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Cancer doesn't kill, Cachexia does

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lilitalienboi16:
Hello Claudia, thank you for sharing your testimony. I'm glad the Lord was merciful in his dealings with you. Cancer is an awful thing.

What I have learned from my class as far as cancer statistics and radiation. These are straight out of my in class notes:

Cancer currently claims 1 million lives each year in America.
Its the #2 killer of Americans behind cardiovascular disease.
Cancer is a disease of old age. People are living longer now and so we are getting the diseases of older age.

Environmental risk factor: Radiation

Solar radiation (UV)

Creates thiamine dimers
This causes DNA to buckle which results in errors in replication
700,000 non-melanoma skin cancers a year and the number is going up
Approximately 2 million cases world way
Largely curable, mostly basal and squamous cell carcinomas
One can be exposed to various wave-lengths of UV which determines whether its UV A, B or C
A is long wave length and used in tanning salons
B is short wave length, less than 350 nm
The most serious skin cancer is melanoma
35,000 deaths a year
132,000 deaths worldwide
One of the genes rendered nonfunctional by UV exposure is the p53 gene
P53 is involved in more cancer than any other gene

Ionizing radiation

Comes in several forms

X-rays

At the turn of the last century, in the 1900’s, workers that worked with x-rays developed a disproportionate amount of leukemia's
3 to 4 times the general population
It has been estimated that one cancer will develop for about every 1-million x-rays
That's 300-400 people a year
Do a risk-benefit analysis in deciding whether to get an x-ray or not

CAT Scans have 30 times more radiation than x-rays
X-rays that are used to treat cancer are used at very high doses and as a consequence of that the chance of causing secondary tumors is much greater

Decay of radioactive compounds
We have seen this in the survivors of the bombings of Hiroshima and Nagasaki
Many of the survivors developed various kinds of cancer

There are two measure when we evaluate the carcinogenic potential of radiation

The ability of radiation to penetrate tissue

RAD (radiation equivalent mean)
This is the amount absorbed by tissue

How much damage is it going to do to the tissue that it just penetrated

REM (radiation equivalent in man)
This is basically RADs corrected for the biological effectiveness of the particular form  of radiation in doing damage

Example: alpha particles which are emitted by radioactive elements are far more damaging than x-rays

About 20 times more damaging
1 RAD of x-ray exposure is equal to 1 REM
1 RAD of alpha particle exposure is equal to 20 REM

The annual dose of UV exposure is between 0.3-0.4 REMS
80% of this comes from just being alive

The other 20% comes from medicinal sources
Last year we had between 300-400 million x-rays given

Risk factor: Viruses

There are viruses that will transform normal cells into a tumor cell
We refer to these viruses as:
Oncogenic viruses, tumor viruses or transforming viruses
Viruses are causative agents from an epidemiologic perspective of certain human cancers
On a world wide bases viruses cause 15-20% of all cancer
Everything we know about cancer we have learned from studying and understanding viruses and their role in cancer

Hepatitis B Virus (HBV)
A major risk factor for hepatocellular carcinoma
Responsible for a significant amount of world wide cancers
Virus attacks hepatocytes
This tell us that the hepatocytes have a receptor for the virus
The virus can cause acute liver damage
5-10% of individuals that are infected by this virus will not have the viral infection resolved
From the population, these are the chronic virus carries and will show greater incidence of liver cancer

Epidemiological studies have shown that about 10% of adults in the USA get infected by HBV. Of that, less than 1%will be chronic carries of the virus
In China 100% of adults have been exposed to HBV and 10-15% will be chronic carriers
This shows that the virus is associated with the cancer

Experimentally you can inject HBV into mice and see if they develop cancer
You can also inject HBV into cells in tissue culture and see if they develop cancer
You can also isolate cells from a patient operated on for hepatocellular carcinoma and see if the virus is part of it
There is a several year lag time. Populations in Asia are exposed during childhood and don't develop the cancer until their 30’s-40’s

