Evidence map›Paper›PMID 10791772›Full record

ReviewJournal of mammary gland biology and neoplasia2000

Function of the IGF-I receptor in breast cancer.

E Surmacz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 214 citations in OpenAlex.

  1. Genetic architecture of mammographic density as a risk factor for breast cancer: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. The role of IGF-1 in obesity, cardiovascular disease, and cancer.Medical journal of the Islamic Republic of Iran · 2019
    Review
  9. Article
  10. SerumInternational journal of clinical and experimental pathology · 2018
    Article
  11. Article
  12. Article
  13. Drug delivery approaches for breast cancer.International journal of nanomedicine · 2017
    Review
  14. Dual roles of CCN proteins in breast cancer progression.Journal of cell communication and signaling · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Pregnancy-associated plasma protein-A expression in human breast cancer.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2014
    Article

21 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

E SurmaczKimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. surmacz1@jeflin.tju.edu
Thomas Jefferson University · US

Funding

IGF 1R IN BREAST CANCERR29DK048969 · NIDDK · THOMAS JEFFERSON UNIVERSITY · PI SURMACZ, EVA · 1994 to 1998
–
NIDDK NIH HHS DK 48969
6 · The paper itself

Abstract

The insulin-like growth factor-I receptor (IGF-IR) is a transmembrane tyrosine kinase regulating various biological processes such as proliferation, survival, transformation, differentiation, cell-cell and cell-substrate interactions. Different signaling pathways may underlie these pleiotropic effects. The specific pathways engaged depend on the number of activated IGF-IRs, availability of intracellular signal transducers, the action of negative regulators, and is influenced by extracellular modulators. Experimental and clinical data implicate the IGF-IR in breast cancer etiology. There is strong evidence linking hyperactivation of the IGF-IR with the early stages of breast cancer. In primary breast tumors, the IGF-IR is overexpressed and hyperphosphorylated, which correlates with radio-resistance and tumor recurrence. In vitro, the IGF-IR is often required for mitogenesis and transformation, and its overexpression or activation counteract effects of various pro-apoptotic treatments. In hormone-responsive breast cancer cells, IGF-IR function is strongly linked with estrogen receptor (ER) action. The IGF-IR and the ER are co-expressed in breast tumors. Moreover, estrogens stimulate the expression of the IGF-IR and its major signaling substrate IRS-1, while antiestrogens downregulate IGF-IR signaling, mainly by decreasing IRS-1 expression and function. On the other hand, overexpression of IRS-1 promotes estrogen-independence for growth and transformation. In ER-negative breast cancer cells, usually displaying a more aggressive phenotype, the levels of the IGF-IR and IRS-1 are often low and IGF is not mitogenic, yet the IGF-IR is still required for metastatic spread. Consequently, IGF-IR function in the late stages of breast cancer remains one of the most important questions to be addressed before rational anti-IGF-IR therapies are developed.

Indexed as

Breast NeoplasmsFemaleHumansInsulin Receptor Substrate ProteinsPhosphoproteinsReceptor, IGF Type 1Receptors, EstrogenSignal TransductionInsulin Receptor Substrate ProteinsIRS1 protein, humanPhosphoproteinsReceptor, IGF Type 1Receptors, Estrogen

Identifiers

PMID10791772
OpenAlexW1526859945

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.