Evidence map›Paper›PMID 17960465›Full record

ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2008

Telomere shortening and telomerase expression during multistage carcinogenesis of intraductal papillary mucinous neoplasms of the pancreas.

Yasushi Hashimoto, Yoshiaki Murakami, Kenichiro Uemura, Yasuo Hayashidani, Takeshi Sudo, Hiroki Ohge, Emi Fukuda, Fumio Shimamoto, Taijiro Sueda, Eiso Hiyama

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Review
  8. Shorter Treatment-Naïve Leukocyte Telomere Length is Associated with Poorer Overall Survival of Patients with Pancreatic Ductal Adenocarcinoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  9. Leukocyte Telomere Length and Its Interaction with Germline Variation in Telomere-Related Genes in Relation to Pancreatic Adenocarcinoma Risk.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  10. Molecular Diagnosis of Cystic Neoplasms of the Pancreas: a Review.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2020
    Review
  11. Review
  12. Prediagnostic Leukocyte Telomere Length and Pancreatic Cancer Survival.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
  13. Review
  14. Review
  15. Article
  16. Cyst Fluid Telomerase Activity Predicts the Histologic Grade of Cystic Neoplasms of the Pancreas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  17. Pancreatic adenocarcinoma pathology: changing "landscape".Journal of gastrointestinal oncology · 2015
    Review
  18. Review
  19. Telomeres and telomere dynamics: relevance to cancers of the GI tract.Expert review of gastroenterology & hepatology · 2013
    Review
  20. 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

10 authors at 2 institutions in 1 country.

Yasushi HashimotoDepartment of Surgery, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan. hashimoto_yss@ybb.ne.jp
Yoshiaki Murakami
Kenichiro Uemura
Yasuo Hayashidani
Takeshi Sudo
Hiroki Ohge
Emi Fukuda
Fumio Shimamoto
Taijiro Sueda
Eiso Hiyama
Hiroshima University · JPPrefectural University of Hiroshima · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intraductal papillary mucinous neoplasm (IPMN) of the pancreas has been increasingly identified as a precursor to infiltrating ductal adenocarcinoma. Telomerase activation in response to telomere crisis followed by telomere shortening is thought to be a crucial event in the development of most human cancers. The aim of this study was to determine when this event occurs in the context of histologically defined IPMN progression. We analyzed telomerase expression in 68 IPMN samples and assessed telomere length by quantitative fluorescence in situ hybridization in samples taken from 17 sequential IPMN patients that included 37 individual loci. Samples from pancreatic ductal adenocarcinomas (PDACs, n=15) and chronic pancreatitis patients (n=10) were also examined. Telomeres were significantly shortened in 36 (97.3%) of 37 IPMN loci, with average telomere length decreasing with IPMN progression. Notably, even adenoma IPMNs demonstrated a 50% reduction of telomere length in 7 of 14 foci examined. Marked telomere shortening was observed from the in situ IPMN carcinoma stage (P<0.001; vs borderline IPMNs) through the invasive stage, although telomerase had been activated, indicating that telomeres had shortened to a critical length by this histological grade. Up-regulated human telomerase reverse transcriptase expression was detectable and increased gradually with cancer development and was primarily observed at the borderline IPMN stage and then in more advanced histopathologies. Progressive telomere shortening predominantly occurs during early IPMNs carcinogenesis before telomerase activation and progression from borderline to carcinoma in situ IPMNs is the critical stage of IPMNs carcinogenesis at which telomere dysfunction occurs.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma, MucinousAdultAgedAged, 80 and overCarcinoma, Pancreatic DuctalCarcinoma, PapillaryDisease ProgressionDNA, NeoplasmEnzyme ActivationFemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMaleMiddle AgedDNA, NeoplasmTelomerase

Identifiers

PMID17960465
OpenAlexW1998062816

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.