Is metastatic cancer different from primary cancer?

[sameeralord]

Hello everyone,

Lets say there is a guy with colorectal carinoma and he developed metastasis in liver.

1. My question is now this guy has a liver cancer as well. Does this liver cancer contain dysplastic cells from colon or does it contain dysplastic hepatocytes. In simple words what I'm asking is in metastatic liver cancer is it the liver cells that are growing out of control or is it in this case cells from the colon has got implanted in liver and this colon cells are growing out of control in the liver.

2. If it is colon cells, does that mean metastatic cancer of liver would not affect the function of liver that much because liver cells are still normal. As opposed to a primary liver cancer where liver cells itself grow out of control and function is bound to be affected.

Thanks a lot

 

[atyy]

http://www.cancerquest.org/metastases-form-new-tumors.html suggests http://www.sciencedirect.com/science/article/pii/S0092867406014140. The last sections have some descriptions of what happens when different organs are colonized by metastatic cells.

 

[Andy Resnick]

Hello everyone,

Lets say there is a guy with colorectal carinoma and he developed metastasis in liver.

1. My question is now this guy has a liver cancer as well. Does this liver cancer contain dysplastic cells from colon or does it contain dysplastic hepatocytes. In simple words what I'm asking is in metastatic liver cancer is it the liver cells that are growing out of control or is it in this case cells from the colon has got implanted in liver and this colon cells are growing out of control in the liver.

2. If it is colon cells, does that mean metastatic cancer of liver would not affect the function of liver that much because liver cells are still normal. As opposed to a primary liver cancer where liver cells itself grow out of control and function is bound to be affected.

Thanks a lot

Cells comprising secondary tumors are similar to the primary tissue, not the secondary tissue. Either way, tumors can alter host organ function by depriving the host organ with sufficient blood (oxygen) supply, among other things.

The real question about secondary tumors is why they are so host tissue-specific: for example, kidney cancer preferentially metastasizes into bone. The pithy way docs ask the question is "soil or seed?"

 

[mathwonk]

as far as the host subject is concerned, it seems it also means he/she has less chance of eradicating it, if it has metastasized. I realize your question was more scientific in nature, but as an old guy with lots of friends experiencing these, it affects survival.

 

[sameeralord]

Thanks for everyone for clearing this up

@Andy: "The real question about secondary tumors is why they are so host tissue-specific: for example, kidney cancer preferentially metastasizes into bone."

Isn't this because anatomical routes. Eg in prostate cancer, via the prostatic venous plexus, easily spread to vertebral venous plexus and then metastasizes in vertebrae. Or are there other reasons?

 

[Andy Resnick]

Thanks for everyone for clearing this up

@Andy: "The real question about secondary tumors is why they are so host tissue-specific: for example, kidney cancer preferentially metastasizes into bone."

Isn't this because anatomical routes. Eg in prostate cancer, via the prostatic venous plexus, easily spread to vertebral venous plexus and then metastasizes in vertebrae. Or are there other reasons?

It's unclear- AFAIK, tumors primarily metastasize by shedding cells that enter and exit the bloodstream and circulate everywhere.

 

[mathwonk]

I know cases where cancers have metastasized to the expected preferred locations and others, presumably detected later, where cancers have gone "everywhere". An interesting phenomenon to me are a few cases where the spread and growth of cancer cells was limited by sticking closely to a particular diet. The reduction was quite measurable while the diet was adhered to strictly. This diet was neither recommended nor endorsed by a doctor, but although difficult to maintain, worked to some extent, at least temporarily.

This is a very interesting and challenging scientific problem, since significantly metastasized cancer can be fatal in a short time, and pose to patients the choice of an unpleasant period of chemotherapy, hoping to buy more good time, or of just passing the final months without treatment but only palliative care. Unfortunately the original cancer can be hard to detect early enough to prevent this scenario. I also know of some very lucky cases where isolated tumors that would have developed into serious situations, were detected early by accident, while looking for a different problem.

One scientific question that puzzles me is how a parasite like this which kills its host, can be evolutionarily viable for so long, and even seems to be increasingly flourishing. Maybe the whole human race is considered to be the host, and that race is not disappearing? But that is puzzling too since the disease is not contagious.

 

[Choppy]

One scientific question that puzzles me is how a parasite like this which kills its host, can be evolutionarily viable for so long, and even seems to be increasingly flourishing. Maybe the whole human race is considered to be the host, and that race is not disappearing? But that is puzzling too since the disease is not contagious.

Cancer is not a parasitic disease.

The current way of thinking is that cancer is a natural part of life. It occurs as a result of genetic damage. Damage events happens all the time, in every cell of your body, every day. The result from the normal metaboloic processes that release reactive oxygen species, from environmental carcinogens, and even from background radiation. Normally the damage is either efficiently repaired, or it is recognized as unrepairable and the cell commits a form of cellular suicide (apoptosis).

Interestingly it's that damage that leads to changes in the gene sequence, or mutations. And from a certain point of view, those mutations are what drive the random walk of evolution.

Unfortunately you get situations where those mutations directly interfere with the cell's ability to recognize damage, to commit suicide, or at least to maintain its quiescent, differentiated state where it performes whatever function it's meant to perform, and instead it begins to move through its cell cycle unchecked. This is cancer.

A single cell will then continue to replicate, often unnoticed, because it's small at first and a few abberant cells won't interfer with much. But typically after about 30 doublings or so, you get to 10⁹ cells - an approximate mass of 1 g. It's somewhere around this stage with most cancers that you transition into a clinical presentation. Physically the patient notices an odd "lump" or enough resources are taken away from the regular cells that the afflicted organ or tissue doesn't do what it's supposed to anymore.

 

[mathwonk]

Thanks Choppy, I had some similar thoughts on further reflection myself. In regard to the original question, it seems this distinction between cancer of the host organ versus cancer of a distant organ that has traveled there, is important for treatment, since at least in some cases one needs to treat the original cancer type, even in the new location. So again this distinction can affect survivial rates, since a bad cancer that has metastasized can be more threatening than a less scary local one. One also needs different analyses to determine these things since a CT scan can detect cancer but one may need a biopsy to identity it. So cost of different types of care comes into play as well as accessibility of various sites in the body.