kumar

Hello,

Cancer is caused by some mutations in genes of cells and those cells
can be thought have become something different than normal healthy
cells. I have few questions:-

1. Does our immune system recognize those cells with mutations as
"something different" than normal cells?

2. Does our immune system start working on those cancer cells
immediately on their getting mutations or not?

3. If not, how tumor is developed? Is it(tumor development) immune
system's oriented or cancer cells's oriented?

4. Does some non-infection type inflamatory immune responses starts
during initial or later stages on getting cancer?

5. Do cancer patients esp. before or after spread, commonly develop
some iron or B12/Folic acid or anemic imbalances? Can imbalances in pH
of different body's parts cause cancer's mutations?

6. Can you tell me relations of our innate or aquired immunity with
cancer? I mean about role of our immunity for handling cancer?

Let us understand it in three stages. 1) On getting mutations 2) Within
Tumor stage 3) On spread.
Best wishes.

steph

Sure, that's the immune system's main job. It only fights infections in its spare time


If they express the antigens necessary to stimulate the imune cells. Cancers
don't always do that.


Some cancer cells escape immune surveillance - there's your cancer


Sometimes early, sometimes late, sometimes never

Anaemia mimicing iron deficiency is common in advanced cancer, but note I saidd mimicing.


Er.......?

kumar

Thanks but cancer is not an infection.

Are all cancer cells are encapsuled in tumor? If yes, how these are encapsuled in cancer?


Yes, but how these are encapsuled in tumor?


Can you differenciate between infection and non-infection based inflamatory response?


Can you explain it in some detail esp. iron defficient and otherwise?

steph

Really? Whaddya know? I didn't say it was, but your comprehension skils seem a little rusty

You need to read some basic biology. If you had a grasp of some basic
concepts, this discussion wouldn't be like trying to open a tin of beans with a banana...


See what I said above. Don't use words you don't understand.

Why would I want to?

I could, but no. If you'd like to enroll in a medical school for 5 or 6
years, I'm sure you'd get the idea.


Assuming you're an axe-grinding troll, I'll leave it at that

kumar

Sorry, I think I made you bit angry. We may not find awnser of my
questions in biology books, therefore trying to know from senier people in this field. Thanks.

mike mcwilliams

Kumar actually asks good questions despite his seeming inability to
understand the answers. He/She is also quite persistent, having been
posting various questions regarding autoimmunity for a little over a month.

The way I see it, answering the questions can't hurt, but trying to
provide an education in biology over usenet isn't a great idea either.

cheers.

kumar

Hello,

Cancer is caused by some mutations in genes of cells and those cells
can be thought have become something different than normal healthy
cells. I have few questions:-

1. Does our immune system recognize those cells with mutations as
"something different" than normal cells?

2. Does our immune system start working on those cancer cells
immediately on their getting mutations or not?

3. If not, how tumor is developed? Is it(tumor development) immune
system's oriented or cancer cells's oriented?

4. Does some non-infection type inflamatory immune responses starts
during initial or later stages on getting cancer?

5. Do cancer patients esp. before or after spread, commonly develop
some iron or B12/Folic acid or anemic imbalances? Can imbalances in pH
of different body's parts cause cancer's mutations?

6. Can you tell me relations of our innate or aquired immunity with
cancer? I mean about role of our immunity for handling cancer?

Let us understand it in three stages. 1) On getting mutations 2) Within
Tumor stage 3) On spread.
Best wishes.

steph

That's why I suggested medical school..........

steph

Sure, that's the immune system's main job. It only fights infections in its spare time


If they express the antigens necessary to stimulate the imune cells. Cancers
don't always do that.


Some cancer cells escape immune surveillance - there's your cancer


Sometimes early, sometimes late, sometimes never

Anaemia mimicing iron deficiency is common in advanced cancer, but note I saidd mimicing.


Er.......?

bryan heit

There is no doubt that our immune system can identify cancerous cells.
In mouse models you can get complete remission of some tumors with
nothing more then a vaccination. This has yet to work in humans, but
there has been some clinical trials where definite anti-tumor immunity
has been observed.

The problem is that tumors rapidly evolve mechanisms to avoid the immune
system. Generally this is done by producing chemicals such as IL-4,
IL-10 and TGF-beta. This has the effect of turning off the cells which
would normally kill the tumor cells.

No one really knows. The problem is that a lot of cancers are
associated (initially) with an infection, so you're never really sure if
an early response is against the cancer or the infectious agent.

But the answer is probably "no". If you make a mouse which lacks the
cells which mediate anti-cancer responses (T, B and NK cells, called a
beige-SCID mouse) you don't see increased rates of cancer compared to
controls. This suggests that these cells are not preventing cancers
from forming. But you do tend to see faster progression of the tumor,
suggesting that once a tumor is formed, these cells may act to slow it down.

