Are all the different cancers really that different or is it all just cancer and we just specify where it formed?
In: Biology
I want to thank everyone for all these good overviews and explanations! Cancer is such a broad topic and will always be an important one to research. In the past months I have learned more than I ever wanted to, but it’s good.
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The problem with cancer is that it is your own body that makes it.
Its like a softwhere bug where a programmer has missplaced a decimal point. So instead of creating 10.000 Cells of X type at Y location, the body has been instructed to create 1000.000 Cells. So you get a huge lumps of the same cells where there shouldnt be. Taking up space and nutriment(cell food) that shoud be used on other stuff.
When cancer spreads its becouse small chunks of the cancerius cells breaks off and is transfered to other places of the body repeating the process and clogging up the “machinery”.
And since its all “your cells” the immune system dosnt see it as a treath and dosnt employ its defences.
Thats also why its so difficult to treat, becouse its different from person to person, there are no 2 alike. So the doctors/medicin have to target vary specific stuff vary precisely.
Your cells have many ways to trigger the same reactions within them. Even the same types of cancers may have different parts of a same reaction pathway damaged. There are also mutations in cancer that, although they won’t affect the diseases behavior, might make the cancer resist different types of treatments. The smallest difference in a cell’s mutation could be what determines whether a patient can survive/go into remission or only delay the disease.
Think of it this way, if you wanted to make scrambled eggs, there are so many ways you could scramble the eggs. You could use a fork, an egg beater, knives, or a blender, and the end product would be the same. If someone wanted to stop you from making scrambled eggs, they would need to know what specific way you use to make them, and also know if you have any alternate way of making them. If they went in blind and took your forks without knowing you use an egg beater, then they’d change nothing. Cancer is the same way. You can reach the same issues in a cel through so many different ways. Then, you have to partly hope that the treatment you use damages the specific mechanism that mutated or that it hurts a part of the cell’s DNA that the cancer isn’t already ignoring.
The reason we name cancers based on where they start is because during the time in history when people were naming cancers, that’s the most obvious difference they could see in the autopsy.
Normal cells have to make new normal cells, but only when it’s needed. We need to make new blood and skin cells to replace old ones…but it’s a delicate balance, we can’t make too much or to few. Same with lung tissue. The cells get old or damaged and need to be replaced
Normal cells interpret a lot of different chemical signals to know when it’s time to make new cells. Some signals are like traffic signals, and say when to speed up production and when to stop making new cells. If the DNA in a cell gets damaged, the cell might have problems “interpreting the traffic signals”
If DNA is damaged and the cell thinks a red light is always on, or a green light never turns on…no one cares, the cell just dies.
Cancer is when a cell becomes broken in a way where it mis-reads the signals, and shit gets wild. Maybe a green light is broken and never turns OFF, or a red light it broken and the cell can’t stop. The cell makes a new cell when it wasn’t supposed to. This “baby” cell has the same defect, and continues misreading the signals… and so on. That’s when cancer happens.
The old names like “lung cancer” stick because it’s still easiest to “see” where it is, and it doesn’t make much difference to the patients which gene is broken. Doctors and researchers today may characterize a cancer by which specific gene is broken, because some drugs work better at killing specific cancers.
So there are two basic types of cellular pathways that affect cancerous cells. You can basically lump these into pro-cancerous and anti-cancerous.
The “pro-cancerous” pathways aren’t actually promoting cancer in the body, but they are systems when they function incorrectly cause cancerous conditions to occur. As an example, there is a chemical pathway that tells cells that they need to reproduce and make more cells. This pathway can go haywire and always be triggered and the cell will reproduce at a much higher rate than usual.
Then we have anti-cancerous pathways. These are pathways that are supposed to stop cancerous conditions from happening. My favorite one of these is basically a suicide pathway. If your cell determines that something is wrong with it’s function it is programmed to basically explode (lyse) and kill itself. If fact it’s estimated that many people get “cancer” multiple times in their life, but the your cells identify and suicides before it is able to become full fledged cancer and damage the body. Another one is called contact inhibition. Basically of a cell is pressed up against something it knows not to keep making more because it won’t fit, but in cells with this function impaired there is no check on it’s normal growth cycle and can promote cancer.
