Evidence map›Paper›PMID 23835331›Full record

ArticleDiabetes2013

Insulin receptor phosphorylation by endogenous insulin or the insulin analog AspB10 promotes mammary tumor growth independent of the IGF-I receptor.

Emily Jane Gallagher, Nyosha Alikhani, Aviva Tobin-Hess, Jeffrey Blank, Nicholas J Buffin, Zara Zelenko, Norbert Tennagels, Ulrich Werner, Derek LeRoith

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Insulin and cancer: a tangled web.The Biochemical journal · 2022
    Review
  5. Article
  6. Hyperinsulinemia in Obesity, Inflammation, and Cancer.Diabetes & metabolism journal · 2021
    Review
  7. Article
  8. Article
  9. Disrupting Insulin and IGF Receptor Function in Cancer.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Article
  12. Obesity, Type 2 Diabetes, and Cancer Risk.Frontiers in oncology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Insulin glargine affects the expression ofIranian journal of basic medical sciences · 2018
    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

9 authors at 1 institution in 1 country.

Emily Jane GallagherDivision of Endocrinology, Diabetes and Bone Diseases, Samuel Bronfman Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Nyosha Alikhani
Aviva Tobin-Hess
Jeffrey Blank
Nicholas J Buffin
Zara Zelenko
Norbert Tennagels
Ulrich Werner
Derek LeRoith
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous hyperinsulinemia and insulin receptor (IR)/IGF-I receptor (IGF-IR) phosphorylation in tumors are associated with a worse prognosis in women with breast cancer. In vitro, insulin stimulation of the IR increases proliferation of breast cancer cells. However, in vivo studies demonstrating that IR activation increases tumor growth, independently of IGF-IR activation, are lacking. We hypothesized that endogenous hyperinsulinemia increases mammary tumor growth by directly activating the IR rather than the IGF-IR or hybrid receptors. We aimed to determine whether stimulating the IR with the insulin analog AspB10 could increase tumor growth independently of IGF-IR signaling. We induced orthotopic mammary tumors in control FVB/n and hyperinsulinemic MKR mice, and treated them with the insulin analog AspB10, recombinant human IGF-I, or vehicle. Tumors from mice with endogenous hyperinsulinemia were larger and had greater IR phosphorylation, but not IGF-IR phosphorylation, than those from control mice. Chronic AspB10 administration also increased tumor growth and IR (but not IGF-IR) phosphorylation in tumors. IGF-I led to activation of both the IGF-IR and IR and probably hybrid receptors. Our results demonstrate that IR phosphorylation increases tumor growth, independently of IGF-IR/hybrid receptor phosphorylation, and warrant consideration when developing therapeutics targeting the IGF-IR, but not the IR.

Indexed as

Molecular Targeted TherapyAnimalsBreast NeoplasmsCell Line, TumorDiabetes Mellitus, ExperimentalFemaleHumansHyperinsulinismHypoglycemic AgentsInsulinInsulin-Like Growth Factor IMammary Neoplasms, ExperimentalMetabolic SyndromeMiceMice, TransgenicObesityHypoglycemic AgentsInsulininsulin, Asp(B10)-Insulin-Like Growth Factor IReceptor, IGF Type 1

Identifiers

PMID23835331
PMCPMC3781483
OpenAlexW2145594480

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.