ReviewCold Spring Harbor perspectives in medicine2017
Evolution of Premalignant Disease.
Review in Cold Spring Harbor perspectives in medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency.Cancer discovery · 2026Article
- Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.Molecular biomedicine · 2026Review
- PCMR: a comprehensive precancerous molecular resource.Scientific data · 2025Article
- Article
- Defining precancer: a grand challenge for the cancer community.Nature reviews. Cancer · 2024Review
- Epithelial‑derived head and neck squamous tumourigenesis (Review).Oncology reports · 2024Review
- Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models.The American journal of pathology · 2024Article
- The Role of Specialized Pro-Resolving Lipid Mediators in Inflammation-Induced Carcinogenesis.International journal of molecular sciences · 2023Review
- The actin cytoskeleton: Morphological changes in pre- and fully developed lung cancer.Biophysics reviews · 2022Review
- Lessons Learned from Donor Cell-Derived Myeloid Neoplasms: Report of Three Cases and Review of the Literature.Life (Basel, Switzerland) · 2022Article
- Evaluating statistical approaches to define clonal origin of tumours using bulk DNA sequencing: context is everything.Genome biology · 2022Review
- Epigallocatechin-3-Gallate Delivery in Lipid-Based Nanoparticles: Potentiality and Perspectives for Future Applications in Cancer Chemoprevention and Therapy.Frontiers in pharmacology · 2022Review
- Crosstalk between cancer stem cells and the tumor microenvironment drives progression of premalignant oral epithelium.Frontiers in oral health · 2022Review
- Aldehyde dehydrogenase 1B1 is a potential marker of colorectal tumors.Histology and histopathology · 2021Article
- Understanding oncogenicity of cancer driver genes and mutations in the cancer genomics era.FEBS letters · 2020Review
- Redistribution, homing and organ-invasion of neoplastic stem cells in myeloid neoplasms.Seminars in cancer biology · 2020Review
- A multi-omics approach to understanding the field effect in bladder cancer.Translational andrology and urology · 2019Article
- An analysis of genetic heterogeneity in untreated cancers.Nature reviews. Cancer · 2019Review
- Clonal Hematopoiesis with Oncogenic Potential (CHOP): Separation from CHIP and Roads to AML.International journal of molecular sciences · 2019Review
- High MYC Levels Favour Multifocal Carcinogenesis.Frontiers in genetics · 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
3 authors.
Funding
Abstract
Where does cancer come from? Although the cell-of-origin is difficult to pinpoint, cancer clones harbor information about their clonal ancestries. In an effort to find cells before they evolve into a life-threatening cancer, physicians currently diagnose premalignant diseases at frequencies that substantially exceed those of clinical cancers. Cancer risk prediction relies on our ability to distinguish between which premalignant features will lead to cancer mortality and which are characteristic of inconsequential disease. Here, we review the evolution of cancer from premalignant disease, and discuss the concept that even phenotypically normal cell progenies inherently gain more malignant potential with age. We describe the hurdles of prognosticating cancer risk in premalignant disease by making reference to the underlying continuous and multivariate natures of genotypes and phenotypes and the particular challenge inherent in defining a cell lineage as "cancerized."
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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.