About 23 years ago a vaccine was developed for HBV

There are other carcinogens that will exacerbate this chronic infection and that includes:
Alcohol
Contributes to cirrhosis of the liver
Aflatoxin
Potent mutagen for liver cells

Human papillomavirus (HPV)

A risk factor that can cause malignant and benign neoplasms
Cervical and other anogenital carcinomas
Cervical cancer occurs less frequently in nuns
Cervical cancer occurs more frequently in women who have had multiple sex partners
Cervical cancer occurs more frequently in women who are married to men whose first wife had cervical carcinomas

All these events suggest a venereal transmitted disease
Squamous cell skin carcinomas

In 1983 a distinct papillomavirus was isolated from a cervical carcinoma sample
HPV16 was found to be involved in 50% of all cervical cancers
HPV18 was found to be involved in another 20%
HPV33 was found to be involved in another 10%

Today we know that 90-99% of all cervical cancers are virally caused by HPV
There are other strains of HPV that will cause genital infections but they are not transforming viruses
Like HBV there is a long lag period that could be several decade

Today there is a vaccine, Gardasil, that can be used for HBV

Epstein-Barr virus (EPV)

First virus that was implicated in cancer
Associated with Burkitt’s and other B-cell lymphomas
Burkitt’s lymphoma is a lymphoma of childhood prevalent in parts of Africa
Associated with nasopharyngeal carcinoma in parts of China
Very rare to see Epstein-Barr virus to be implicated in cancer in other places

There is a geographic restriction

90% of people around the world are infected with EPV
They either have no symptoms or they have infectious mononucleosis
Individuals who have mononucleosis, the cell that is infected is the B-lymphocyte
Cell will have limited proliferation but it will not be transformed
Prevalent to the area where Burkitt’s lymphoma runs rampant in Africa is also Malaria
Parasites don't want you dead, they want to derive to nutrients from you
It depressed our immune system which may lead EPV to have a far greater affect on them then other people around the world

Human immunodeficiency virus (HIV)
Cancers caused:
Lymphomas
Kaposi’s sarcoma
Angogenital carcinomas



Risk factor: Heredity
 The vast majority of patients with cancer have no inherited their disease
They will not pass their disease on to children
However, even though cancer is not considered a inherited disease, there are incidences that increases to susceptibility of the disease that can now be passed onto the offspring
That includes some rare forms of cancer as well as genetic diseases 
That includes some rare forms of cancer as well as genetic diseases 

Figure: Examples of inherited cancers

As we’ve seen before FAP is an inherited genetic condition that leads to the formation of lots of benign tumors and a small population of individuals who have that can lead to colon cancer
Wilms’ tumor has an inherited susceptibility as well as retinoblastoma
There are also diseases of genetic instability and diseases of immunodeficiency’s and individuals with those diseases show an increase in development in certain types of cancers
What you cant see in the illustration is that the gene that was inherited, it was always a defective tumor suppressor gene
If we have these rare susceptibilities it is going to be because of defective tumor suppressor genes

Figure: Mode of inheritance
The mode of inheritance suggest that the susceptibility is determined by single genes and that they are transmitted in a genetically dominate fashion
Large C that dad has the actual cancer gene
In this case, half of the offspring’s will inherit the susceptibility gene
The gene functions in a dominate fashion
Even in the presence of another normal gene, these individuals will almost certainly develop the cancer
These inherited cancers represent a group that have a “direct-effect” on the cells that will ultimately become the neoplastic cells
This has to be contrasted with certain other disorders such as those of genetic instability or inherited immunodeficiency where the effect is going to be an indirect one
The effect is not going to be on a cell that is going to be the cancer cell but it will be on a cell  that maybe involved with preventing the onset of disease
   
An example of a “direct-effect”:
Retinoblastoma
The inherited gene is ultimately going to manifest its activity in retinal cells
These individuals will have an increased predisposition of developing that disorder

