Evidence map›Paper›PMID 20801951›Full record

ArticleEndocrine-related cancer2010

Mammalian target of rapamycin inhibition abrogates insulin-mediated mammary tumor progression in type 2 diabetes.

Yvonne Fierz, Ruslan Novosyadlyy, Archana Vijayakumar, Shoshana Yakar, Derek LeRoith

Open access · bronzeAbstract read
In one paragraph

Article in Endocrine-related cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Hyperinsulinaemia in cancer.Nature reviews. Cancer · 2020
    Review
  4. Article
  5. Obesity, Type 2 Diabetes, and Cancer Risk.Frontiers in oncology · 2020
    Review
  6. A Review on Dietary Intervention in Obesity Associated Colon CancerAsian Pacific journal of cancer prevention : APJCP · 2019
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Insulin and IGFs in obesity-related breast cancer.Journal of mammary gland biology and neoplasia · 2013
    Review
  16. Article
  17. Article
  18. Obesity and cancer risk: evidence, mechanisms, and recommendations.Annals of the New York Academy of Sciences · 2012
    Review
  19. Article
  20. Insulin-like growth factor receptor inhibitors: baby or the bathwater?Journal of the National Cancer Institute · 2012
    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

5 authors at 1 institution in 1 country.

Yvonne FierzDivision of Endocrinology, Diabetes and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Ruslan Novosyadlyy
Archana Vijayakumar
Shoshana Yakar
Derek LeRoith
Icahn School of Medicine at Mount Sinai · US

Funding

Mechanisms for the pro-metastatic effects of hyperinsulinemia on breast cancerR01CA128799 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEROITH, DEREK · 2008 to 2018
$3.7M
NCI NIH HHS 1R01CA128799NCI NIH HHS R01 CA128799
6 · The paper itself

Abstract

Type 2 diabetes increases breast cancer risk and mortality, and hyperinsulinemia is a major mediator of this effect. The mammalian target of rapamycin (mTOR) is activated by insulin and is a key regulator of mammary tumor progression. Pharmacological mTOR inhibition suppresses tumor growth in numerous mammary tumor models in the non-diabetic setting. However, the role of the mTOR pathway in type 2 diabetes-induced tumor growth remains elusive. Herein, we investigated whether the mTOR pathway is implicated in insulin-induced mammary tumor progression in a transgenic mouse model of type 2 diabetes (MKR mice) and evaluated the impact of mTOR inhibition on the diabetic state. Mammary tumor progression was studied in the double transgenic MMTV-Polyoma Virus middle T antigen (PyVmT)/MKR mice and by orthotopic inoculation of PyVmT- and Neu/ErbB2-driven mammary tumor cells (Met-1 and MCNeuA cells respectively). mTOR inhibition by rapamycin markedly suppressed tumor growth in both wild-type and MKR mice. In diabetic animals, however, the promoting action of insulin on tumor growth was completely blunted by rapamycin, despite a worsening of the carbohydrate and lipid metabolism. Taken together, pharmacological mTOR blockade is sufficient to abrogate mammary tumor progression in the setting of hyperinsulinemia, and thus mTOR inhibitors may be an attractive therapeutic modality for breast cancer patients with type 2 diabetes. Careful monitoring of the metabolic state, however, is important as dose adaptations of glucose- and/or lipid-lowering therapy might be necessary.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisBlood GlucoseBody WeightBreast NeoplasmsDiabetes Mellitus, Type 2Disease Models, AnimalEatingFemaleInsulinMiceMice, TransgenicSirolimusTOR Serine-Threonine KinasesTriglyceridesAntibiotics, AntineoplasticBlood GlucoseInsulinmTOR protein, mouseSirolimusTOR Serine-Threonine KinasesTriglycerides

Identifiers

PMID20801951
PMCPMC4082826
OpenAlexW2139143788

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.