Rapid-onset cancer - Article - Rapid-onset cancer review

Sep 23, 2026

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Human cancers are often described as developing over decades, yet “rapid-onset” cancers can emerge in months in humans and in as little as days in mice. Rapid progression is linked to conditions such as early developmental contexts, immune deficiency, or viral infection. The article reviews rapid-onset cancers through the “hallmarks of cancer,” emphasizing how viruses are especially capable of driving malignant transformation quickly. It contrasts slow multi-step carcinogenesis with genetically engineered, congenital, and virus-induced rapid cases.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages8

Reading Time20 min

AccessFree to download

What is “rapid-onset” cancer?

Multistep carcinogenesis: “slow-onset cancer”

Tumour Virus Research 19 (2025) 200312 Contents lists available at ScienceDirect Tumour Virus Research journal [homepage:](homepage: www.journals.elsevier.com/tumour-virus-research)[ www.journals.elsevier.com/tumour-virus-research](homepage: www.journals.elsevier.com/tumour-virus-research) | Rapid-onset cancer
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Andrea Bilger , Paul F. Lambert
McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, 1111 Highland Avenue, Madison, WI, 53705, USA | | | | --- | --- | --- | | A R T I C L E I N F O | | A B S T R A C T | | Keywords: Rapid Slow Onset Cancer Virus Congenital
Carcinogenesis | | Human cancers are generally thought to develop over the course of decades. Such slow progression is well documented for a variety of cancers that we designate “slow-onset” cancers.“Rapid-onset” cancers, in contrast, can develop in a matter of months in humans or in as little as 9 days in mice. These cancers often develop under conditions that might be expected to accelerate cancer development: early development, immune deficiency, or viral infection. We will discuss rapid-onset cancers in the context of the "hallmarks of cancer" – properties cells must acquire in order to become malignant – focusing on how viruses are particularly well suited to causing rapid-onset cancer. | 1. What is “rapid-onset" cancer? To understand what it means for a cancer to develop rapidly, we need to know what it means for cancers to develop slowly. This review will summarize some of the decades of data on cancer development in tissues where available evidence supports a multistep process that requires decades in people or several months in rodent models: “slow onset”cancers. We will then describe a variety of “rapid onset” cancers: genetically engineered, congenital, and virus-induced cancers in patients and/or animals where onset occurs in as little as months in people or weeks in animal models. Some of these rapid-onset cancers are also"early-onset" cancers – cancers that develop in young patients or animals; others – particularly virus-induced cancers – can develop rapidly even in adults. 2. Multistep carcinogenesis: “slow-onset cancer” Cancer is generally considered a disease of aging, with a median age at diagnosis in the United States of 67 [1,2]. In the 1950s, analysis of cancer mortality statistics, relating the frequency of deaths from cancer to the age of those deaths, suggested that many cancers result from the accumulation of six to seven mutations [1]. A correction for mutations that confer a proliferative advantage reduced this number to 4–5 mutations per cancer cell [2]. Mutational analysis has largely validated this hypothesis for a variety of cancers, revealing an average of 4–5 cancer driver mutations – including mutations that confer a proliferative advantage – for nearly 2700 cancers of 38 types [3]. Analyses of cancer latency in cases likely initiated by exposure to chemicals such as asbestos (mesothelioma) or arsenic (bladder cancer) suggest such cancers develop over the course of decades, with a median time to onset of 40+ years [4–7]. Analyses of lesions of increasing Abbreviations: DEN, diethylnitrosamine; 4-NQO, 4-Nitroquinoline 1-oxide; CRC, colorectal cancer; WNT, Wingless-related integration site; APC, Adenomatous Polyposis Coli; RAS, Rat Sarcoma; PI3K, Phosphatidylinositol 3 Kinase; DNA, Deoxyribonucleic Acid; FAP, Familial Adenomatous Polyposis; HPV, Human Papilloma Virus; E5, Early gene 5; E6, Early gene 6; E7, Early gene 7; PTEN, Phosphatase and Tensin homolog; CRE, Causes Recombination; MMTV, Mouse Mammary Tumor Virus; PyMT, Polyoma Middle T antigen; ERBB2, Erythroblastic leukemia viral gene homolog 2; PTPRH, Protein Tyrosine Phosphatase Receptor Type H; RB, Retinoblastoma; MYCN, Myelocytomatosis Viral Oncogene Neuroblastoma-Derived homolog; MDM2, Mouse Double Minute 2, human homolog of; CDKN1B, Cyclin Dependent Kinase Inhibitor 1B; LIN28B, Lineage abnorm

FAQs

What distinguishes rapid-onset cancer from slow-onset cancer?

Rapid-onset cancers can develop in months in humans and within very short timeframes in mice, whereas slow-onset cancers progress over decades. The review contrasts rapid emergence with slow, multi-step accumulation.

Which conditions may accelerate cancer development toward a rapid onset?

The article links rapid-onset cancers to early developmental contexts, immune deficiency, and viral infection. These conditions can shorten the timeline to malignancy.

How does the paper explain the mechanism behind slow-onset cancer?

Slow-onset cancer is described as a multistep process involving stepwise accumulation of mutations over long latency periods. Evidence is discussed using mutation counts and latency analyses.

Sep 23, 2026

Uploaded by Logic