A simple algebraic cancer equation: calculating how cancers may arise with normal mutation rates | BMC Cancer | Full Text
Background The purpose of this article is to present a relatively easy to understand cancer model where transformation occurs when the first cell, among many at risk within a colon, accumulates a set of driver mutations. The analysis of this model yields a simple algebraic equation, which takes as inputs the number of stem cells, mutation and division rates, and the number of driver mutations, and makes predictions about cancer epidemiology. Methods The equation [p = 1 - (1 - (1 - (1 - u) d ) k ) Nm ] calculates the probability of cancer (p) and contains five parameters: the number of divisions (d), the number of stem cells (N × m), the number of critical rate-limiting pathway driver mutations (k), and the mutation rate (u). In this model progression to cancer
Abstract Background The purpose of this article is to present a relatively easy to understand cancer model where transformation occurs when the first cell, among many at risk within a colon, accumulates a set of driver mutations. The analysis of this model yields a simple algebraic equation, which takes as inputs the number of stem cells, mutation and division rates, and the number of driver mutations, and makes predictions about cancer epidemiology. Methods The equation [p = 1 - (1 - (1 - (1 - u)d)k)Nm] calculates the probability of cancer (p) and contains five parameters: the number of…
saved by
related reading
- Cancer risk across mammalsnature.com
- The Lower Bound to the Evolution of Mutation Rates - PMCncbi.nlm.nih.gov
- Somatic mutation landscapes at single-molecule resolutionnature.com
- A systematic CRISPR screen defines mutational mechanisms underpinning signatures caused by replication errors and endogenous DNA damagenature.com
- ��|�z���������g��Ʋέp����www3.ha.org.hk
- Epigenetic regulation during cancer transitions across 11 tumour typesnature.com
- What Mormon Family Trees Tell Us About Cancer - The Atlantictheatlantic.com
- Similar but different: distinct roles for KRAS and BRAF oncogenes in colorectal cancer development and therapy resistance - PMCncbi.nlm.nih.gov
- Pancreatic Cancer - PMCncbi.nlm.nih.gov
- Going Founder Mode On Cancer - by Elliot Hershbergcenturyofbio.com
- Why are early-onset colorectal cancer rates spiking?communitymorgue.com
- Somatic evolution: We contain multitudes - Ruxandra Tesloianuruxandratesloianu.com