The paper itself

Abstract

Compared with normal cells, tumor cells have undergone an array of genetic and epigenetic alterations. Often, these changes underlie cancer development, progression, and drug resistance, so the utility of model systems rests on their ability to recapitulate the genomic aberrations observed in primary tumors. Tumor-derived cell lines have long been used to study the underlying biologic processes in cancer, as well as screening platforms for discovering and evaluating the efficacy of anticancer therapeutics. Multiple -omic measurements across more than a thousand cancer cell lines have been produced following advances in high-throughput technologies and multigroup collaborative projects. These data complement the large, international cancer genomic sequencing efforts to characterize patient tumors, such as The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC). Given the scope and scale of data that have been generated, researchers are now in a position to evaluate the similarities and differences that exist in genomic features between cell lines and patient samples. As pharmacogenomics models, cell lines offer the advantages of being easily grown, relatively inexpensive, and amenable to high-throughput testing of therapeutic agents. Data generated from cell lines can then be used to link cellular drug response to genomic features, where the ultimate goal is to build predictive signatures of patient outcome. This review highlights the recent work that has compared -omic profiles of cell lines with primary tumors, and discusses the advantages and disadvantages of cancer cell lines as pharmacogenomic models of anticancer therapies.

Indexed as

Cell Line, TumorAntineoplastic AgentsEpigenesis, GeneticGenetic HeterogeneityHigh-Throughput Screening AssaysHumansModels, BiologicalNeoplasmsAntineoplastic Agents

Identifiers

PMID26248648
PMCPMC4828339

What OpenQuestion holds

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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.