An example of a “indirect-effect”:
A consequence of not dominant genes but recessive genes
In order for the disorder ot be manifested, both parents must carry the gene
This is why its far rare

Xeroderma pigmentosum

is a condition of genetic instability.
It doesn't allow DNA to be repaired effectively
Particularly DNA that has been damaged by UV exposure
The defect is in a gene that encodes a DNA repair enzyme called UV-specific endonuclease
Rare condition-occurs in 1 out of 250 million children born

Inherited immunodeficiency known as Ataxia telangiectasia
This is an inherited immunodeficiency
Just like acquired immunodeficiency like AIDs, just like patients that are on immunosuppressive drugs, individuals with ataxia telangiectasia are much more susceptible to the development of cancer
If the immune system is not functioning properly then the chances of developing tumors particularly tumors lymphocytes and other immune cells increases
We see in patients with ataxia telangiectasia an increase in lymphomas and in some cases leukemia’s
There maybe a viral connection


Environmental risk factor: Occupation risk factors
Boys who cleaned chimney soot and developed scrotal carcinomas
Asbestos workers got cancer as well as their wife’s who washed their laundry
Got a rare form of lung cancer called mesothelioma
Occupation carcinogens account for about 5% of cancers
Our concerns are that today we are using new chemicals and we don't know the affect they will have on us until 20 years

Environmental risk factor: Hormones

Back in the 1940’s, a lot of pregnant women were given synthetic estrogen known as DES.
In the 1970’s their daughters were found to have been developing vaginal and cervical cancer after the 10-20 year lag period
This was the first evidence that estrogen can be problematic

Women still do take extra estrogen
Important effect in ameliorating the ravages of menopause
Beneficial and preventing the development of osteoporosis

Our evidence is not complete
For a period of time women were told that if they took progesterone along with estrogen it will prevent the adverse effect of estrogen
Large studies then came along and showed it not to be true
Other studies came to show that it may not be so clear
Most evidence suggest that extra estrogen is not a good thing to have because it's a promoting agent for breath and cervical epithelial cells

Environmental risk factor: Diet

There are study’s that suggest that dietary components can be responsible for anywhere up to 30% or so of the cancers we see

Figure: Dietary factors and cancer risk
The problem with this illustration is that the studies that have been done are not nearly as incontrovertible as were those that have shown tobacco smoke and radiation to be major carcinogens
A lot of the studies that have shown some of these dietary components have either been controversial or in some cases contradictory

High Fat
Increased risk of colorectal and possibly breast carcinomas

Figure: Breast cancer death rates vs dietary fat intake
As you consume more dietary fat the incidence of breast cancer goes up
The greatest consumers consists of the USA, Canada, Great Britain
The lowest consumers consists of Thailand and some Asian countries
There’s a problem with this illustration, its that there can be many other differences within a country besides just their consumption of dietary fat
Studies showed that rats on a high fat diet and high rates of mammary tumor
Its not always like this when you go out into the general population
Even studies that have not been able to show conclusively show the association between dietary fat and breast cancer have shown a correlation between dietary fat and colorectal carcinomas

There is a 2-fold increase in the risk of colorectal carcinoma in individuals that consume around 44% of their daily diet in fat as compared to those who consume under 30%
The risk for endometrial carcinoma is 2-5 times greater for women who weight more than 165 pounds as compared to women who weight less than 125 pounds
The basis for this association is on the fact that fat cells produce estrogen
Now you have multiple sources of estrogen
Estrogen drives the proliferation of endometrial epithelium cells
Increased proliferation beyond the norm will lead to endometrial carcinoma
Estrogen also drives for proliferation of breast epithelial cells.
It appears that there is a relatively small contribution to the increase in breast cancer

Cured, smoked and pickled foods

Increased risk for stomach cancers
Japan has a much higher risk for stomach cancer than here

