ReviewCell cycle (Georgetown, Tex.)2014
The other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axis.
Review in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 45 citations in OpenAlex.
- Somatic BRCA alterations in breast cancer are associated with distinct biological and clinical patterns according to germline BRCA status.ESMO open · 2026Article
- Characterization of tumor microenvironment infiltration and therapeutic responses of cell cycle-related genes' signature in breast cancer.Journal of cancer research and clinical oncology · 2023Article
- KIF14 affects cell cycle arrest and cell viability in cervical cancer by regulating the p27World journal of surgical oncology · 2022Article
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- Combined RNA/tissue profiling identifies novel Cancer/testis genes.Molecular oncology · 2021Article
- Article
- Functional genomics of AP-2α and AP-2γ in cancers: in silico study.BMC medical genomics · 2020Article
- Double Agent:Cancer management and research · 2020Review
- Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology.Journal of Cancer · 2020Review
- MicroRNA Assisted Gene Regulation in Colorectal Cancer.International journal of molecular sciences · 2019Article
- Prognostic significance of mutated genes in megakaryocytic disorders.Oncology reviews · 2019Article
- The biological characteristics of transcription factors AP-2α and AP-2γ and their importance in various types of cancers.Bioscience reports · 2019Review
- Dual-functionality of RASSF1A overexpression in A375 cells is mediated by activation of IL-6/STAT3 regulatory loop.Molecular biology reports · 2018Article
- Review
- Evaluating the Remote Control of Programmed Cell Death, with or without a Compensatory Cell Proliferation.International journal of biological sciences · 2018Review
- There are only four basic modes of cell death, although there are many ad-hoc variants adapted to different situations.Cell & bioscience · 2018Review
- Integrated Oncogenomic Profiling of Copy Numbers and Gene Expression in Lung Adenocarcinomas withoutJournal of Cancer · 2018Article
- Review
- A mononucleotide repeat in PRRT2 is an important, frequent target of mismatch repair deficiency in cancer.Oncotarget · 2017Article
- Revisiting the hallmarks of cancer.American journal of cancer research · 2017Review
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 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cancer-regulatory genes are dichotomized to oncogenes and tumor-suppressor gene s, in reality they can be oncogenic in one situation but tumor-suppressive in another. This dual-function nature, which sometimes hampers our understanding of tumor biology, has several manifestations: (1) Most canonically defined genes have multiple mRNAs, regulatory RNAs, protein isoforms, and posttranslational modifications; (2) Genes may interact at different levels, such as by forming chimeric RNAs or by forming different protein complexes; (3) Increased levels of tumor-suppressive genes in normal cells drive proliferation of cancer progenitor cells in the same organ or tissue by imposing compensatory proliferation pressure, which presents the dual-function nature as a cell-cell interaction. All these manifestations of dual functions can find examples in the genes along the CCND-CDK4/6-RB axis. The dual-function nature also underlies the heterogeneity of cancer cells. Gene-targeting chemotherapies, including that targets CDK4, are effective to some cancer cells but in the meantime may promote growth or progression of some others in the same patient. Redefining "gene" by considering each mRNA, regulatory RNA, protein isoform, and posttranslational modification from the same genomic locus as a "gene" may help in better understanding tumor biology and better selecting targets for different sub-populations of cancer cells in individual patients for personalized therapy.
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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.