Evidence map›Paper›PMID 18676863›Full record

ArticleCancer research2008

Rat prolactinoma cell growth regulation by epidermal growth factor receptor ligands.

George Vlotides, Emily Siegel, Ines Donangelo, Shiri Gutman, Song-Guang Ren, Shlomo Melmed

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. EGFR/ErbB2-Targeting Lapatinib Therapy for Aggressive Prolactinomas.The Journal of clinical endocrinology and metabolism · 2021
    Trial
  4. Trial
  5. Review
  6. Review
  7. Article
  8. Article
  9. Approach to the Patient With Prolactinoma.The Journal of clinical endocrinology and metabolism · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Emerging and Novel Treatments for Pituitary Tumors.Journal of clinical medicine · 2019
    Review
  15. Article
  16. Over-expression of LRIG1 suppresses biological function of pituitary adenoma via attenuation of PI3K/AKT and Ras/Raf/ERK pathways in vivo and in vitro.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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 1 country.

George VlotidesDepartment of Medicine, Cedars-Sinai Medical Center, University of California School of Medicine, Los Angeles, California 90048, USA.
Emily Siegel
Ines Donangelo
Shiri Gutman
Song-Guang Ren
Shlomo Melmed
Cedars-Sinai Medical Center · US

Funding

Mechanisms of Pituitary TumorigenesisR01CA075979 · NCI · CEDARS-SINAI MEDICAL CENTER · PI MELMED, SHLOMO · 1999 to 2012
$3.5M
NCI NIH HHS CA 075979NCI NIH HHS R01 CA075979
6 · The paper itself

Abstract

Epidermal growth factor (EGF) regulates pituitary development, hormone synthesis, and cell proliferation. Although ErbB receptor family members are expressed in pituitary tumors, the effects of EGF signaling on pituitary tumors are not known. Immunoprecipitation and Western blot confirmed EGF receptor (EGFR) and p185(c-neu) protein expression in GH3 lacto-somatotroph but not in adrenocorticotropic hormone-secreting AtT20 pituitary tumor cells. EGF (5 nmol/L) selectively enhanced baseline ( approximately 4-fold) and serum-induced (>6-fold) prolactin (PRL) mRNA levels, whereas gefitinib, an EGFR antagonist, suppressed serum-induced cell proliferation and Pttg1 expression, blocked PRL gene expression, and reversed EGF-mediated somatotroph-lactotroph phenotype switching. Downstream EGFR signaling by ERK, but not phosphoinositide-3-kinase or protein kinase C, mediated the gefitinib response. Tumors in athymic mice implanted s.c. with GH3 cells resulted in weight gain accompanied by increased serum PRL, growth hormone, and insulin growth factor 1. Gefitinib decreased tumor volumes and peripheral hormone levels by approximately 30% and restored normal mouse body weight patterns. Mice treated with gefitinib exhibited decreased tumor tissue ERK1/2 phosphorylation and down-regulated tumor PRL and Pttg1 mRNA abundance. These results show that EGFR inhibition controls tumor growth and PRL secretion in experimental lacto-somatotroph tumors. EGFR inhibitors could therefore be useful for the control of PRL secretion and tumor load in prolactinomas resistant to dopaminergic treatment, or for those prolactinomas undergoing rare malignant transformation.

Indexed as

AnimalsAntineoplastic AgentsBase SequenceBlotting, WesternCell DivisionCell Line, TumorCell ProliferationDNA PrimersErbB ReceptorsFemaleFlow CytometryGefitinibGene ExpressionImmunoprecipitationLigandsMiceAntineoplastic AgentsDNA PrimersErbB ReceptorsGefitinibLigandsQuinazolines

Identifiers

PMID18676863
PMCPMC2497431
OpenAlexW1968392567

What OpenQuestion holds

Textmetadata
LicenceTDM
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.