Nitrites found in preserved foods
Nitrites are converted to nitrosamines in the liver
Nitrosamines are a very potent carcinogen

Vitamin C may prevent the conversion of nitriles to nitrosamines, evidence not conclusive

Aflatoxin

One of the most potent carcinogens known to man
It's a contaminant, a poison produced by molds found on improperly stored peanuts and grains
Causes hepatocellular carcinoma
It causes a mutation in the p53 tumor suppressor gene

Saccharin (artificial sweetener)
Shown to cause bladder cancer in rats
The rats were given a high dosage which is unrealistic to what humans consume
No correlation in human populations so no real evidence

Vitamin C
Is an antioxidant, may decreases risk of stomach cancer (evidence not conclusive)

Vitamin A and beta-carotene
Decreases risk of lung and other epithelial cancers

Vitamin E and selenium
No known cancer fighting properties

Fiber
Decreased risk of colon cancer by forcing the movement of food through the colon faster thereby decreasing the amount of time toxins may be in contact with epithelial tissues of the colon.
Increases peristalsis

Environmental risk factor: Alcohol

Its related to an increase risk of the following cancers:
Oral cavity
Pharynx
Larynx
Esophagus

Prolonged drinking can lead to cirrhosis of the liver
This is an inflammatory response

Individuals with cirrhosis of the liver will have an increased susceptibility to liver cancer or hepatocellular carcinoma
Many individuals who drink also smoke
Now we have two carcinogens

Moderate alcohol consumption is 1 drink for women and 2 for men a day
Moderate cig smoking is 1-2 packs a day
Mod smoking and Mod drinking each on their own cause an increase of oral and pharyngeal cancer that is 2 times greater than if you don't drink or smoke.
If you do both together you have a 4 fold increase

Heavy drinking is more than 4 drinks a day
Heavy smoking is more than 2 packs a day
Heavy smoking and Heavy drinking each on their own cause an increase of oral and pharyngeal carcinomas about 7 fold
If you do both, 40 times the increased
This is called a synergistic effect
The effects of each is greater than the additive effects of each separately

Environmental risk factor: Tobacco smoke

Accounts for nearly 1/3 of all cancer deaths in the United States
It is responsible for 80% of all lung cancers
This contributes about 30% to the death rate
A very significant amount of cancer mortality can be eliminated by eliminating tobacco

Smoking has also been implicated in the following
Cancers of the oral cavity
Cancers of the pharynx
Cancers of the larynx
Cancers of the esophagus
Cancers of the bladder
Canners of the kidney
Cancers of the pancreas

Figure: per capital cigarette consumption vs year vs lung cancer death rate
Lung cancer starts to go up around 1930 as does smoking.
Smoking began in 1910 and 20 years later lung cancer rates go up
That period is known as a Lag Period
This lag period , 20 years, is known to be relatively characteristic of many carcinogens
Many agents take that long, 20 years, for that multistep process of various mutations occurring giving cells increased potential for division/proliferation followed by more aggressive types of tumors appearing

Figure: Annual lung cancer death rates for males and females in the US
Men start smoking in 1910 and lung cancer rates went up in 1930
Women began smoking in the 1940
World War II occurred in 1940 so women filled in the standard typical jobs that men had at home
Not only did they take on mens jobs, they took on their habits to which smoking was probably the worst of all
So 1940 women began smoking and 1960 lung cancer rates go up in women
This is pretty dramatic evidence
The evidence suggests a very strong association between cigarette smoking and lung cancer
It doesn't show that it causes it but it shows a strong association between the two

Some facts:

There exists a close dose relationship between cigarette consumption and the development of lung cancer
The more you smoke, the greater your chancers are of getting this disease
The risk for smokers ranged between 5 and 25 times more of that than a non-smoker
Those that are light smokers will have an intermediate risk
Mortality due to cig smoking is enhanced in the presence of other carcinogens
If you stop smoking your rate stops at that point
You have a lower risk of mortality that stops at the point you stop smoking
Over the period of 20 years your chance will go down to almost that of a non-smoker

