We all know that certain products increase one’s probability of getting particular types of cancers. For example - cigarettes::lung cancer, red meat::colon cancer, and chewing tobacco::oral cancer. I guess this question can apply to all of the various relationships, but let’s use the simple one of chewing tobacco::mouth cancer.
An assumption: the higher the amount of tobacco that one chews as well as the longer time period that one chews it will increase the probability of contracting mouth cancer. I’m by no means a medical professional, but this seems obvious. For simplificaton purposes, let’s just say that all tobacco comes in “units” of consistent strength and each unit is consumed by all users 10 times a day, everyday.
Assumption 2: Allen will take 5 years to contract oral cancer based on the usage level that has been stated. This length of usage until getting cancer varies from person to person, and is currently unknowable in advance. But let’s say that Allen quits after 3 years. He quits for an amount of time reasonable enough for his entire mouth to be cleansed of all of the cancer-causing agents, let’s say 1 month.
After this month is finished, he foolishly decides to start chewing tobacco again.
After the long-winded intro, here’s the question:
Will Allen now contract cancer in exactly 2 years, exactly 5 years, or some time in between? In other words, does Allen’s body have a “memory” that will remember the past use?
This question comes to me from my Health class when I was a high school sophomore (18 years ago). The teacher who was probably 55 years old or so proudly proclaimed that she smoked a pack a day for 25 years and then quit for the last 10. She said that her body had fully recovered and that her lungs were like brand new. She clearly had no way of knowing this, but one of the class comedians (with the initials JJ) told her that she might as well start back up again since she knows she’s in the clear for the next 25 years.
First, consider what cancer is. It is an unregulated dividing of cells; either growing cells lose the ability to stop dividing or non-dividing cells gain the ability to start dividing again. This is due to DNA mutation, caused by carcinogens or other factors like DNA repair or replication errors. Carcinogens, which we are worried about, mostly act at random throughout the genome. There are a lot of genes that control the cell growth cycle, and there are a number of mutations which can cause cancer. So you have to get unlucky. You start with a set of mutations, which you have inherited. These are sometimes capable of causing cancer by themselves but not usually. Then you add acquired mutations. Exposure to carcinogens only increases the number of mutations occuring in the cells, and does not guarantee that a particular cell or tissue will develop cancer, even if it is bathed in the carcinogen.
The mouth is a reasonable example. The lining of the mouth consists of several kinds of cells (all subject to cancer – including epithelium, tongue, and salivary glands and ducts), but you can think of them in two general classes: there are basal stem cells responsible for dividing and generating more apical cells (closer to the surface). The apical cells form the majority of cells in the mouth, and are shed and replaced. If a carcinogen affects a stem cell, it doesn’t matter how long you have stopped chewing tobacco, because all cells from that stem cell (and the stem cell itself) are one step along the road to cancer. If a carcinogen affects a later apical cell, then that effect is temporary, until that cell is shed.
Your health teacher had probably shed a lot of cells in her lungs that were affected by smoke. Certainly the vast majority of her bronchial lining, except for the few bronchial stem cells, had been shed. But her cancer risk would always be elevated above normal. What one sees is an increased cancer risk for smokers which increases until one quits, and then decreases, but never returns to the level of a never-smoker.
One can enter her data here into a risk calculator, which displays the total number of cancer cases by year. The slope of the curve (in cases/year) should be the risk. One can see that the risk for cancer always increases with age, as that is the number one risk factor for cancer. For someone who smoked and quit, the curve has a slope somewhere between that of a never-smoker and a smoker.
The 1 month without the chew will make no difference, whatsoever to when Alan contracts oral cancer - 1 month is not enough time to make an appreciable difference on very much.
However, lets say that he stops for 5 years, instead of 1 month - then, I dunno. I imagine factors such as his age, his overall health, his diet, etc will all play factors. My guess is that if he has truly cleansed his palate (so to speak) and gone back to a “Never Chewed” level of cancer risk, it would again be 5 years before he got CA.
I would be interested to see what other people have to say.
Allen plays Russian roulette as a hobby. He plays it regularly for several years and, luckily, survives it. He gets tired of it and quits for a while. Then he starts back up. How long until it kills him this time around?
Cancer is not a monolithic thing. There are various kinds, and they often don’t cross over. For example, if a woman has breast cancer, that same cancer will not crop up later in the colon, where a different cancer would be to blame.
Carcinogens vary widely in “how likely this will cause that.” Cigarette smoking probably tilts the odds toward lung cancer to a greater degree than red meat tilts the odds toward colon cancer.
I speak of “odds” because that’s the word used by the only oncologist I ever spent much time with. He laid out the odds of one treatment against another, as to being cancer-free 5 years later. He keeps up on the latest research, and he plays the odds in choosing the best treatment options. He also lays all the figures on the table, so the patient can make an informed decision.
As to the Original Poster’s Question, the figures you may have seen about how long it takes a substance to produce cancer are based on statistical averages. Some tobacco chewers get cancer in a year, some never get it (and die from something else.) There is no solid schedule.
Do you want to roll the dice in your mouth? How lucky do you feel? :eek:
I don’t think that’s a great example. The link between diet and colon cancer is far from resolved. To a large extent, it is diffiucult to dissect out the putative risk of certain nutrients (eg. red meat) from the putative benefits of others (eg. fruits and vegetables). That is a pedantic way of saying that, for example, people who eat lots of red meat or animal fat tend to ingest less fruits and vegetables, and vice versa.
Certainly, no causal relationship has been established between the ingestion of red meat and the development of colon cancer (AFAIK).
Here’s a study from a very reputable group. They conclude that red meat is a “marginal factor” for colon cancer. In fact, by my reading of their paper, I’d say that’s almost an overstatement.
Thanks for all of the replies. In response to edwino, based on what you’re saying, the probability that Allen develops mouth cancer of any stem cell is the same the thousandth time he uses it as it is the first time. Clearly, repeated uses will increase the chance of developing cancer, but previous uses have no bearing on future ones. So basically, the Russian Roulette metaphor is appropriate?
Not necessarily, Jackknifed Juggernaut (airbag saved my life…)
Most cancers are not one-step mutations. Some are, and your supposition is basically correct, assuming the actual chemical carcinogens are flushed out completely between chaws. A much more typical cancer, though, is one where a whole pathway of genes gets mutated, and many of the checks on unregulated division are removed (not just one). This has been well studied in colon cancer. For many sporadic cases of colon cancer, several cell-cycle checkpoint genes are mutated: first APC, which can be inherited (it stands for adenomatous polyposis of the colon), then K-ras, then the cell adhesion molecule DCC (which allows the cells the “sense” when they are done dividing by contact with other cells; loss of it permits overgrowth), then p53. Further aggressive cancers have other mutations which allow metastasis.
Mutations in APC alone cause a adenomatous polyp, which are removed during standard colonoscopy. APC + K-ras mutations cause an intermediate polyp, which still isn’t cancer. Only with loss of DCC and p53 do you get a true colon cancer. This was famously worked out for a good percentage of sporadic and inherited colon cancers, but it is not the only way to colon cancer, nor does it happen in the same way in other tissues.
I’ll just add that one does see all kinds of precancerous lesions in mouth cancer as well. But cancer does not have to be predicated by precancerous lesions, nor do mutations have to occur in any particular order. So even with no precancerous lesions in the mouth, your epithelial stem cells could very well be acquiring mutations in the wrong genes and be well on the way to cancer, with or without precancerous lesions. So each time Allen puts tobacco in his hypothetical mouth, he increases the possibility that one of the millions of epithelial stem cells in his mouth acquires one of possibily hundreds of cancer causing mutations.