Evidence map›Paper›PMID 15509777›Full record

ArticleMolecular and cellular biology2004

Involvement of insulin receptor substrate 2 in mammary tumor metastasis.

Julie A Nagle, Zhefu Ma, Maura A Byrne, Morris F White, Leslie M Shaw

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Therapeutic delivery of albumin-binding siRNA targeting IRS2 to diverse cell types reduces mammary tumor growth.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
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  9. Embryonic Programs in Cancer and Metastasis-Insights From the Mammary Gland.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Article
  12. Night-Shift Work Duration and Risk of Colorectal Cancer According toCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  13. Article
  14. Article
  15. Article
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  18. Review
  19. Article
  20. Article

14 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

5 authors at 2 institutions in 1 country.

Julie A NagleDivision of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Zhefu Ma
Maura A Byrne
Morris F White
Leslie M Shaw
Beth Israel Deaconess Medical Center · USHoward Hughes Medical Institute · US

Funding

Regulating IRS-proteins by Ser/Thr PhosphorylationR01DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1992 to 2014
$5.0M
Insulin Receptor Substrate Function in Breast CancerR01CA090583 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHAW, LESLIE M · 2002 to 2011
$2.9M
INSULIN RECEPTOR REGULATION BY MULTISITE PHOSPHORYLATIONR29DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1987 to 1989
–
INTERACTION BETWEEN INSULIN RECEPTORS AND CELL PROTEINSR55DK038712 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1991 to 1991
–
NCI NIH HHS CA90583NCI NIH HHS R01 CA090583NIDDK NIH HHS DK38712NIDDK NIH HHS R01 DK038712
6 · The paper itself

Abstract

The insulin receptor substrate (IRS) proteins are adaptor molecules that integrate signals generated by receptors that are implicated in human breast cancer. We investigated the specific contribution of IRS-2 to mammary tumor progression using transgenic mice that express the polyoma virus middle T antigen (PyV-MT) in the mammary gland and IRS-2-null (IRS-2(-/-)) mice. PyV-MT-induced tumor initiation and growth were similar in wild-type (WT) and IRS-2(-/-) mice. However, the latency and incidence of metastasis were significantly decreased in the absence of IRS-2 expression. The contribution of IRS-2 to metastasis is intrinsic to the tumor cells, because IRS-2(-/-) mammary tumor cells did not metastasize when grown orthotopically in the mammary fat pads of WT mice. WT and IRS-2(-/-) tumors contained similar numbers of mitotic cells, but IRS-2(-/-) tumors had a higher incidence of apoptosis than did WT tumors. In vitro, IRS-2(-/-) mammary tumor cells were less invasive and more apoptotic in response to growth factor deprivation than their WT counterparts. In contrast, IRS-1(-/-) tumor cells, which express only IRS-2, were highly invasive and were resistant to apoptotic stimuli. Collectively, our findings reveal an important contribution of IRS-2 to breast cancer metastasis.

Indexed as

AnimalsApoptosisBase SequenceBreast NeoplasmsCell Line, TumorDNA, NeoplasmFemaleHumansInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMitosisDNA, NeoplasmInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsIRS1 protein, humanIrs1 protein, mouseIRS2 protein, humanIrs2 protein, mousePhosphoproteins

Identifiers

PMID15509777
PMCPMC525494
OpenAlexW2108072032

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.