Chronic installation of tobacco products intraarticularly into experimental animals or exposure of experimental animals to cig smoke will cause them to develop lung cancer
If you expose lung cells in culture to cig smoke they will become transformed
They will under go neoplastic transformation
Now we have both sides, the epidemiologic and the experimental
We can no longer say that cig smoke is associated with lung cancer but we can now say that cig smoke can cause cancer 

There are between 2,000-3,000 chemical components and derivative es of those components in a single puff of cig cmoke
Benzopyrine, Nickle carbonyls and dimethyltriosemines are known chemical carcinogens
Benzopyrine has been observed to bind to p53
The risk for pipe smokers, cigar smokers and those who chew tobacco is much greater than a nonsmoker but not as high as a cig smoker

Every time a person puffs a cig it is diluting that stream with 7 volumes of air
If you are standing next to that individual you are getting considerably less
It depends on environment, outdoors vs indoors

Figure: Geographic variation in cancer incidence

Colon cancer
Highest Incidence: USA
34 cases per 100,000 people
20 times more than india
Lowest Incidence: India
1.8 cases per 1000,000

Prostate cancer
Highest Incidence: USA
91 cases per 100,000 people
70 times more than china
Lowest-Incidence: China
1.3 cases per 100,000

Melanoma
Highest Incidence: Australia
31 cases per 100,000 people
155 times more than japan
Lowest Incidence: Japan
0.2 cases per 100,000 people

Why is this?  There are two possibilities
Populations have exposure to different environmental factors
Populations have genetic variability (they’re genetically different than we are)

We can find out by studying migrant populations

We see that after 1 to 2 generations the patterns become identical indicating that the cancer is based on exposure to environmental factors
The number next to the country with lowest-incidence is referred to as the Minimum Intrinsic Level

The minimum intrinsic level is the lowest level of cancer in a population that cannot be decreased any further. Everything above that is environmentally caused
It is believed that the cancer rate cannot drop below that
Anything above this is environmentally caused
Over 90% of all colorectal carcinomas, on a world wide bases, is environmentally caused.


I have an exam on all this material on monday and much more. Its alot to memorize.. heh. Well, back to my studies, I have another 3 pages of notes to cram into my head. I hope someone finds this educational. I'm enjoying studying it, its just alot to take in!

P.S. If you're interested in more information, mechanisms, more facts etc... I'll be glad to share more of my notes :)

lilitalienboi16:
Ah what the heck, since im studying this right now, ill share more. Currently memorizing the differences between normal cells and cancer cells:

The history of a cell as it divides involves

Cell growth
Duplication of the genetic material
Division of a parent cell into two daughter cells
This is the cycle

Figure: The cell cycle

The cell cycle includes the following phases

G1 phase is gap 1 where the cell is metabolically active but not involved in replication 
S phase is the synthesis phase where the cell will duplicate its genetic material (DNA)
G2 phase is gap 2 where the cell is preparing for cell division
M phase is the actual division of a parent cell into two daughter cells
Progression through this cycle is controlled and regulated precisely

There is a cell cycle control system
It is a cyclin-dependent kinase system
It is responsible for activating all the proteins and enzymes needed at every stage to complete that stage and at the end of that to deactivate those protein once the process is completed
It also has to make sure that every stage is complete before the next stage begins
So DNA replication has to be finished before mitosis can begin

There are checkpoints in this cycle
Checkpoint at G1
Checkpoint at G2

It takes a cell between 20-24 hours to divide (20 hrs for real fast cells)

We can divide this out as follows:
One hour for Mitosis
Eight hours for G1
Eight hours for S
Three hours for G2

3 Different categories of cells

Cells that are always dividing and divide rapidly
Example: cells of the epithelial cells or Immune cells

Cells that occasional divide
Example: Fibroblast

Cells that never divide
Nervous tissue cells, cardiac cells and skeletal muscle cells

