However, this definition does not accurately reflect current knowledge of how most cancers develop. 
It assumes, mostly incorrectly, one exposure is the sole cause of a cancer such that we can start to clock on cancer latency at that exposure.  It also ignores the possibility the cancer being considered would have developed absent the exposure but the exposure accelerated cancer development.  Lastly, it also ignores the randomness in when a cancer is diagnosed.  For example, when there are signs and symptoms or when detected incidentally.About 20-30 percent of persons >65 years have a pre-leukaemia process termed age-related clonal haematopoiesis (ARCH) or clonal haematopoiesis of indeterminate potential 1-2 percent of these persons per year will develop leukaemia.  The question is when to start the clock to estimate cancer latency in these persons.  The antecedent mutations resulting in clonal haematopoiesis may have occurred years before these persons developed leukaemia.  However, when the final mutation(s) resulting in leukaemia development is unknown but is probably close to when the leukaemia was detected.  Should we start the clock to calculate cancer latency when the 1st mutations causing ARCH or CHIP occurred, when the final mutation(s) occurred or somewhere in between?  The decision is obviously arbitrary.  One strategy, starting with the 1st mutation, might result in a very long estimate of cancer latency and the other, a very brief estimate of cancer latency.  Choosing either model is entirely arbitrary and without a scientific basis.  Also, some persons receiving anti-cancer drugs such as DNA polymerase-II-inhibitors cancer develop a new cancer within a median of 2-3 years.  Others receiving alkylating drugs have a median interval to cancer diagnosis of 5-7 year.
There is also the mistaken notion that cancers accumulate mutations gradually and in a predictable linear order.  For example, in a study in pancreas cancer the authours tracked DNA copy number changes and DNA-rearrangements and showed cancer development is not gradual and often does not follow a linear mutation acquisition model.  A substantial proportion of cancers had complex rearrangement patterns associated with mitotic errors consistent with punctuated equilibrium as the principal evolutionary trajectory resulting the simultaneous knockout of driver mutations.  Considerable data indicate cancer development is almost always a complex, multi-step process further complicating attempts to define and/or estimate cancer latency.  Most cancers do not have a cause but rather several or even many causes.

The bottom line is defining cancer latency is not as simple as it once seemed.  It is difficult or impossible to know at which event or mutation to start to clock to measure cancer latency.  It is equally difficult to know when to stop the clock given the stochastic nature of when cancers are diagnosed.  Importantly, even in genetically-identical twins with the same driver mutation intervals to develop cancer vary substantially.  And there are other confonders we discuss above.  We clearly need a new definition of cancer latency or abandon the concept of cancer latency entirely in the modern era of cancer biology.