Evidence map›Paper›PMID 18836286›Full record

ArticleCancer biology & therapy2008

Copy number alterations in pancreatic cancer identify recurrent PAK4 amplification.

Shuaili Chen, Theresa Auletta, Ostap Dovirak, Christina Hutter, Karen Kuntz, Samira El-ftesi, Jude Kendall, Haiyong Han, Daniel D Von Hoff, Raheela Ashfaq and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer biology & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.4field-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

65 citing papers in PubMed, 172 citations in OpenAlex.

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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Shuaili ChenCold Spring Harbor Laboratory, Cold Spring Harbor, New York, New York, USA.
Theresa Auletta
Ostap Dovirak
Christina Hutter
Karen Kuntz
Samira El-ftesi
Jude Kendall
Haiyong Han
Daniel D Von Hoff
Raheela Ashfaq
Anirban Maitra
Christine A Iacobuzio-Donahue
Ralph H Hruban
Robert Lucito
Cold Spring Harbor Laboratory · USJohns Hopkins University · USTranslational Genomics Research Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI JAFFEE, ELIZABETH M. · 1993 to 2022
$54.6M
Validation of Amplified Genes in Pancreatic CancerP01CA109552 · NCI · TRANSLATIONAL GENOMICS RESEARCH INST · PI VON HOFF, DANIEL D · 2005 to 2009
$15.2M
Application of Genomic Microarrays to Breast CancerK01CA093634 · NCI · COLD SPRING HARBOR LABORATORY · PI LUCITO, ROBERT · 2002 to 2006
$683k
NCI NIH HHS CA109552-0141NCI NIH HHS CA62924NCI NIH HHS K01 CA093634NCI NIH HHS K01CA93634-01NCI NIH HHS P01 CA109552NCI NIH HHS P50 CA062924
6 · The paper itself

Abstract

Pancreatic cancer is one of the most lethal of all cancers. The median survival is six months and less than 5% of those diagnosed survive five years. Recurrent genetic deletions and amplifications in 72 pancreatic adenocarcinomas, the largest sample set analyzed to date for pancreatic cancer, were defined using comparative genomic hybridization The recurrent genetic alterations identified target a number of previously well-characterized genes, as well as regions that contain possible new oncogenes and tumor suppressor genes. We have focused on chromosome 19q13, a region frequently found amplified in pancreatic cancer and demonstrate how boundaries of common regions of mutation can be mapped and how a gene, in this case PAK4 amplified on chromosome19q13, can be functionally validated. We show that although the PAK4 gene is not activated by mutation in cell lines with gene amplification, an oncogenic form of the KRAS2 gene is present in these cells and oncogenic KRAS2 can activate PAK4. In fact in the three samples we identified with PAK4 gene amplification, the KRAS2 gene was activated and genomically amplified. The kinase activity of the PAK4 protein is significantly higher in cells with genomic amplification as compared to cells without amplification. Our study demonstrates the utility of analyzing copy number data in a large set of neoplasms to identify genes involved in cancer. We have generated a useful dataset which will be particularly useful for the pancreatic cancer community as efforts are undertaken to sequence the pancreatic cancer genome.

Indexed as

Gene DosageGene Expression Regulation, NeoplasticAnimalsCell Line, TumorChromosomes, Human, Pair 19Gene AmplificationHumansMaleMiceModels, GeneticMutationNeoplasm Transplantationp21-Activated KinasesPancreatic NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)KRAS protein, humanp21-Activated KinasesPAK4 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID18836286
PMCPMC7323936
OpenAlexW1981580511

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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.