ArticleCell cycle (Georgetown, Tex.)2015
Amplified centrosomes may underlie aggressive disease course in pancreatic ductal adenocarcinoma.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- African-Americans and Indigenous Peoples Have Increased Burden of Diseases of the Exocrine Pancreas: A Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2019Pooled it
- Stress adaptation pathways and HA-CD44 signaling maintain the survival of pancreatic cancer cells with centrosome amplification.Cell communication and signaling : CCS · 2026Article
- Nek2A prevents centrosome clustering and induces cell death in cancer cells via KIF2C interaction.Cell death & disease · 2024Article
- Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease.JCI insight · 2024Article
- Epigenetic alterations impede epithelial-mesenchymal transition by modulating centrosome amplification and Myc/RAS axis in triple negative breast cancer cells.Scientific reports · 2023Article
- Centrosomal protein 120 promotes centrosome amplification and gastric cancer progression via USP54-mediated deubiquitination of PLK4.iScience · 2023Article
- KIF24 depletion induces clustering of supernumerary centrosomes in PDAC cells.Life science alliance · 2022Article
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- Kinesin Family Member C1 (KIFC1) Regulated by Centrosome Protein E (CENPE) Promotes Proliferation, Migration, and Epithelial-Mesenchymal Transition of Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- 2-methoxyestradiol sensitizes breast cancer cells to taxanes by targeting centrosomes.Oncotarget · 2020Article
- Article
- PLK4: a promising target for cancer therapy.Journal of cancer research and clinical oncology · 2019Review
- Inhibition of polo-like kinase 4 (PLK4): a new therapeutic option for rhabdoid tumors and pediatric medulloblastoma.Oncotarget · 2017Article
- Multinucleated polyploidy drives resistance to Docetaxel chemotherapy in prostate cancer.British journal of cancer · 2017Article
- Amplified centrosomes and mitotic index display poor concordance between patient tumors and cultured cancer cells.Scientific reports · 2017Article
- The more the messier: centrosome amplification as a novel biomarker for personalized treatment of colorectal cancers.Journal of biomedical research · 2016Review
- A centrosome clustering protein, KIFC1, predicts aggressive disease course in serous ovarian adenocarcinomas.Journal of ovarian research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Centrosome amplification (CA), the presence of centrosomes that are abnormally numerous or enlarged, is a well-established driver of tumor initiation and progression associated with poor prognosis across a diversity of malignancies. Pancreatic ductal adenocarcinoma (PDAC) carries one of the most dismal prognoses of all cancer types. A majority of these tumors are characterized by numerical and structural centrosomal aberrations, but it is unknown how CA contributes to the disease and patient outcomes. In this study, we sought to determine whether CA was associated with worse clinical outcomes, poor prognostic indicators, markers of epithelial-mesenchymal transition (EMT), and ethnicity in PDAC. We also evaluated whether CA could precipitate more aggressive phenotypes in a panel of cultured PDAC cell lines. Using publicly available microarray data, we found that increased expression of genes whose dysregulation promotes CA was associated with worse overall survival and increased EMT marker expression in PDAC. Quantitative analysis of centrosomal profiles in PDAC cell lines and tissue sections uncovered varying levels of CA, and the expression of CA markers was associated with the expression of EMT markers. We induced CA in PDAC cells and found that CA empowered them with enhanced invasive and migratory capabilities. In addition, we discovered that PDACs from African American (AA) patients exhibited a greater extent of both numerical and structural CA than PDACs from European American (EA) patients. Taken together, these findings suggest that CA may fuel a more aggressive disease course in PDAC patients.
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Registered trials
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.