From /u/ Peoplma on reddit
"I thought I would clear up some misconceptions about the new "Nature publication" claiming ecigs are as harmful as cigarettes (which they call tcigs, for tobacco cigarettes, in an apparently deliberate attempt to blur the line between the two, but we may have done that to ourselves by calling it "ecig" in the first place).
First of all, it is not a Nature paper, it is an abstract in a journal called Clinical Cancer Research. A person who reports for Nature's scientific news team attended a scientific meeting called the Joint Conference on Molecular Origins of Lung Cancer. The "paper" causing all the hype, is not a paper, it is an abstract of a talk or poster that one of the scientists presented there, and the proceedings from it were put on Clinical Cancer Research's website. The work has not been peer reviewed or published yet, apart from in the proceedings from that conference (which is not peer reviewed).
Second, from the abstract of their work recorded in the proceedings, they used a cell model with an artificially knocked out tumor suppressor gene (p53) and an artificially activated tumor promoting gene (KRAS).
Third, the study found that high concentrations of nicotine in both smoke and vapor made cells grow faster than low or 0 concentrations of nicotine. This is a well known result, nicotine induces cell proliferation of some cell types, but it is not recognized by the CDC as a carcinogen.
Thanks for reading"
From /u/ SpOoKy_EdGaR on reddit
"Very good observation. I am interested in going into cancer research (currently a pre-health post-bac student at an ivy university, worked in blood cancer before this - only saying this so you know I take this very seriously) and thus paid especially close attention to the cancer lecture.
What we learned is that p53, the tumor suppressor gene, is mutated in over 50% of cancers (Hollstein et al, 1991, Science - taken from my lecture slide). The p53 gene is at a crucial intersection of cell replication, where cells that are growing too large, have damaged DNA, or other forms of cell damage/mutation, are basically told by p53 stop, you're ....ed up, you're too big/damaged and then p53 directs them to either destroy themselves (apoptosis) or repair themselves, if it is deemed possible by p53. Similarly, oncogenes (KRAS is one) promote cell growth, and when oncogenes are mutated to be over-active, well, obviously… cells grow at an insane rate.
Putting these basics together: with upregulated oncogene activity (KRAS), your cells are going to grow larger and take up more resources than they should (typical of tumor cells). Now that you have these cells, AND now that you lack p53 function (the guy who basically decides who is healthy/needs repair/suicides due to excessive damage) the body has no method of preventing cells from replicating via mitosis (cell proliferation) even if they are abnormally large / damaged.
The whole point of learning about this was that it is rare for p53 / oncogene mutation to occur from the radiation/carcinogens we are exposed to in everyday life. Things like smoking, excessive UV radiation, exposure to radioactive materials are what cause the excessive radiation to a point where you are more likely to have mutations in p53 and oncogenes. Basically, among the tens of thousands of genes, mutating p53 and oncogenes are only a few targets out of many. The chances are low - but when you do things that expose you to high carcinogen concentrations (SMOKING), you are basically constantly damaging your cellular DNA, and you have a much higher likelihood to mutate p53/oncogenes since you're barraging your cells with carcinogens so often.
Back to the study (it is a study, the abstract is a summary of the study that will undergo peer review for publication)…. I don't really scientifically understand why, given such contrived condition that promote cancer outright, the researchers stick "tcigs" or "ecigs" into the equation. The "tcigs" are normally what bring about the conditions of mutated p53/oncogene activity due to their carcinogenic content (smoking cigarettes = constant damage to DNA). The way these researchers did this, it seems like they could have stuck in grape juice and said the same thing - "gJuice correlated with genetic expression similar in tcigs". The whole point is that they've basically contrived a genetic environment for each cell to guarantee to become "cancerous", i.e. proliferation while damaged DNA/excessively large.
The one conclusion that seems "useful" is that nicotine causes similar genetic expression in cells that have already mutated their cancer-regulating genes. Since that's the common denominator between "tcigs" and "ecigs", all they're really saying is "look, nicotine has a certain effect when you guarantee conditions of cancer". I guess there is some benefit to this somewhere - but for practical purposes, it really doesn't do much in the name of trying to argue against ecigs as "equally as harmful as cigarettes". That is not at all what this study tested. Kudos for noticing that right when you read it, OP."
, we all have the potential for cancer. We are all born with cancer causing cells. It's all about what will trigger them. I can remember thinking, "wow, that's crazy!" Sometime it's as simple as stress that can cause these cells to start firing, regenerating in place of healthy cells.