Cells are going to vary with the length of time that it takes them to undergo a cell division
All of that variation is going to occur in the G1 phase
G1 can vary from a couple hours to several weeks

Cells that never divide are permanently arrested in G1

For virtually all other cells passage through G1 is not continuous except for some of the very rapidly dividing cells
There is a very slow progression through G1

We can divide G1 into component parts
For most cells they will spend most of G1 in a quiescent state
We have termed this G0
Cells stay in G0 until they get some kind of message that pushes them through the cycle

Fibroblasts for example will stay in G0 until there is a physiologic need for the cell to divide
For example if there is a wound to which it will leave G0 and move from G1 and into the S phase

G1 is a decision point for cells
Do they become arrested or continue on with the cycle?

How the p53 gene arrests the cell cycle in G1

DNA gets damaged

Somehow the p53 gene is aware of the DNA damage

p53 encodes more p53 protein which is going to bind to a regulatory region of the p21 gene and stimulate the p21 gene to produce a cyclin-dependent kinase inhibitor protein
p53 activates p21 which produces an inhibitor protein which stops the cycle
Division has stopped so DNA can get repaired
Once DNA is repaired the inhibitor protein will become deactivated again and the cycle will continue
 
Now you have mutated p53 by either smoking (benzopyrene and its derivatives target p53) or say by eating contaminated peanuts that contained aflatoxin (aflatoxin binds to p53 and mutates it)
Now you can’t stop the cell cycle
What you are going to do is continue the cycle with damaged DNA
Damaged DNA will lead to more mutations and ultimately transformation of the cell from a normal to neoplastic cell. Cancer on the horizon.

What keeps the cell in G0?
The Rb protein
It is found in high concentrations in the nucleus
It is the product of the Rb tumor suppressor gene
Tumor suppressor genes retard cell growth.
In retinoblastoma, the RB GENE is mutated or deleted.

A basic defect that occurs in cancer cells is that they are going to proliferate unregulated and uncontrolled so how do we study this?
One of the major advances to cancer research occurred with the development of tissue culture techniques
When we learned to maintain cells alive outside the body of an organism by controlling the temperature, atmospheric pressure, pH, the environment, the nutrients, the growth factors, if we give all of these kinds of entities to cells we can keep them alive for a long period of time
This leads to an ability to effectively study them
The basic unregulated growth of cancer cells we see in an organism is very closely correlated to their behavior in tissue culture.

Figure: Properties of normal cells and cancer cells

Density-dependent inhibition of growth
Present in normal cells and absent in cancer cells

Tumor cells can have expression of growth factor gene which results in synthesis of their own growth factors resulting in autocrine signaling
Tumor cells may also have a mutation on their growth factor receptor resulting in a continually activated receptor as well as an activated kinase

Adhesiveness
High in normal cells and low in cancer cells
If a normal cell is forming an association with another cell or an association with the ECM (Extra cellular matrix) it is making contact with it and sticking to it
Tumor cells are less adhesive
This property correlates with metastasis

Normal cells need that adhesiveness for a number of a reasons
It tells the cells when to divide
Keeps cells in place

Contact inhibition
Present in normal cells and absent in tumor cells

If we took normal cells and put them into a petri dish that we covered in ECM we would discover that normal cells will move around the petri dish until they make contact with another cell and the ECM and then they will stop
They will do this until they form a single monolayer of cells across the dish
This property is referred to as contact inhibition

On the other hand if we put tumor cells into the dish they will not demonstrate contact inhibition
They will make contact with each other and continue to move and divide
They will not form a single organized monolayer
They will form a multilayer complex
They do not demonstrate contact inhibition

Anchorage dependence
Present in normal cells and absent in tumor cells
Normal cells in culture, if they are to divide, they have to attach to a surface
They can’t divide in suspension
They need to hold onto something even if it’s the plastic of the petri dish
Tumor cells are anchorage independent

