Evidence map›Paper›PMID 14647146›Full record

ArticleBritish journal of cancer2003

Incidence, mechanism and prognostic value of activated AKT in pancreas cancer.

M G Schlieman, B N Fahy, R Ramsamooj, L Beckett, R J Bold

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

120 citing papers in PubMed, 256 citations in OpenAlex.

  1. Oral mTOR inhibitor everolimus in patients with gemcitabine-refractory metastatic pancreatic cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009
    Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. TargetingWorld journal of clinical oncology · 2023
    Review
  8. Pancreatic Cancer: Beyond Brca Mutations.Journal of personalized medicine · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Isoforms of MUC16 activate oncogenic signaling through EGF receptors to enhance the progression of pancreatic cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  18. Article
  19. Article
  20. Review

60 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.

M G SchliemanDepartment of Surgery, University of California Davis Medical Center, Sacramento, CA 95817, USA.
B N Fahy
R Ramsamooj
L Beckett
R J Bold
University of California, Davis · USUniversity of California Davis Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When activated, the serine/threonine kinase AKT mediates an antiapoptotic signal implicated in chemoresistance of various cancers. The mechanism(s) of AKT activation are unknown, though overexpression of HER-2/neu has been implicated in breast cancer. Therefore, we determined the incidence of activated AKT in human pancreatic cancer, whether HER-2/neu is involved in AKT activation, and if AKT activation is associated with biologic behaviour. HER-2/neu expression and AKT activation were examined in seven pancreatic cancer cell lines by Western blotting. The in vitro effect of HER-2/neu inhibition on AKT activation was similarly determined. Finally, 78 pancreatic cancer specimens were examined for AKT activation and HER-2/neu overexpression, and correlated with the clinical prognostic variable of histologic grade. HER-2/neu was overexpressed in two of seven cell lines; these two cell lines demonstrated the highest level of AKT activation. Inhibition of HER-2/neu reduced AKT activation in vitro. AKT was activated in 46 out of 78 (59%) of the pancreatic cancers; HER-2/neu overexpression correlated with AKT activation (P=0.015). Furthermore, AKT activation was correlated with higher histologic tumour grade (P=0.047). Thus, it is concluded that AKT is frequently activated in pancreatic cancer; this antiapoptotic signal may be mediated by HER-2/neu overexpression. AKT activation is associated with tumour grade, an important prognostic factor.

Indexed as

AdenocarcinomaAntibodies, MonoclonalEnzyme ActivationErb-b2 Receptor Tyrosine KinasesHumansPancreatic NeoplasmsPrognosisProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTumor Cells, CulturedAKT1 protein, humanAntibodies, MonoclonalErb-b2 Receptor Tyrosine KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID14647146
PMCPMC2376856
OpenAlexW1964717481

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Registered trials

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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.