For cancer to occur it’s estimated that you need between 4-8 of these genetic pathways to become mutated and both types. My info is a bit old but as of a few years ago they have identified around 15 pro-cancerous genetic pathways and 11 anti-cancerous pathways. If you think about it a cancer can be any permutation of those mutations so a cancer in the same tissue between two different people can be completely different and that just going by what we understand now, without full and complete understanding of cellular mechanics.
Cancers really are that different, though they are similar in ways that are unrelated to the current naming system. The way we name them is leftover from a time when we truly had no understanding of what caused them, so we classified them by location and tissue type affected.
If we were to scrap the old system and start over, we would probably classify them differently. And I think we should because it would allow it to be taught at a lower educational level. If we could the push cancer biology down to, say, upper level undergraduate coursework, we could make a lot more progress.
I am not conversant enough in cancer biology to do it myself. But I think it would still identify the starting tissue, then maybe the cell cycle phase/biological pathway(s) involved, and whether it results in gain or loss of function, and then you’d still need to include the extent of spread.
In the simplest form, cancer is the uncontrolled replication of cells.
I’m most* cases the cellular system for self destruction is broken (apoptosis). This leads to the unchecked propagation of mutated cells that are ultimately harmful to the host.
Everyone reading this post has had a cancer cell develop as part of typical cell division through mitosis – but that cell of ours just had the ability to monitor, self diagnose, and self terminate due to that error.
The different types of cancer typically speak to what kind of cell is effected, and why the cell is a) replicating too much and b) why it isn’t self destructing in response to that mutation
Different mutations cause different cancers. Cancer is as broad a term as *virus*.
Imagine you had a recipe for a really good soup, and so you share it by copying it by hand and giving a copy to someone else.
You then inadvertently make a mistake in your copy.
If the mistake is a simple typo, like you misspelled celrey, the next person will usually catch that and change it back to celery. However, if a mistake isn’t caught, your friend will continue to make the soup as you described.
Maybe instead of a pinch of salt, you carelessly wrote down a cup of salt. Or instead of adding celery, you accidentally wrote cilantro. Either way, the soup ends up tasting like crap (cilantro tastes like soap, change my mind), but the solution to fixing the soup is completely different.
Let’s use lung cancer as an example.
The most rudimentary understanding is a location based diagnosis. “You have lung cancer.” That’s to say, you have a cancer that originated in the lung.
The next level of understanding is knowing the histology. That is how this cancer appears under the microscope. This is based on the appearance or the staining of those specific cells. Most common specific types in the lung include adenocarcinoma (a tumor arising from glandular tissue), a squamous cell carcinoma (tumor arising from epithelial tissue), or neuroendocrine tumors like a small cell carcinoma. We have historically broken up lung tumors into “Small Cell” [SCLC] and “Non-Small Cell” cancers [NSCLC] (adenocarcinomas, squamous cell carcinomas, and large cell carcinomas) because the treatment recommendation and prognosis differs significantly for a SCLC and a NSCLC. To dive even deeper, these are just the most common typical lung cancers. You can also have a lymphoma that arises from lymphoid tissue in the lung, a sarcoma that arises from muscle or connective tissue in the lung, an adenoid cystic carcinoma that arises from glandular tissue in the lung, and the treatment paradigms for these more rare tumors usually follows the paradigm of tumors of the same histology rather than tumors of the same location (i.e. I would treat a sarcoma of the lung like a sarcoma of the leg and NOT like a NSCLC).
So as you can see, even with this fairly rudimentary understanding of things, the type of cancer makes a difference even if it is arising from the same location. Now, to take a deeper dive into this, there has been an explosion of knowledge regarding the biologic makeup of these cancers over the last decade. For example, many lung cancers (and other cancer cells as well) have receptors [PD-1 or PD-L1 receptors] on their surface that allow them to avoid detection, and thus killing, by our immune system. We now give many of these patients “immunotherapy” which is basically a medication that blocks these receptors and allows our body’s own immune cells to detect these cancer cells and kill them. These treatments are more “targeted” to specific cells and thus have fewer side effects than conventional chemotherapies which use more of a shotgun approach. While this is not a curative treatment in and of itself, it has extended the life expectancy of patients with less toxicity than conventional chemotherapy. Similarly there are other “targeted” therapies for patients with lung cancers and other specific mutations that we are using more and more and in some cases seeing a significant improvement in life expectancy.
So this may not have been an ELI5, but you can see how knowledge of the specific cancer matters more and more because it significantly influences our treatment decisions.
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