Evidence map›Paper›PMID 12483521›Full record

ArticleOncogene2002

In vitro chemo- and radio-resistance in small cell lung cancer correlates with cell adhesion and constitutive activation of AKT and MAP kinase pathways.

Alison C Kraus, Ines Ferber, Sven-Oliver Bachmann, Hannah Specht, Anja Wimmel, Markus W Gross, Juergen Schlegel, Guntram Suske, Marcus Schuermann

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  3. Article
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  16. Article
  17. Oncotarget · 2017
    Article
  18. Article
  19. Article
  20. Targeting the Mammalian Target of Rapamycin in Lung Cancer.The American journal of the medical sciences · 2016
    Review
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

9 authors at 1 institution in 1 country.

Alison C KrausDepartment of Haematology and Oncology, Centre for Internal Medicine, University Hospital, Philipps-Universität Marburg, D35033 Marburg, Germany.
Ines Ferber
Sven-Oliver Bachmann
Hannah Specht
Anja Wimmel
Markus W Gross
Juergen Schlegel
Guntram Suske
Marcus Schuermann
Philipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most small cell lung cancer (SCLC) patients relapse within 12 months of starting combination chemotherapy plus radio-therapy, due to the development of acquired chemo- and radio-resistance. This phenomenon relates to the induction of tumour differentiation, resulting in apoptosis-resistant, morphologically variant (v-SCLC) cells, which lack the neuroendocrine expression of classic (c-) SCLC cells. In this study spontaneously adherent SCLC sublines were shown by differential gene expression analysis to provide an in vitro model of variant differentiation in SCLC, with down-regulation of neuroendocrine markers and up-regulation of epithelial differentiation markers cyclin D1, endothelin, the cell adhesion molecules CD 44 and integrin subunits alpha2, beta3 and beta4. The sensitivity of adherent SCLC sublines to etoposide, cyclophosphamide and gamma radiation was significantly diminished relative to parent suspension cell lines. Western blot analysis using phosphorylation-specific antibodies to Akt and MAP kinase revealed markedly elevated activation in adherent SCLC sublines, paralleled by increased levels of phosphorylated Bad protein and activated NF-kappaB. Subcultivation of the adherent sublines on uncoated surfaces reversed their adherent phenotype immediately and under these conditions Akt activity reverted to low levels. These results suggest that c-SCLC cells can differentiate spontaneously to v-SCLC and that the associated cellular adhesion may trigger Akt-dependent inhibition of apoptosis in SCLC cells, thus leading to acquired chemo- and radio-resistance.

Indexed as

Cell AdhesionMAP Kinase Signaling SystemProtein Serine-Threonine KinasesAntineoplastic AgentsBase SequenceCarcinoma, Small CellDNA PrimersGamma RaysHumansLung NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionTumor Cells, CulturedAKT1 protein, humanAntineoplastic AgentsDNA PrimersProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID12483521
OpenAlexW1966333562

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.