Evidence map›Paper›PMID 21106881›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

HER2/ErbB2 receptor signaling in rat and human prolactinoma cells: strategy for targeted prolactinoma therapy.

Hidenori Fukuoka, Odelia Cooper, Jun Mizutani, Yunguang Tong, Song-Guang Ren, Serguei Bannykh, Shlomo Melmed

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. 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
3.7field-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

36 citing papers in PubMed, 67 citations in OpenAlex.

  1. EGFR/ErbB2-Targeting Lapatinib Therapy for Aggressive Prolactinomas.The Journal of clinical endocrinology and metabolism · 2021
    Trial
  2. Trial
  3. Approach to the Patient With Prolactinoma.The Journal of clinical endocrinology and metabolism · 2023
    Review
  4. Review
  5. Pituitary Tumorigenesis-Implications for Management.Medicina (Kaunas, Lithuania) · 2023
    Review
  6. Review
  7. Pituitary Apoplexy: Risk Factors and Underlying Molecular Mechanisms.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Emerging and Novel Treatments for Pituitary Tumors.Journal of clinical medicine · 2019
    Review
  19. Article
  20. The Treatment of Refractory Pituitary Adenomas.Frontiers in endocrinology · 2019
    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

7 authors at 1 institution in 1 country.

Hidenori FukuokaCedars-Sinai Medical Center, Department of Academic Affairs, 8700 Beverly Boulevard Plaza North, Los Angeles, CA 90048, USA.
Odelia Cooper
Jun Mizutani
Yunguang Tong
Song-Guang Ren
Serguei Bannykh
Shlomo Melmed
Cedars-Sinai Medical Center · US

Funding

ErbB Family in Pituitary TumorsK23DK085148 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI COOPER, ODELIA · 2009 to 2013
$844k
PTTG1 regulates anti-cancer drug responseK99CA138914 · NCI · CEDARS-SINAI MEDICAL CENTER · PI TONG, YUNGUANG · 2010 to 2011
$324k
NCI NIH HHS CA07597NCI NIH HHS K99 CA138914NIDDK NIH HHS K23 DK085148NIDDK NIH HHS K23DK085148-01
6 · The paper itself

Abstract

Dopamine agonist resistance or intolerance is encountered in approximately 20% of prolactinoma patients. Because human epidermal growth factor receptor 2 (HER2)/ErbB2 is overexpressed in prolactinomas and ErbB receptor ligands regulate prolactin (PRL) gene expression, we tested the role of HER2/ErbB2 in prolactinoma hormone regulation and adenoma cell proliferation to assess the rationale for targeting this receptor for prolactinoma therapy. As we showed prolactinoma HER2 overexpression, we generated constitutively active HER2-stable GH3 cell transfectants (HER2CA). PRL mRNA levels were induced approximately 250-fold and PRL secretion was enhanced 100-fold in HER2CA cells, which also exhibited increased proliferation. Lapatinib, a dual tyrosine kinase inhibitor (TKI) of both epidermal growth factor receptor (EGFR)/ErbB1 and HER2, blocked receptor signaling, and suppressed PRL expression more than gefitinib, a TKI of EGFR/ErbB1. Lapatinib also suppressed colony formation in soft agar more than gefitinib. Oral lapatinib treatment caused tumor shrinkage and serum PRL suppression both in HER2CA transfectant-inoculated Wistar-Furth rats and in estrogen-induced Fischer344 rat prolactinomas. In cultured human cells derived from resected prolactinoma tissue, lapatinib suppressed both PRL mRNA expression and secretion. These results demonstrate that prolactinoma HER2 potently induces PRL and regulates experimental prolactinoma cell proliferation. Because pituitary HER2 signaling is abrogated by TKIs, this receptor could be an effective target for prolactinoma therapy.

Indexed as

Signal TransductionAnimalsCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleGefitinibGene Expression Regulation, NeoplasticHumansLactotrophsLapatinibMolecular Targeted TherapyProlactinProlactinomaQuinazolinesRatsErb-b2 Receptor Tyrosine KinasesGefitinibLapatinibProlactinQuinazolinesRNA, Messenger

Identifiers

PMID21106881
PMCPMC3089034
OpenAlexW2138542239

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.