Evidence map›Paper›PMID 22068913›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Redefining the relevance of established cancer cell lines to the study of mechanisms of clinical anti-cancer drug resistance.

Jean-Pierre Gillet, Anna Maria Calcagno, Sudhir Varma, Miguel Marino, Lisa J Green, Meena I Vora, Chirayu Patel, Josiah N Orina, Tatiana A Eliseeva, Vineet Singal and 7 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed, 3 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.

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

265 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Guideline
  3. Tissue specificity of in vitro drug sensitivity.Journal of the American Medical Informatics Association : JAMIA · 2018
    Pooled it
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  14. Translational 3DFrontiers in immunology · 2026
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205 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

17 authors.

Jean-Pierre GilletLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Anna Maria Calcagno
Sudhir Varma
Miguel Marino
Lisa J Green
Meena I Vora
Chirayu Patel
Josiah N Orina
Tatiana A Eliseeva
Vineet Singal
Raji Padmanabhan
Ben Davidson
Ram Ganapathi
Anil K Sood
Bo R Rueda
Suresh V Ambudkar
Michael M Gottesman

Funding

Mechanisms of non-classical multidrug resistance in cancerZIABC010830 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GOTTESMAN, MICHAEL · 2009 to 2025
$19.6M
Intramural NIH HHS
6 · The paper itself

Abstract

Although in vitro models have been a cornerstone of anti-cancer drug development, their direct applicability to clinical cancer research has been uncertain. Using a state-of-the-art Taqman-based quantitative RT-PCR assay, we investigated the multidrug resistance (MDR) transcriptome of six cancer types, in established cancer cell lines (grown in monolayer, 3D scaffold, or in xenograft) and clinical samples, either containing >75% tumor cells or microdissected. The MDR transcriptome was determined a priori based on an extensive curation of the literature published during the last three decades, which led to the enumeration of 380 genes. No correlation was found between clinical samples and established cancer cell lines. As expected, we found up-regulation of genes that would facilitate survival across all cultured cancer cell lines evaluated. More troubling, however, were data showing that all of the cell lines, grown either in vitro or in vivo, bear more resemblance to each other, regardless of the tissue of origin, than to the clinical samples they are supposed to model. Although cultured cells can be used to study many aspects of cancer biology and response of cells to drugs, this study emphasizes the necessity for new in vitro cancer models and the use of primary tumor models in which gene expression can be manipulated and small molecules tested in a setting that more closely mimics the in vivo cancer microenvironment so as to avoid radical changes in gene expression profiles brought on by extended periods of cell culture.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAntineoplastic AgentsCell Line, TumorCell SurvivalDrug Screening Assays, AntitumorFemaleGene Expression ProfilingHumansOvarian NeoplasmsOvaryReverse Transcriptase Polymerase Chain ReactionTranslational Research, BiomedicalTumor Cells, CulturedTumor Suppressor Protein p53Antineoplastic AgentsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22068913
PMCPMC3219108

What OpenQuestion holds

Textmetadata
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.