Evidence map›Paper›PMID 28720843›Full record

ArticleBritish journal of cancer2017

Clinical study of genomic drivers in pancreatic ductal adenocarcinoma.

Michael T Barrett, Ray Deiotte, Elizabeth Lenkiewicz, Smriti Malasi, Tara Holley, Lisa Evers, Richard G Posner, Timothy Jones, Haiyong Han, Mark Sausen and 6 more

Open access · hybridAbstract readClinical Study
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 35 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 7 institutions in 1 country.

Michael T BarrettMayo Clinic in Arizona, Scottsdale, AZ 85259, USA.
Ray DeiotteISSAC Corp, Colorado Springs, CO 80919, USA.
Elizabeth LenkiewiczMayo Clinic in Arizona, Scottsdale, AZ 85259, USA.
Smriti MalasiMayo Clinic in Arizona, Scottsdale, AZ 85259, USA.
Tara HolleyMayo Clinic in Arizona, Scottsdale, AZ 85259, USA.
Lisa EversMayo Clinic in Arizona, Scottsdale, AZ 85259, USA.
Richard G PosnerNorthern Arizona University, Flagstaff, AZ 86011, USA.
Timothy JonesISSAC Corp, Colorado Springs, CO 80919, USA.
Haiyong HanTranslational Genomics Research Institute, Phoenix, AZ 85004, USA.
Mark SausenJohns Hopkins University, Baltimore, MD 21218, USA.
Victor E VelculescuJohns Hopkins University, Baltimore, MD 21218, USA.
Jeffrey DrebinUniversity of Pennsylvania, Philadelphia, PA 19104, USA.
Peter O'DwyerUniversity of Pennsylvania, Philadelphia, PA 19104, USA.
Gayle JamesonVirginia G Piper Cancer Center at Honor Health, Scottsdale, AZ 85258, USA.
Ramesh K RamanathanMayo Clinic Cancer Center, Phoenix, AZ 85054, USA.
Daniel D Von HoffTranslational Genomics Research Institute, Phoenix, AZ 85004, USA.
Mayo Clinic in Arizona · USHonorHealth · USISSAC (United States) · USJohns Hopkins University · USTranslational Genomics Research Institute · USUniversity of Pennsylvania · USMayo Clinic Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDA) is a lethal cancer with complex genomes and dense fibrotic stroma. This study was designed to identify clinically relevant somatic aberrations in pancreatic cancer genomes of patients with primary and metastatic disease enrolled and treated in two clinical trials.

methodsTumour nuclei were flow sorted prior to whole genome copy number variant (CNV) analysis. Targeted or whole exome sequencing was performed on most samples. We profiled biopsies from 68 patients enrolled in two Stand Up to Cancer (SU2C)-sponsored clinical trials. These included 38 resected chemoradiation naïve tumours (SU2C 20206-003) and metastases from 30 patients who progressed on prior therapies (SU2C 20206-001). Patient outcomes including progression-free survival (PFS) and overall survival (OS) were observed.

resultsWe defined: (a) CDKN2A homozygous deletions that included the adjacent MTAP gene, only its' 3' region, or excluded MTAP; (b) SMAD4 homozygous deletions that included ME2; (c) a pancreas-specific MYC super-enhancer region; (d) DNA repair-deficient genomes; and (e) copy number aberrations present in PDA patients with long-term (⩾ 40 months) and short-term (⩽ 12 months) survival after surgical resection.

conclusionsWe provide a clinically relevant framework for genomic drivers of PDA and for advancing novel treatments.

Indexed as

Base SequenceSequence DeletionAdultAgedAged, 80 and overAntineoplastic Combined Chemotherapy ProtocolsBiopsyCarcinoma, Pancreatic DuctalCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Disease-Free SurvivalDNA Copy Number VariationsDNA Mutational AnalysisDNA RepairEnhancer Elements, GeneticExome5'-methylthioadenosine phosphorylaseCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18KRAS protein, humanMalate Dehydrogenasemalic enzyme 2; humanMicrotubule-Associated ProteinsProto-Oncogene Proteins p21(ras)Purine-Nucleoside PhosphorylaseSmad4 ProteinSMAD4 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28720843
PMCPMC5558689
OpenAlexW2736517046

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.