Ipilimumab, the first cancer immunotherapy for metastatic melanoma, is the first drug to be FDA approved in many years. Ipilimumab is sold as Yervoy by Bristol-Meyers Squibb. Interleukin-2, the last drug to have been approved for treating melanoma was approved in 1998 and only benefits 10-15% of patients with advanced disease. Dacarbazine, a chemotherapy approved in 1975, shows similar efficacy.
Zelboraf – the targeted cancer therapy vemurafenib – benefits ~80% of the patients who test positive for the B-raf mutation. Vemurafenib was also FDA approved in 2011 for metastatic melanoma. There are ongoing tests for the combination of vemurafenib (Zelboraf) and ipilimumab (Yervoy) with optimism for finding a very effective treatment for melanoma.
Cancer immunotherapy works by promoting the normal body immune system attempts to kill foreign cells, but not the body’s own cells. Tumor cells are the body’s own cells, but the changes that lead to excessive growth make the cells slightly different. If that difference were identified, then the body’s immune system could kill those tumor cells. Normally CTLA-4 blocks the immune response and protects the body’s regular cells. Ipilimumab binds to the receptors on immune cells in place of the CTLA-4 and dials down the prevention of immune cells from killing the regular cells. The goal is for the immune system to now kill the tumor cells preferentially over the regular cells, which was observed for 20-30% of the patients. There is a difficult balance where the more powerful immune system does attack the body’s regular cells as well and leads to auto-immune disorder side effects like rashes and trouble with digestion.
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Ipilimumab, the first cancer immunotherapy for metastatic melanoma, is the first drug to be FDA approved in many years. Ipilimumab is sold as Yervoy by Bristol-Meyers Squibb. Interleukin-2, the last drug to have been approved for treating melanoma was approved in 1998 and only benefits 10-15% of patients with advanced disease. Dacarbazine, a chemotherapy approved in 1975, shows similar efficacy.
Zelboraf – the targeted cancer therapy vemurafenib – benefits ~80% of the patients who test positive for the B-raf mutation. Vemurafenib was also FDA approved in 2011 for metastatic melanoma. There are ongoing tests for the combination of vemurafenib (Zelboraf) and ipilimumab (Yervoy) with optimism for finding a very effective treatment for melanoma.
Cancer immunotherapy works by promoting the normal body immune system attempts to kill foreign cells, but not the body’s own cells. Tumor cells are the body’s own cells, but the changes that lead to excessive growth make the cells slightly different. If that difference were identified, then the body’s immune system could kill those tumor cells. Normally CTLA-4 blocks the immune response and protects the body’s regular cells. Ipilimumab binds to the receptors on immune cells in place of the CTLA-4 and dials down the prevention of immune cells from killing the regular cells. The goal is for the immune system to now kill the tumor cells preferentially over the regular cells, which was observed for 20-30% of the patients. There is a difficult balance where the more powerful immune system does attack the body’s regular cells as well and leads to auto-immune disorder side effects like rashes and trouble with digestion.
Ipilimumab, the first cancer immunotherapy for metastatic melanoma, is the first drug to be FDA approved in many years. Ipilimumab is sold as Yervoy by Bristol-Meyers Squibb. Interleukin-2, the last drug to have been approved for treating melanoma was approved in 1998 and only benefits 10-15% of patients with advanced disease. Dacarbazine, a chemotherapy approved in 1975, shows similar efficacy.
Zelboraf – the targeted cancer therapy vemurafenib – benefits ~80% of the patients who test positive for the B-raf mutation. Vemurafenib was also FDA approved in 2011 for metastatic melanoma. There are ongoing tests for the combination of vemurafenib (Zelboraf) and ipilimumab (Yervoy) with optimism for finding a very effective treatment for melanoma.
Cancer immunotherapy works by promoting the normal body immune system attempts to kill foreign cells, but not the body’s own cells. Tumor cells are the body’s own cells, but the changes that lead to excessive growth make the cells slightly different. If that difference were identified, then the body’s immune system could kill those tumor cells. Normally CTLA-4 blocks the immune response and protects the body’s regular cells. Ipilimumab binds to the receptors on immune cells in place of the CTLA-4 and dials down the prevention of immune cells from killing the regular cells. The goal is for the immune system to now kill the tumor cells preferentially over the regular cells, which was observed for 20-30% of the patients. There is a difficult balance where the more powerful immune system does attack the body’s regular cells as well and leads to auto-immune disorder side effects like rashes and trouble with digestion.
Biotherapies are based on the idea that the body's own immune system is capable of killing cancer cells, a process known as cell aptosis. In fact, many have theorized that everyone has millions of cancer cells in their bodies every day, as cancer cells are normal cells that have changed or mutated. Normally, a person's immune system is able to kill these mutated cells on its own such that these cells never get a chance to replicate and grown into a tumor, or spread. However, in some people, their body's immune system is not killing the cancer cells and they do begin to form tumors, and sometimes spread.
