Evidence map›Paper›PMID 18854834›Full record

ArticleBritish journal of cancer2008

Co-expression of KLK6 and KLK10 as prognostic factors for survival in pancreatic ductal adenocarcinoma.

F Rückert, M Hennig, C D Petraki, D Wehrum, M Distler, A Denz, M Schröder, G Dawelbait, H Kalthoff, H-D Saeger and 3 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 70 citations in OpenAlex.

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  7. Identifying Biomarkers Using Support Vector Machine to Understand the Racial Disparity in Triple-Negative Breast Cancer.Journal of computational biology : a journal of computational molecular cell biology · 2023
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  19. A 65‑gene signature for prognostic prediction in colon adenocarcinoma.International journal of molecular medicine · 2018
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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

13 authors at 5 institutions in 3 countries.

F RückertVisceral, Thoracic and Vascular Surgery, University Hospital Carl Gustav Carus, Technical University of Dresden, Fetscherstrasse 74, Dresden 01307, Germany. Felix.Rueckert@uniklinikum-dresden.de
M Hennig
C D Petraki
D Wehrum
M Distler
A Denz
M Schröder
G Dawelbait
H Kalthoff
H-D Saeger
E P Diamandis
C Pilarsky
R Grützmann
TU Dresden · DEUniversity Hospital Carl Gustav Carus · DEEvangelismos Hospital · GRMount Sinai Hospital · CAUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kallikreins play an important role in tumour microenvironment and as cancer biomarkers in different cancer entities. Previous studies suggested an upregulation of KLK10 and KLK6 in pancreatic ductal adenocarcinoma (PDAC). Therefore, we evaluated the clinicopathological role of these kallikreins and their value as biomarkers in PDAC.Differential expression was validated by DNA-microarrays and immunohistochemistry in normal and malignant pancreatic tissues. Sera concentrations of both kallikreins were evaluated using ELISA. In silico analysis of possible protein interactions and gene silencing of KLK10 in vitro using siRNAs gave further insights in the pathomechanisms.Gene expression analysis and immunohistochemistry demonstrated a strong expression for KLK10 and KLK6 in PDAC. Statistical analysis showed that co-expression of these kallikreins correlated with an R1-resection status (P=0.017) and worse outcome for overall survival (P=0.031). Multivariate analysis proofed that co-expression is an independent prognostic factor for survival (P=0.043). Importantly, KLK10 knockdown in AsPC-1 cells significantly reduced cell migration, whereas computational analysis suggested interaction of KLK6 with angiogenetic factors as an important mechanism.Co-expression of KLK10 and KLK6 plays an unfavourable role in PDAC. Our results suggest that this effect is likely mediated by an interaction with the factors of the extracellular matrix and enhancement of cancer cell motility.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementEye ProteinsGene Expression ProfilingGene SilencingHumansImmunohistochemistryKallikreinsNerve Growth FactorsPancreatic NeoplasmsPigment Epithelium-Derived FactorPrognosisSerpinsEye ProteinsKallikreinsKLK10 protein, humanKLK6 protein, humanNerve Growth FactorsPigment Epithelium-Derived FactorSerpins

Identifiers

PMID18854834
PMCPMC2579692
OpenAlexW2129685551

What OpenQuestion holds

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LicenceCC BY
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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.