ArticleNature communications2016
Functional annotation of rare gene aberration drivers of pancreatic cancer.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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
55 citing papers in PubMed, 88 citations in OpenAlex.
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- DNA Origami-Cyanine Nanocomplex for Precision Imaging of KRAS-Mutant Pancreatic Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cryo-EM structure and regulation of human NAD kinase.Science advances · 2025Article
- A protein expression atlas on tissue samples and cell lines from cancer patients provides insights into tumor heterogeneity and dependencies.Nature cancer · 2024Article
- Homeostatic regulation of NAD(H) and NADP(H) in cells.Genes & diseases · 2024Review
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- Simultaneous screening of overexpressed genes in breast cancer for oncogenic drivers and tumor dependencies.Scientific reports · 2024Article
- A de novo missense variant in EZH1 associated with developmental delay exhibits functional deficits in Drosophila melanogaster.Genetics · 2023Article
- The genomic landscape of familial glioma.Science advances · 2023Article
- In vivo functional characterization of EGFR variants identifies novel drivers of glioblastoma.Neuro-oncology · 2023Article
- Glioma epileptiform activity and progression are driven by IGSF3-mediated potassium dysregulation.Neuron · 2023Article
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- Nicotinamide adenine dinucleotide kinase promotes lymph node metastasis of NSCLC via activating ID1 expression through BMP pathway.International journal of biological sciences · 2023Article
- (-)-Epigallocatechin Gallate is a Noncompetitive Inhibitor of NAD Kinase.ACS medicinal chemistry letters · 2022Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 1 country.
Funding
Abstract
As we enter the era of precision medicine, characterization of cancer genomes will directly influence therapeutic decisions in the clinic. Here we describe a platform enabling functionalization of rare gene mutations through their high-throughput construction, molecular barcoding and delivery to cancer models for in vivo tumour driver screens. We apply these technologies to identify oncogenic drivers of pancreatic ductal adenocarcinoma (PDAC). This approach reveals oncogenic activity for rare gene aberrations in genes including NAD Kinase (NADK), which regulates NADP(H) homeostasis and cellular redox state. We further validate mutant NADK, whose expression provides gain-of-function enzymatic activity leading to a reduction in cellular reactive oxygen species and tumorigenesis, and show that depletion of wild-type NADK in PDAC cell lines attenuates cancer cell growth in vitro and in vivo. These data indicate that annotating rare aberrations can reveal important cancer signalling pathways representing additional therapeutic targets.
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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.