Evidence map›Paper›PMID 30172883›Full record

ArticleTranslational oncology2018

Proteome Profiling of Primary Pancreatic Ductal Adenocarcinomas Undergoing Additive Chemoradiation Link ALDH1A1 to Early Local Recurrence and Chemoradiation Resistance.

V O Oria, P Bronsert, A R Thomsen, M C Föll, C Zamboglou, Luciana Hannibal, S Behringer, M L Biniossek, C Schreiber, A L Grosu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-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

18 citing papers in PubMed, 29 citations in OpenAlex.

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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

16 authors at 5 institutions in 1 country.

V O OriaInstitute of Molecular Medicine and Cell Research, Freiburg, Germany; Faculty of Biology, University of Freiburg, Freiburg, Germany; Spemann Graduate School of Biology and Medicine, Freiburg, Germany.
P BronsertInstitute of Surgical Pathology, University Medical Center, Freiburg, Germany; German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; Tumorbank Comprehensive Cancer Center Freiburg, Medical Center- University of Freiburg, Germany; Faculty of Medicine, University of Freiburg, Germany.
A R ThomsenGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; Faculty of Medicine, University of Freiburg, Germany; Department of Radiation Oncology, Medical Center - University of Freiburg, Germany.
M C FöllInstitute of Molecular Medicine and Cell Research, Freiburg, Germany; Faculty of Biology, University of Freiburg, Freiburg, Germany.
C ZamboglouGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; Faculty of Medicine, University of Freiburg, Germany; Department of Radiation Oncology, Medical Center - University of Freiburg, Germany.
Luciana HannibalLaboratory of Clinical Biochemistry and Metabolism, Department for Pediatrics, Medical Center, University of Freiburg, Freiburg, Germany.
S BehringerLaboratory of Clinical Biochemistry and Metabolism, Department for Pediatrics, Medical Center, University of Freiburg, Freiburg, Germany.
M L BiniossekInstitute of Molecular Medicine and Cell Research, Freiburg, Germany.
C SchreiberInstitute of Pathology, UKSH Campus Lübeck, Lübeck, Germany.
A L GrosuGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; Faculty of Medicine, University of Freiburg, Germany; Department of Radiation Oncology, Medical Center - University of Freiburg, Germany.
L BolmClinic of Surgery, UKSH Campus Lübeck, Lübeck, Germany.
D RadesDepartment of Radiation Oncology, UKSH Campus Lübeck, Lübeck, Germany.
T KeckClinic of Surgery, UKSH Campus Lübeck, Lübeck, Germany.
M WernerInstitute of Surgical Pathology, University Medical Center, Freiburg, Germany; German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; Tumorbank Comprehensive Cancer Center Freiburg, Medical Center- University of Freiburg, Germany; Faculty of Medicine, University of Freiburg, Germany.
U F WellnerClinic of Surgery, UKSH Campus Lübeck, Lübeck, Germany.
O SchillingInstitute of Molecular Medicine and Cell Research, Freiburg, Germany; Institute of Surgical Pathology, University Medical Center, Freiburg, Germany; German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) Heidelberg, Germany; BIOSS Centre for Biological Signaling Studies, University of Freiburg, Freiburg, Germany. Electronic address: oliver.schilling@mol-med.uni-freiburg.de.
Universitäres Kinderwunschzentrum Lübeck · DEUniversity Medical Center Freiburg · DEUniversity of Freiburg · DEGerman Cancer Research Center · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis with frequent post-surgical local recurrence. The combination of adjuvant chemotherapy with radiotherapy is under consideration to achieve a prolonged progression-free survival (PFS). To date, few studies have determined the proteome profiles associated with response to adjuvant chemoradiation. We herein analyzed the proteomes of primary PDAC tumors subjected to additive chemoradiation after surgical resection and achieving short PFS (median 6 months) versus prolonged PFS (median 28 months). Proteomic analysis revealed the overexpression of Aldehyde Dehydrogenase 1 Family Member A1 (ALDH1A1) and Monoamine Oxidase A (MAOA) in the short PFS cohort, which were corroborated by immunohistochemistry. In vitro, specific inhibition of ALDH1A1 by A37 in combination with gemcitabine, radiation, and chemoradiation lowered cell viability and augmented cell death in MiaPaCa-2 and Panc 05.04 cells. ALDH1A1 silencing in both cell lines dampened cell proliferation, cell metabolism, and colony formation. In MiaPaCa-2 cells, ALDH1A1 silencing sensitized cells towards treatment with gemcitabine, radiation or chemoradiation. In Panc 05.04, increased cell death was observed upon gemcitabine treatment only. These findings are in line with previous studies that have suggested a role of ALDH1A1 chemoradiation resistance, e.g., in esophageal cancer. In summary, we present one of the first proteome studies to investigate the responsiveness of PDAC to chemoradiation and provide further evidence for a role of ALDH1A1 in therapy resistance.

Identifiers

PMID30172883
PMCPMC6121830
OpenAlexW2889515835

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.