One idea of how this works is the "danger hypothesis". Simply put, the
immune system doesn't respond until it perceives a danger; in the case
of a tumor this would occur when the tumor became large enough to damage the surrounding tissue.

Tumors develop through a fairly well characterized series of mutations.
The immune system doesn't have a whole lot to do with making these
mutations, although most tumors regulate the immune system to their
advantage. Generally speaking all tumors start off as a normal cell (or
perhaps as stem cells). The first stage involves a mutation in a single
gene which regulates cell division or DNA repair. This results in a
faster-then-normal dividing cell. You don't have a tumor yet; rather
you have a small ball of cells which are a little off. It is believed
that in 60% or more of tumors this initial mutational event is driven by
the presence of a pathogen.

The next stage in tumor development involves a few more mutations. Most
of these allow for even faster cell division, but you also begin to see
mutations (or at least changes in gene expression) which allow the
proto-tumor to grow larger then a few mm in diameter. This includes
genes which promote the growth of new blood vessels and the suppression
of the immune system. At this point you get what doctors call a
"pre-cancerous mass". Basically, it's almost a tumor, but it's small
enough to not cause damage to the surrounding tissue and it is not
growing too rapidly or metastiszing.

A few mutations alter and you get a non-invasive tumor. This basically
means you have a rapidly growing mass of cells. These cells are
developing their own blood network, and are actively suppressing local
immune responses. Often this mass will grow so quickly that it out
paces the formation of new blood vessels, resulting in a core of dead
tissue. The rapid growth of this tumor will damage surrounding tissue.

The final stage involves a few more mutations, resulting in a metastatic
cancer. This final stage is not nescisarily characterized by faster
cell division, but rather by a loss of cell-cell contact. The cancer
cells become motile, and begins to spread through the body
(metatstisis). By this stage most cancers are essentially incurable.
Unfortunately for the patient, this is often the stage at which cancer
is detected. This is why self-examinations and regular checkups are so
highly recommended. The earlier you detect cancer the easier it is to
treat, and the more likely it is treatment will work.

No one really knows. We do know that this inflammation is essential for
the growth of the tumor, but different tumors become inflamed at
different points; some right from the beginnings, others during the
conversion from a pre-cancerous mass to a true tumor. Diffuse tumors
(i.e. leukemia) do not get inflamed until quite late in disease progression.

Not that I'm aware of. In general, if you lead a healthy lifestyle your
cancer risk decreases. Proper diet, exercise, etc, goes a long ways.
But how exactly this works is not well understood. pH doesn't really
effect mutation rates (I wrote about that in another message).


Innate immunity tends to help cancer. One of the most important parts
of tumor development is the formation of new blood vessels. Without
this the tumor can only grow to be a couple of mm in size. Innate
immunity, notably neutrophils, will infiltrate tumors and cause new
blood vessels to form. This occurs through a process where the
neutrophil forms a channel as it crawls through a tumor. As it crawls
it releases chemicals like IL-8 and VEGF. these chemicals will stick to
the channel, and promote the growth and recruitment of the cells which
for the walls of a blood vessel. There are a lot of interesting EM
images where you can literally see a blood vessel crawling along behind
a neutrophil within a tissue. Pretty cool stuff.

This infiltration has to be carefully balanced by the tumor - too much
and the inflammation will kill the tumor; too little and the tumor wont
get enough blood. Clinical trials using TNF (a pro-innate chemical) and
anti-TNF (which would reduce TNF levels in a tumor) found that both
treatments reduced tumor growth; largely through driving the number of
neutrophils off of the optimum.

Adaptive immunity tends to be anti-tumor. During cancer you will find B
and T cells specific to tumor antigens, and against pathogen antigens
associated with the tumor. However, tumors produce a large number of
immune regulators which tend to dampen these cells. As such you tend to
see a lot of these anti-tumor cells floating around, but they aren't
very active so they have little effect on the tumor.

Interestingly, in most tumors it is the innate immune system, not the
tumor itself, which dampens the adaptive immune responses. For reasons
that aren't well understood, macrophage inside of tumors turn into what
is called a "type II" macrophage. These cells produce the chemicals
which dampen the adaptive immune system, and produce the chemicals which
recruit neutrophils. Why this happens is not entirely clear, and
probably depends on the tumor. We do know that tumors produce some of
the same chemicals as the macrophage, so it may be that the tumor
initiates the type-II response, and the macrophage cause it to perpetuate.

A lot of research has gone into activating these tumor-specific adaptive
cells. To date we haven't been very successful, but work in mice has
demonstrated that it is possible, and if we overcome the tumors
dampening effects, these cells can completely destroy the tumor.

Bryan