Biotherapies work to stimulate the body's own immune system so that it can be more effective at killing cancer cells. Different biotherapy treatments approach this process in various ways. For example, some stimulate your body to produce more NK (natural killer) cells. Others, for example, stimulate your body to produce more T-cells. Both NK and T-cells are used by your body to target and kill melanoma. The following are examples of biotherapies used in fighting melanoma:
Biotherapies are based on the idea that the body's own immune system is capable of killing cancer cells, a process known as cell aptosis. In fact, many have theorized that everyone has millions of cancer cells in their bodies every day, as cancer cells are normal cells that have changed or mutated. Normally, a person's immune system is able to kill these mutated cells on its own such that these cells never get a chance to replicate and grown into a tumor, or spread. However, in some people, their body's immune system is not killing the cancer cells and they do begin to form tumors, and sometimes spread.
Biotherapies work to stimulate the body's own immune system so that it can be more effective at killing cancer cells. Different biotherapy treatments approach this process in various ways. For example, some stimulate your body to produce more NK (natural killer) cells. Others, for example, stimulate your body to produce more T-cells. Both NK and T-cells are used by your body to target and kill melanoma. The following are examples of biotherapies used in fighting melanoma:
First patients are screened with Cobas 4800, to confirm the BRAF V600 mutation - only patients with this mutation are expected to respond to Zelforab (Vemurafenib.)
Vemurafenib is taken twice a day in pill form, approximately every 12 hours. In contrast, dacarbazine is administered every three weeks by IV. Patients should inform any other doctor or dentist that you are taking Vemurafenib before they care for you. Avoid sunlight and sunlamps. They should use lip balm and a broad-spectrum sunscreen with SPF 30 or higher. It is necessary to get regularly screened for new moles (squamous cell carcinomas), that grow more frequently when using Vemurafenib, and that will need to be quickly removed.
Vemurafenib is a treatment that extends life and reduces tumors. It is not a cure. While 74% of the patients showed regression, compared with ~5% for Dacarbazine, the regression only lasted from 2-18 months. Two explanations for the recurrence have been identified. The cancer cells find an alternative path to excessive growth through cell surface protein, or an upstream gene on the pathway, N-ras mutates and the cancer growth resumes. 3 The successful results are encouraging for metastatic melanoma patients as well as other cancers that are caused through these pathways, especially by the same V600E mutation.
At this time vemurafenib treatment costs ~$10,000 per month.
The Phase III trials, led by Dr. Paul B Chapman of New York’s Memorial Sloan-Kettering Cancer Center, and a large multidisciplinary team treated late stage melanoma patients with dacarbazine or vemurafenib in a direct comparison.1 After six months, 84% of patients taking vemurafenib were alive, compared to 64% of patients on dacarbazine1. Vemurafenib also shrank the tumors in nearly half of patients, while the dacarbazine shrank tumors for only 6%. After these significant findings, the patients in the dacarbazine group were switched to vemurafenib because the observed survival rate was so much better2. The results of these trials led to FDA approval for the treatment of late-stage melanoma on August 17, 2011 3. Vemurafenib is sold under the name Zelboraf and produced by Genentech. At the same time, a the key matching diagnostic test, Cobas 4800, was approved to confirm the BRAF V600E mutation in metastatic melanoma patients.
The mutation in the B-Raf gene produces a protein that interferes with regular programmed cell death. The targeted cancer therapy, vemurafenib, pinpoints the V600E mutation and restores the function of programmed cell death, thus reducing the unwanted cell division and growth (cancer). It was observed that vemurafenib worked on other mutations in of the B-raf gene, too. The successful design and implementation of a targeted cancer therapy is a significant advance in the treatment of metastatic melanoma and a promising indicator for other key mutation based cancers. BRAF is the most frequently mutated protein kinase in human cancers5. More than 30 mutations of the B-raf gene associated with human cancers have been identified. The research on the B-raf mutation started before 1990 6 8, the work with vemurafenib (first identified as PLX4032) began over five years ago. The original PLX4032 was identified in experiments designed to target theV600E mutation 7.
The conventional treatment is with the chemotherapy drug dacarbazine, which was approved thirty six years before. Tumor shrinkage in people who received Zelboraf was 48.4 percent compared to 5.5 percent for those who received dacarbazine chemotherapy 4. Melanoma that occurs independently of the mutation is not expected to respond to vemurafenib. This treatment is a key example of personalized medicine and targeted cancer therapy.
Vemurafenib (sold as Zelboraf) is a recently approved chemotherapy available for melanoma treatment. For the 60% of melanoma patients whose cancer is caused by the V600E BRAF mutation,it restores normal cell growth by blocking the mutation's overactive cell growth. This new targeted chemotherapy was shown to extend survival time and shrink tumors better than dacarbazine, the standard of care choice for treating metastatic melanoma.