Protease secretion
Low in normal cells but high in tumor cells
Tumor cells produce large amounts of proteases and secrete those proteases

These digestive enzymes assist in:
Breaking through a basement membrane
Dissolving the material that constitutes the spaces within the capillaries or lymphatic
Dissolve collagen and elastin that is found in the ECM
Tumor cells have a large amount of metallocollagenases

Angiogenesis
Tumor cells demonstrate this property
Angiogenesis is the development of blood vessels
If a tumor is to grow beyond a million cell it needs its own blood supply
Up to a million cells it does ok
What the tumor cell does is it secretes growth factors that affect endothelial cells and causes out growths of those cells to grow directly into the tumor
Endothelial cells line capillaries in neighboring tissues
These capillaries are much more permeable to the tumor cells
They are a little bit defective
The tumor is creating its own blood supply

Judah Folkman outlined all of the pathways involved in angiogenesis
Worked out the signaling pathways with many of the factors involved in angiogenesis
The most critical is called VEGF (vascular endothelial growth factor)
At one point he began to think that if these vessels play such an important role in metastasis why not try and block the process by blocking the formation of blood vessels
He started his experiment on mice and use inhibitors of VEGF and other components within the angiogenesis pathway and indeed he showed that he can block metastasis

Differentiation
Present in normal cells but blocked in tumor cells 
Many cancers and in particular leukemia’s fail to differentiate appropriately 

There is a rare form of leukemia called an erythroleukimia
Most leukemia’s are of white blood cells, this one is of red
Differentiation stops at the erythroblast stage but division goes on
You get a large number of cells but they are all erythroblasts and not erythrocytes

Apoptosis
Present in normal cells but least likely to happen in cancer cells
BCL prevents apoptosis

Unstable genetic material
Aneuploidy (abnormal # of chromosomes) as well as translocations contribute to unstable genetic material in tumor cells

Gene amplification
Too many copies of a gene
Occurs 1000x more frequently in tumor cells than normal cells

Gene amplification can cause problems
Too much proteases
Too much growth factors
Not only critical for the development of the disease but also correlated with the treatment of the disease
Most tumors are response to chemotherapeutic drugs and then a drug resistant clone inevitably grows out
That drug resistant clone then becomes the major population of that clone
It is believed that the development of drug resistant clones is a consequence of gene amplification
One way is that whatever the target enzyme is of a particular drug, the gene for that enzyme gets amplified
The amount of drug that is used can’t deal effectively with the growth of the cell
It is closely correlated with the severity and prognosis of the disease
The more gene copies you have of something, the worst the prognosis will be

In summary the properties of tumor cells that correlate to invasiveness and metastatic properties are:

The loss of adhesiveness, contact inhibition and anchorage dependence

Why are they missing these properties?
Tumor cells are missing integrin’s and other CAM’s

Excessive protease secretion and angiogenesis 

microlink:
WOW. A lot of info to digest. Thanks.

lilitalienboi16:

--- Quote from: microlink on October 26, 2013, 02:13:31 PM ---WOW. A lot of info to digest. Thanks.

--- End quote ---

My pleasure, I got lots and lots of more information ;)

Love sharing this stuff, biology is one of my great passions along with medicine! :D

loretta:
Effective Solutions to Cancer Thwarted by Big Pharma (posted earlier by Arcturus)

This documentary is absolutely shocking, how the organized medical fraternity backed by the pharmaceutical industry has lobbied to stall alternative treatments for cancer. Yet hardly surprising,  the deceit and cover-up is akin to what is happening in Christendom and is of God.  Whether we live (thanks to alternative therapies) or die (from conventional cancer treatments) is also of God. All is of God

The question is, should we take out health insurance?! :)

How Dr. Lorraine Day M.D., reversed her severe, advanced cancer by rebuilding her immune system by natural therapies, so her body could heal itself.
http://www.drday.com/

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