In one person, of one epithelium, which is all exposed to that carcinogen equally, in the same duration, frequency and intensity?
Hello Michaela.
That is a 600 million dollars' question. There may be no such a study to demonstrate extensive frequency in all type of cells present in the body (~250 cell types are present), as you asked why. It is called 'susceptibility', ill-defined. Different susceptibilities may come from different cellular activities of each unique cell that would have different metabolic activities, molecular machinery and biochemical responses due to the different contents of cell organelles in each cell phenotype. Sorry not to provide a full explanation for why.
Regards.
Hello Michaela.
That is a 600 million dollars' question. There may be no such a study to demonstrate extensive frequency in all type of cells present in the body (~250 cell types are present), as you asked why. It is called 'susceptibility', ill-defined. Different susceptibilities may come from different cellular activities of each unique cell that would have different metabolic activities, molecular machinery and biochemical responses due to the different contents of cell organelles in each cell phenotype. Sorry not to provide a full explanation for why.
Regards.
Good question! As answered above, it's really hard to explain why. The phenomenon you mentioned is called cell context-dependent. Different tissues or cells are specific to a certain kind of carcinogen. For example, H. pylori infection is always associated with gastric carcinoma, and F. nucleatum infection promotes colorectal cancer, highlighting the complexity of carcinogen on tissue-specific carcinogenesis. That's why different cancers need distinct chemotherapies and strategies.
There is many variables that can influence the outcome of an exposure to carcinogen and they operate on different hierarchical level, such as toxicokinetics level (absorption, distribution, metabolism and elimination of carcinogens), toxicogenomics level (gene expression and/or sequence variations in tumor-suppressor genes, DNA repair genes, genes involved in the detoxification of DNA-interacting species, transporters, metabolic activators of proximate carcinogens...). The question is rather general and so is this answer.
Carcinogenesis process can depend on the number of mitochondria in the cells (and also, among others, functions/metabolism of the cells).
As a result, observed by us effect of carcinogen acting can depend on the number of mitochondria in the cells (and also, among others, functions/metabolism of the cells).
For this reason, this can sometimes be an illusion that "a carcinogen causes/contributes to mutation in one certain cell or certain group of cells and not in another cell/group of cells".
This is the reason why Cancer research is evergreen.!!!
In my point of view,
Carcinogen cannot target the same site in different tissue types to cause identical mutations. It's just a chance factor.!
The cell could initiate variuos pathways in response to that carcinogen. for example, it could be p53 dependent or independent!!!
Even if we subject two different cells for the same site specific mutegenesis, still they give two different outcome. Because they might differ with respect to the number of active genes in that cell.!!
hope my answer is convincing.
--best regards
In my opinion a carcinogen causes DNA mutations, which can lead to cancer initiation (transformation), in similar way in all cells. But at once after cancer transformation, mutations caused by cancer development depend on cell types. If so, then by observing the final result, we can draw the wrong conclusions.
- Badges
- Science topic
- Similar topics
- Medicine
- Oncology
- Cancer Research
- Cancer Biology