Evidence map›Paper›PMID 25807104›Full record

ArticlePloS one2015

Functional EpoR pathway utilization is not detected in primary tumor cells isolated from human breast, non-small cell lung, colorectal, and ovarian tumor tissues.

Scott D Patterson, John M Rossi, Katherine L Paweletz, V Dan Fitzpatrick, C Glenn Begley, Leigh Busse, Steve Elliott, Ian McCaffery

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Pan-Cancer Analysis Based onFrontiers in oncology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. MiRNA-323-5p Promotes U373 Cell Apoptosis by Reducing IGF-1R.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

8 authors at 1 institution in 1 country.

Scott D PattersonDepartment of Medical Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
John M RossiDepartment of Molecular Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
Katherine L PaweletzDepartment of Molecular Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
V Dan FitzpatrickDepartment of Molecular Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
C Glenn BegleyDepartment of Oncology Research, Amgen Inc., Thousand Oaks, California, United States of America.
Leigh BusseDepartment of Molecular Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
Steve ElliottDepartment of Oncology Research, Amgen Inc., Thousand Oaks, California, United States of America.
Ian McCafferyDepartment of Molecular Sciences, Amgen Inc., Thousand Oaks, California, United States of America.
Amgen (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several clinical trials in oncology have reported increased mortality or disease progression associated with erythropoiesis-stimulating agents. One hypothesis proposes that erythropoiesis-stimulating agents directly stimulate tumor proliferation and/or survival through cell-surface receptors. To test this hypothesis and examine if human tumors utilize the erythropoietin receptor pathway, the response of tumor cells to human recombinant erythropoietin was investigated in disaggregated tumor cells obtained from 186 patients with colorectal, breast, lung, ovarian, head and neck, and other tumors. A cocktail of well characterized tumor growth factors (EGF, HGF, and IGF-1) were analyzed in parallel as a positive control to determine whether freshly-isolated tumor cells were able to respond to growth factor activation ex vivo. Exposing tumor cells to the growth factor cocktail resulted in stimulation of survival and proliferation pathways as measured by an increase in phosphorylation of the downstream signaling proteins AKT and ERK. In contrast, no activation by human recombinant erythropoietin was observed in isolated tumor cells. Though tumor samples exhibited a broad range of cell-surface expression of EGFR, c-Met, and IGF-1R, no cell-surface erythropoietin receptor was detected in tumor cells from the 186 tumors examined (by flow cytometry or Western blot). Erythropoiesis-stimulating agents did not act directly upon isolated tumor cells to stimulate pathways known to promote proliferation or survival of human tumor cells isolated from primary and metastatic tumor tissues.

Indexed as

Breast NeoplasmsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsEpidermal Growth FactorEpoetin AlfaErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleHepatocyte Growth FactorHT29 CellsHumansInsulin-Like Growth Factor IMaleEpidermal Growth FactorEpoetin AlfaErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHepatocyte Growth FactorInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metReceptor, IGF Type 1Receptors, Erythropoietin

Identifiers

PMID25807104
PMCPMC4373902
OpenAlexW1974735369

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.