Evidence map›Paper›PMID 19455144›Full record

ArticleBritish journal of cancer2009

Alternative implication of CXCR4 in JAK2/STAT3 activation in small cell lung cancer.

M Pfeiffer, T N Hartmann, M Leick, J Catusse, A Schmitt-Graeff, M Burger

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  7. Review
  8. Article
  9. Himalayan flora: targeting various molecular pathways in lung cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. [Research Advances of JAK/STAT Signaling Pathway in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2019
    Review
  14. Review
  15. Rosiglitazone Reduces Apoptosis and Inflammation in Lipopolysaccharide-Induced Human Umbilical Vein Endothelial Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  16. Article
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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 1 institution in 2 countries.

M PfeifferDepartment of Internal Medicine, Freiburg University Hospital, Freiburg, Germany.
T N Hartmann
M Leick
J Catusse
A Schmitt-Graeff
M Burger
University Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is an aggressive, rapidly metastasising tumour. Previously, we demonstrated the influence of CXCL12-CXCR4 interaction on processes involved in metastasis and chemoresistance in SCLC. We show here that STAT3 is expressed in both primary SCLC tumour tissues and SCLC cell lines. We investigated the function of STAT3 upon CXCL12 stimulation in SCLC cell lines. Small cell lung cancer cell lines present constitutive phosphorylation of STAT3, and in the reference cell lines NCI-H69 and NCI-H82 constitutive phosphorylation was further increased by CXCL12 stimulation. Further investigating this signalling cascade, we showed that it involves interactions between CXCR4 and JAK2 in both cell lines. However CXCL12-induced adhesion to VCAM-1 could be completely inhibited by the JAK2 inhibitor AG490 only in NCI-H82. Furthermore, CXCR4 antagonist but not AG490 inhibited cell adhesion whereas both antagonisms were shown to inhibit growth of the cells in soft agar, indicating the central involvement of this signalling in anchorage-independent growth of SCLC cells. Most interestingly, while using primary tumour material, we observed that in contrast to non-small-cell lung cancer samples from primary tumour tissues, all analysed samples from SCLC were strongly positive for tyrosine-phosphorylated STAT3. Taken together, these data indicate that STAT3 is constitutively phosphorylated in SCLC and is important in SCLC growth and spreading thus presenting an interesting target for therapy.

Indexed as

Antineoplastic AgentsBlotting, WesternCell AdhesionHumansImmunoenzyme TechniquesImmunoprecipitationJanus Kinase 2Lung NeoplasmsPhosphorylationReceptors, CXCR4Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerSmall Cell Lung CarcinomaSTAT3 Transcription FactorStromal CellsTumor Cells, Culturedalpha-cyano-(3,4-dihydroxy)-N-benzylcinnamideAntineoplastic AgentsCXCR4 protein, humanJAK2 protein, humanJanus Kinase 2Receptors, CXCR4RNA, MessengerSTAT3 protein, humanSTAT3 Transcription FactorTyrphostinsVascular Cell Adhesion Molecule-1

Identifiers

PMID19455144
PMCPMC2714241
OpenAlexW2015787839

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.