Possible Cure For Fatal Skin Cancer?

For a long time now, scientists thought that it's natural for the body's immune system to ignore cancer cells; after all, they're naturally part of one's body, while the immune system is designed to attack foreign invaders. To make it easier to understand, know that cancer cells are actually mutated cells of the human body, ailed with genetic abnormalities caused by a variety of factors including cigarette smoke, chemicals, and other carcinogens (although it could also be hereditary). Now it's clear why one's immune system won't attack cancer cells, right? That, however, isn't an absolute truth. Actually, 20 years ago, scientists discovered that some immune system cells could actually attack skin cancer cells.

Image: Wright State UniversityImage: Wright State UniversityArmed with the knowledge mentioned above, a group of researchers from the Fred Hutchinson Cancer Research Center in Seattle conducted a study on nine patients with fatal skin cancer. Out of the nine, only ONE showed positive results. While the figure might sound dismal, a single success is still better than none. The particular patient is a 52 year old man from Oregon who refuses to grant media interviews. However, we know that the man's tumors had allegedly vanished just two months into the therapy. Furthermore, two years later, all other symptoms disappeared.

*Pictured above, different types of skin cancer.

Skin cancer isn't something which spreads throughout the human body within a day or two. Detected during its early stages, cancerous patches of skin could be easily removed. Unfortunately, in its advanced stages, there's little which could be done. This is the reason why this study is of significance. Skin cancer starts with the melanoma—cells which cause the skin to tan upon exposure to UV rays. When the UV rays damage your cells and cause mutations though, a good summer tan isn't all you're going to get.


Image: WikipediaImage: WikipediaAntigen presentation stimulates T cells to become either killer cells or T helper cells.

The scientists involved in the research used an immune-priming treatment on the test subjects, or more precisely, used the patients' own immune systems to fight the skin cancer. Other recent research delving into the topic often focus on "killer T cells ," which is only natural since they're the lymphocytes (a type of white blood cell) responsible for killing off mutant and tumor cells. The research conducted in this instance, however, used T helper cells or CD4+ T cells (another type of lymphocyte; CD4, by the way, is the surface protein) instead. T helper cells don't have the ability to kill other cells like killer T cells do. T helper cells are more involved in the activation of other cells in the immune system (hence the name "helper").

So, what exactly did the scientists do? First, they drew blood from the patients and located their T helper cells. Afterwards, they cloned the cells in the laboratory. Around 5 billion T helper cells are injected back into the subject's body in the hopes of getting rid of the skin cancer cells. This potential treatment procedure is a lot less toxic than any other and seems not to cause any side effect. It's still early to declare the research successful what with eight of the nine subjects inexplicably failing to recover. I believe though, that this one success could be the start of a whole new approach in skin cancer treatment.

Source: Associated Press, Guardian UK, USA Today

Jun 21, 2008
by Anonymous

Failures could be due to dose?

I was thinking, molecular interactions, rate equations, stable, forward or reverse according to the concentrations of reagents and products.

To simplify ... just an idea ....
Let's assume that it's just a numbers game!
That is the number of defenders relative to the number of attackers is an (the) important factor for success.

They reported:
Approximately, 1 out of 10 success (0.1) required 5 billion (5E12 = 5,000,000,000,000) defenders per person? Therefore to get 10 out of 10 success (100%) we would need to infuse each patient with approximately (5,000,000,000,000 x 1)/0.1 = 50,000,000,000,000 = 50 billion defenders in the same time period?

Could it be that the "dose" - the "concentration of the reagents" - is still too low to saturate the system into a near perfect defense?

Jun 22, 2008
by Anonymous

T cell therapy for skin cancer

This therapy does look promising. However, it is very impractical due to the large amount of patient specific manipulation required.

Also, only one of nine patients responded.

Another therapy had Phase 2 clinical trial results presented at ASCO earlier in the month which showed much better results, with a similar low level of side effects, and is completely practical coming in an off the shelf vial.

This is called Oncovex and has given 6 complete responses (ie disease iradications, as per the one in the New England Journal paper) of 43 patients in which its been tested, with six others achieving a partial response, also by an immunlogical mechanism (in part).

However, as yet the data has not been published, other than presentation at ASCO, and so is pretty low profile at the moment.

It is much more promising than the T cell approach as it gives a higher rate of response and is completely practical.

Unlike the T cell approach, it will also start a Phase 3 clinical trial soon, and thus should rapidly become available for patients more broadly.

I suggest that those who are interested in melanoma look into this further, as the results are stunning and better than anything I've seen before. I was at ASCO, and I saw.

A google search for Oncovex will soon take you to the results.

Jun 29, 2008
by Anonymous

Reason of failure

Cancerogenes damages and transforms the genome of cell in lots of different ways becouse this depends on chance too - so there exists hundreds of posible different types of melanoma cell. That lucky person had melanoma type not resistant to imune cells attack. So, the main differences of his melanoma comparing to the other eight's melanomas must be detected. Kestutis Urba