Evidence map›Paper›PMID 31467540›Full record

ArticleJournal of oncology2019

Overexpression of DCLK1-AL Increases Tumor Cell Invasion, Drug Resistance, and KRAS Activation and Can Be Targeted to Inhibit Tumorigenesis in Pancreatic Cancer.

Dongfeng Qu, Nathaniel Weygant, Jiannan Yao, Parthasarathy Chandrakesan, William L Berry, Randal May, Kamille Pitts, Sanam Husain, Stan Lightfoot, Min Li and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 10% 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, 48 citations in OpenAlex.

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  13. Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022
    Article
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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

15 authors at 5 institutions in 2 countries.

Dongfeng QuDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.ORCID https://orcid.org/0000-0002-9200-3852
Nathaniel WeygantDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Jiannan YaoDepartment of Oncology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0002-4982-4460
Parthasarathy ChandrakesanDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
William L BerryDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Randal MayDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.ORCID https://orcid.org/0000-0001-9397-9964
Kamille PittsDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Sanam HusainDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Stan LightfootDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Min LiDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Timothy C WangDepartment of Digestive and Liver Diseases, Columbia University Medical Center, New York, NY, USA.
Guangyu AnDepartment of Oncology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0003-1597-5188
Cynthia ClendeninDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Ben Z StangerDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Courtney W HouchenDepartment of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.ORCID https://orcid.org/0000-0003-2487-5242
University of Oklahoma Health Sciences Center · USOklahoma State University Oklahoma City · USCapital Medical University · CNUniversity of Pennsylvania · USColumbia University Irving Medical Center · US

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michael S. Businelle · 2018 to 2026
$27.1M
TUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HANNAFON, BETHANY · 2012 to 2022
$21.3M
The role of DCLK1 in the initiation of pancreatic ductal adenocarcinomaR01CA182869 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HOUCHEN, COURTNEY WAYNE · 2015 to 2019
$1.7M
The role of DCLK1 in the initiation of pancreatic ductal adenocarcinoma and colorectal cancerR50CA233186 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI QU, DONGFENG · 2018 to 2022
$448k
NCI NIH HHS P30 CA225520NCI NIH HHS R01 CA182869NCI NIH HHS R50 CA233186NIGMS NIH HHS P20 GM103639
6 · The paper itself

Abstract

Oncogenic KRAS mutation plays a key role in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis with nearly 95% of PDAC harboring mutation-activated KRAS, which has been considered an undruggable target. Doublecortin-like kinase 1 (DCLK1) is often overexpressed in pancreatic cancer, and recent studies indicate that DCLK1+ PDAC cells can initiate pancreatic tumorigenesis. In this study, we investigate whether overexpressing DCLK1 activates RAS and promotes tumorigenesis, metastasis, and drug resistance. Human pancreatic cancer cells (AsPC-1 and MiaPaCa-2) were infected with lentivirus and selected to create stable DCLK1 isoform 2 (alpha-long, AL) overexpressing lines. The invasive potential of these cells relative to vector control was compared using Matrigel coated transwell assay. KRAS activation and interaction were determined by a pull-down assay and coimmunoprecipitation. Gemcitabine, mTOR (Everolimus), PI3K (LY-294002), and BCL-2 (ABT-199) inhibitors were used to evaluate drug resistance downstream of KRAS activation. Immunostaining of a PDAC tissue microarray was performed to detect DCLK1 alpha- and beta-long expression. Analysis of gene expression in human PDAC was performed using the TCGA PAAD dataset. The effects of targeting DCLK1 were studied using xenograft and Pdx1

Identifiers

PMID31467540
PMCPMC6699308
OpenAlexW2964458353

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.