A routinely frustrating part of fighting a disease with a prescription that works for 50% of the patients, is that half the patients will be disappointed – and will suffer side effects and prolonged illness during the trial. If vemurafenib were tried on a random grouping of metastatic melanoma patients, then the success rate would be closer to 50% (60% of 84%), however the selection of those with the V600 BRAF mutation for this exact targeted cancer therapy, resulted in the significant 84% success rate.^1 ^ Research, with results like these are promising for the future of personalized medicine.
There are a number of chemotherapies that are used in melanoma treatment. In some cases they are used on their own, and in other cases they are combined together, or combined with other therapies (such as biotherapies). The following are examples of chemotherapies used in fighting melanoma:
We can get melanoma through genetic predisposition, decreased immune response, and UV radiation. The most common source of UV radiation is sun exposure.
The simplest steps to reducing the likelihood of melanoma are to avoid long sun exposure. Hats, protective swimwear, like rash guards, and sunscreen are all helpful. It is recommended to wear sunscreen daily for your face.
If you work with UV radiation, then protective clothing and eyewear are necessary.
Taking Vitamin D is highly recommended.
We can get melanoma through genetic predisposition, decreased immune response, and UV radiation. The most common source of UV radiation is sun exposure.
The simplest steps to reducing the likelihood of melanoma are to avoid long sun exposure. Hats, protective swimwear, like rash guards, and sunscreen are all helpful. It is recommended to wear sunscreen daily for your face.
If you work with UV radiation, then protective clothing and eyewear are necessary.
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Taking Vitamin D is highly recommended.
There has been a lot of evidence that suggests that vitamin D plays an important part in the prevention and fighting of melanoma. This may seem surprising since the main way people get vitamin D is through exposure to the sun, and sun exposure is something commonly know to cause skin cancer.
The key distinction is between sun exposure and sun over-exposure. In other words, normal sun exposure has not been shown to have any negative effect on melanoma, and in fact, due to the positive effect of producing vitamin D, has actually been show to reduce the risk of melanoma(1). However, over-exposure (i.e. sunburning) has been shown to have a negative effect and is correlated to higher risk of developing melanoma.
There have been many scientific studies done that show the D3 version of vitamin D can be very helpful for some in fighting melanoma. It has been show in some melanoma lines, to stop the melanoma from growing (3), (4), (6), (7). It has also been shown that other mechanisms help to kill melanoma cells(5). Further, another study showed decreased levels of vitamin D3 are associated with increased risk of melanoma. Hence, while it is certainly not guaranteed to work, vitamin D3 should be seriously considered as something to take when fighting melanoma, or trying to prevent its recurrence.
The word "macrobiotic" is Greek and means "long life" or "great life." This diet is a a strict diet that is a philosophy of life and a regime of food. It originated in Japan and emphasizes a balance of food, with a focus on locally grown whole grain cereals, fish, vegetables, seaweed, fermented soy products and fruit. Some studies have shown that this diet can have a positive effect on fighting cancer and melanoma, and many people have testified to its benefit in their battles with cancer.
There is a wide range of evidence that high doses of melatonin can help prevent melanoma, and also can help kill melanoma tumors and help stop them from spreading. See below for a partial listing of studies, some on animals and some on people, supporting the use of melatonin in fighting melanoma. You can also search PubMed.gov for "melanoma melatonin".
It has also been shown that the amount of melatonin taken affects its effectiveness. It is not known what the "ideal" amount to be taken should be, however, many doctors who use melatonin for melanoma treatment will suggest something in the range of 20mg per night. It is best to take it at night because it causes drowsiness.
The word "macrobiotic" is Greek and means "long life" or "great life." This diet is a a strict diet that is a philosophy of life and a regime of food. It originated in Japan and emphasizes a balance of food, with a focus on locally grown whole grain cereals, fish, vegetables, seaweed, fermented soy products and fruit. Some studies have shown that this diet can have a positive effect on fighting cancer and melanoma, and many people have testified to its benefit in their battles with cancer.
Max Gerson was a doctor in Germany in 1881 who developed a protocol for fighting cancer that includes a very strict diet. Essentially, the focus on this diet is on raw, vegan, organic foods and fruit juices consumed in a carefully crafted regimen. Gerson claims to have cured many "incurable" forms of cancer with this protocol, and there is a lot evidence both in support of and against it.
Exercise, detoxification and relaxation are extremely important for the treatment of any disorder, but specifically for creating the ideal internal environment for beating cancers like melanoma. Yoga is a form of exercise, that includes poses ("asanas") as well as meditative breathing and mind-states as well. The mind-body connection is often discussed when it comes to cancer, and treatments that include mind-body components (like yoga) can be extremely effective and emotionally enjoyable.
Exercise, detoxification and relaxation are extremely important for the treatment of any disorder, but specifically for creating the ideal internal environment for beating cancers like melanoma. Yoga is a form of exercise, that includes poses ("asanas") as well as meditative breathing and mind-states as well. The mind-body connection is often discussed when it comes to cancer, and treatments that include mind-body components (like yoga) can be extremely effective and emotionally enjoyable.
