Evidence map›Paper›PMID 39187317›Full record

ArticleIn vivo (Athens, Greece)

Anti-Tumor and Chemosensitizing Effects of the CDK Inhibitor Dinaciclib on Cholangiocarcinoma

Prin Sungwan, Sonexai Kidoikhammouan, Unchalee Thonsri, Charupong Saengboonmee, Sopit Wongkham, Seiji Okada, Wunchana Seubwai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

7 authors.

Prin SungwanBiomedical Science Program, Graduate School, Khon Kaen University, Khon Kaen, Thailand.
Sonexai KidoikhammouanBiomedical Science Program, Graduate School, Khon Kaen University, Khon Kaen, Thailand.
Unchalee ThonsriDepartment of Biochemistry, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.
Charupong SaengboonmeeDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Sopit WongkhamDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Seiji OkadaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan; okadas@kumamoto-u.ac.jp.
Wunchana SeubwaiCenter for Translational Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand; wunchana@kku.ac.th.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimCholangiocarcinoma (CCA) is a highly aggressive disease. Most of CCA patients are diagnosed in an advanced stage of the disease, when it is unresectable and there is chemoresistance, resulting in poor prognosis. However, effective therapeutic regimens and molecular targets for CCA remain poor. Cyclin-dependent kinases (CDKs) are key regulatory enzymes in cell cycle progression. Aberrant CDK activation is a hallmark of cancer. Dinaciclib is a small molecule inhibitor of multiple CDKs, currently under clinical evaluation for treating advanced malignancies. The efficacy of anti-tumor activity of dinaciclib against chemotherapy resistant CCA cells was examined in vitro and in vivo. MATERIALS AND

methodsIn this study, the effect of dinaciclib on growth and cell cycle in CCA cell lines were determined using the MTT assay and cell cycle analysis. The anti-tumor activity of dinaciclib was investigated in CCA-inoculated mice. In addition, the chemosensitizing effect of dinaciclib was investigated in gemcitabine-treated CCA cell lines.

resultsDinaciclib significantly suppressed cell proliferation, induced G

conclusionDinaciclib has the potential to be an effective therapeutic agent to control tumor cell growth of both parental and gemcitabine-resistant CCA cells.

Indexed as

Bridged Bicyclo Compounds, HeterocyclicCell ProliferationCholangiocarcinomaCyclic N-OxidesIndolizinesPyridinium CompoundsXenograft Model Antitumor AssaysAnimalsAntineoplastic AgentsApoptosisBile Duct NeoplasmsCell CycleCell Line, TumorCyclin-Dependent KinasesDeoxycytidineDisease Models, AnimalAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCyclic N-OxidesCyclin-Dependent KinasesDeoxycytidinedinaciclibGemcitabineIndolizinesProtein Kinase InhibitorsPyridinium CompoundsChemosensitizationcholangiocarcinomadinaciclibdrug resistancegemcitabine

Identifiers

PMID39187317
PMCPMC11363801

What OpenQuestion holds

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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.