ReviewOncogene2017
Neomorphic mutations create therapeutic challenges in cancer.
Review in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Osteoradionecrosis After Modern Radiotherapy for Oral Cavity Cancer: Incidence and Risk Factors.Laryngoscope investigative otolaryngology · 2026Article
- Pan-cancer inference and validation of hypermorphic, hypomorphic and neomorphic mutations.Nature genetics · 2026Article
- Functional heterogeneity of TP53 mutants in venetoclax-resistant AML: mechanisms, clinical implications, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Mutation Patterns Define Clinical Heterogeneity in Acute Myeloid Leukemia.Journal of Cancer · 2026Article
- Structural mimicry of UM171 and neomorphic cancer mutants co-opts E3 ligase KBTBD4 for HDAC1/2 recruitment.Nature communications · 2025Article
- Neomorphic Gαo mutations gain interaction with Ric8 proteins in GNAO1 encephalopathies.The Journal of clinical investigation · 2024Article
- CIViCdb 2022: evolution of an open-access cancer variant interpretation knowledgebase.Nucleic acids research · 2023Article
- Restoration of the GTPase activity and cellular interactions of GαScience advances · 2022Article
- The two-hit theory hits 50.Molecular biology of the cell · 2021Article
- Identification of the RP11-21C4.1/SVEP1 gene pair associated with FAT2 mutations as a potential biomarker in gastric cancer.Bioengineered · 2021Article
- Intratumor δ-catenin heterogeneity driven by genomic rearrangement dictates growth factor dependent prostate cancer progression.Oncogene · 2020Article
- PI3K isoforms in cell signalling and vesicle trafficking.Nature reviews. Molecular cell biology · 2019Review
- Targeting the ROS/PI3K/AKT/HIF-1α/HK2 axis of breast cancer cells: Combined administration of Polydatin and 2-Deoxy-d-glucose.Journal of cellular and molecular medicine · 2019Article
- Functional role of SGK3 in PI3K/Pten driven liver tumor development.BMC cancer · 2019Article
- The many faces of mathematical modelling in oncology.The British journal of radiology · 2019Review
- Neomorphic PDGFRA extracellular domain driver mutations are resistant to PDGFRA targeted therapies.Nature communications · 2018Article
- The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers.Nature reviews. Cancer · 2018Review
- Polymerase-mediated ultramutagenesis in mice produces diverse cancers with high mutational load.The Journal of clinical investigation · 2018Article
- A recurrent point mutation in PRKCA is a hallmark of chordoid gliomas.Nature communications · 2018Article
- Systematic Functional Annotation of Somatic Mutations in Cancer.Cancer cell · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Oncogenesis is a pathologic process driven by genomic aberrations, including changes in nucleotide sequences. The majority of these mutational events fall into two broad categories: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph) or activation of oncogenes (hypermorph). The recent surge in genome sequence data and functional genomics research has ushered in the discovery of aberrations in a third category: gain-of-novel-function mutation (neomorph). These neomorphic mutations, which can be found in both tumor suppressor genes and oncogenes, produce proteins with entirely different functions from their respective wild-type (WT) proteins and the other morphs. The unanticipated phenotypic outcomes elicited by neomorphic mutations imply that tumors with the neomorphic mutations may not respond to therapies designed to target the WT protein. Therefore, understanding the functional activities of each genomic aberration to be targeted is crucial in devising effective treatment strategies that will benefit specific cancer patients.
Indexed as
Identifiers
What OpenQuestion holds
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.