Evidence map›Paper›PMID 25907283›Full record

ArticleInternational journal of cancer2015

Microtubule affinity-regulating kinase 2 is associated with DNA damage response and cisplatin resistance in non-small cell lung cancer.

Roland Hubaux, Kelsie L Thu, Emily A Vucic, Larissa A Pikor, Sonia H Y Kung, Victor D Martinez, Mitra Mosslemi, Daiana D Becker-Santos, Adi F Gazdar, Stephen Lam and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-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

26 citing papers in PubMed, 42 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

11 authors at 2 institutions in 2 countries.

Roland HubauxDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Kelsie L ThuDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Emily A VucicDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Larissa A PikorDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Sonia H Y KungDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Victor D MartinezDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Mitra MosslemiDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Daiana D Becker-SantosDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Adi F GazdarHamon Center of Therapeutics, University of Texas South Western, Dallas, TX.
Stephen LamDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Wan L LamDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada, V5Z, 1L3.
Occupational Cancer Research Centre · CAHealth First · US

Funding

Molecular biomarkers of airway and lung linking COPD and Lung CancerR01CA164783 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LAM, STEPHEN C, LENBURG, MARC ELLIOTT · 2011 to 2014
$2.2M
Canadian Institutes of Health Research MOP 86731NCI NIH HHS 1R01CA164783-01NCI NIH HHS R01 CA164783
6 · The paper itself

Abstract

Microtubule affinity-regulating kinases (MARKs) are involved in several cellular functions but few studies have correlated MARK kinase expression with cancer, and none have explored their role in lung cancer. In this study, we identified MARK2 as frequently disrupted by DNA hypomethylation and copy gain, resulting in concordant overexpression in independent lung tumor cohorts and we demonstrate a role for MARK2 in lung tumor biology. Manipulation of MARK2 in lung cell lines revealed its involvement in cell viability and anchorage-independent growth. Analyses of both manipulated cell lines and clinical tumor specimens identified a potential role for MARK2 in cell cycle activation and DNA repair. Associations between MARK2 and the E2F, Myc/Max and NF-κB pathways were identified by luciferase assays and in-depth assessment of the NF-κB pathway suggests a negative association between MARK2 expression and NF-κB due to activation of non-canonical NF-κB signaling. Finally, we show that high MARK2 expression levels correlate with resistance to cisplatin, a standard first line chemotherapy for lung cancer. Collectively, our work supports a role for MARK2 in promoting malignant phenotypes of lung cancer and potentially modulating response to the DNA damaging chemotherapeutic, cisplatin.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinDNA DamageDNA RepairHumansLung NeoplasmsNF-kappa BProtein Serine-Threonine KinasesAntineoplastic AgentsCisplatinMARK2 protein, humanNF-kappa BProtein Serine-Threonine Kinasescisplatin resistanceDNA damage repairlung cancerMARK2NFκB

Identifiers

PMID25907283
PMCPMC4537683
OpenAlexW1973245479

What OpenQuestion holds

Textmetadata
LicenceTDM
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.