Cancer Society seeking volunteers for long-term cancer study

The American Cancer Society is looking for volunteers from the Fredericksburg area to enroll in a long-term cancer research study.

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Skin cancer and tanning beds

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Sunburned? Relief is as close as your pantry

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Alarming Skin Cancer Infographics - The 'Eucerin' Chart Explains the...

The 'Eucerin' chart explains the danger that sun exposure has on the skin. While laying out in the sun, it is always smart to wear a protective shield of sunblock to prevent any serious sun burns, or worse - cancer.

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Kids with melanoma

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Self-Examine For Skin Cancer With This Mobile App

Researchers from the University of Michigan Health System has developed an app that allows users to screen for skin cancer by using their mobile phones.

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An iPhone App for Skin Cancer Diagnosis

A free app is the new coolest thing for DIY skin cancer diagnosis. As long as you're willing to take 23 nude photos of yourself.

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N.Y. bans indoor tanning for 17 younger

New York's Gov. Andrew M. Cuomo, a Democrat, signed a law prohibiting the use of indoor tanning devices by children age 17 and under.

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Transplant, Lymphoma Patients At Greater Risk Of Melanoma

Main Category: Melanoma / Skin Cancer
Also Included In: Transplants / Organ Donations;  Lymphoma / Leukemia / Myeloma
Article Date: 06 Oct 2012 - 0:00 PDT



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New Research Takes Us Another Step Towards Understanding And Treating Melanoma

These proteins are required for melanocyte stem cell self-maintenance and, as such, correct pigmentation throughout the mice's life span. Without these two proteins, the mice's fur turns white. Their research is published in the review Cell Report and paves the way for serious possibilities in terms of stopping the formation of melanomas, tumours that originate from melanocyte cells.

Melanocytes are cells in the organism used for skin, fur and hair pigment. This pigmentation function provides protection from the sun and lends organisms their colour. Malfunctions in these cells may lead to skin cancer known as melanoma. Melanomas are highly aggressive cancers that become very difficult to treat as they develop and metastases occur.

A few years ago, researchers discovered that, in humans, the B-Raf gene (coding gene for protein of the same name) is mutated in more than 50% of melanoma. Spectacular progress has been made in recent years in the treatment of this cancer, thanks to the development of pharmacological inhibitors that target an enzyme: the B-Raf kinase. However, despite this treatment, cancer returns in several patients, indicating that not all cancerous cells have been eliminated. This led researchers to believe that B-Raf is not the only element driving the cancer process.

In this new research, scientists have tried to understand how melanocytes function normally, to then understand their specific role in cancer. To this end B-Raf protein expression, then, in turn, C-Raf protein expression, were removed from mice with black fur (ideal to clearly see any changes in pigmentation).

No changes in pigmentation were observed for mice that only had their B-Raf or C-Raf expression removed by researchers from the line of cells producing melanocytes. Mice that had both coding genes for B-Raf and C-Raf removed simultaneously had a normal colour at birth. However, they progressively lost their pigmentation as they grew. They turned grey from black, before becoming increasingly white.

For Alain Eychène, the research team leader, "these observations represent a fault in melanocyte renewal. Since the colour black is present at birth, the pigment cells clearly exist. However, the progressive whitening of the fur, once B-Raf and C-Raf have been removed from the cell line, proves that both these proteins are required for melanocyte renewal".

As is the case for all cells, melanocytes originate from stem cells; the latter are responsible for renewal during moulting. This research shows that it is specifically this population of stem cells alone that disappears progressively in mutant mice. For Alain Eychène, "This is the first in vivo demonstration of the role of RAF proteins in the self-renewal of stem cells".

The fact that B-Raf and C-Raf are both involved in controlling and renewing pigment stem cells represents another step towards understanding and treating melanoma. By blocking these proteins (using inhibitors) in patients undergoing treatment, it is possible that in time researchers will succeed in eliminating all cancerous stem cells, i.e. the likely cause behind cases of cancer reoccurrence.

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How Melanoma Cells Circumvent The Immune System

Melanoma is so dangerous because it tends to metastasize early on. New treatment approaches utilize, among other things, the ability of the immune defense to search out and destroy malignant cells. Yet this strategy is often only temporarily effective. A research team under the direction of Bonn University has discovered why this is the case: In the inflammatory reaction caused by the treatment, the tumor cells temporarily alter their external characteristics and thus become invisible to defense cells. This knowledge forms an important foundation for the improvement of combination therapies. The results have been published online in the renowned journal Nature.

In Germany, approximately 15,000 people develop melanoma annually and approximately 2,000 people die from it every year. Malignant melanoma is the most frequently fatal skin diseases. The particular malignancy is based on the fact that small tumors can spread via the lymphatic vessels and the bloodstream. For many years, the working group under Prof. Dr. Thomas Tüting, Director of the Laboratory for Experimental Dermatology at the Bonn University Hospital, has investigated the effect of a targeted immune therapy with tumor-specific defense cells.

Tumor cells behave like a wolf in sheep's clothing

In trials on mice who congenitally develop melanoma, the researchers were able to destroy advanced tumors using so-called cytotoxic T-cells. "But they recover after some time - just as they do in patients in the hospital," explain Dr. Jennifer Landsberg and Dr. Judith Kohlmeyer, lead authors of the study. This form of therapy triggers inflammation. Now the researchers have discovered that the melanoma cells change their external characteristics precisely via this accompanying inflammatory reaction. "They behave like wolves in sheep's clothing and thus evade detection and destruction by defense cells," says Marcel Renn, also a lead author of the study.

The immune system can fight tumors - but it can also protect them

On the search for the underlying mechanisms, the researchers pointed histological investigations of tumors in the right direction: Therapy-resistant melanomas demonstrated a significantly stronger inflammatory reaction with many scavenger cells of the immune system, the so-called macrophages. A messenger primarily released from these immune cells - the tumor necrosis factor-alpha - was able to bring about the change in character of the melanoma cells directly in the Petri dish in the laboratory. Cells treated in this way were subsequently hardly detected by the defense cells. "The immune system is like a double-edged sword," explains Prof. Tüting. "It can fight the tumor - but it can also protect it." Such changes in the tumor tissue are probably of great importance for the formation of resistance to therapy. "According to more recent discoveries, treatment with inhibitors which prevent signal transmission in tumor cells is also affected by this," remarks Prof. Tüting.

Melanoma cells lose their typical characteristics

Molecular genetic investigations revealed that melanoma cells from therapy-resistant tumors had lost the characteristics typical for pigment cells. Instead, they demonstrated traits of connective tissue cells. "It is possible that melanoma cells undergo this change in character so easily because they originate from the embryonic development of cells in the neural crest which can also form connective tissue and nerve cells," says Prof. Dr. Michael Hölzel, co-author from the Institute for Clinical Pharmacology and Clinical Chemistry at the Bonn University Hospital.

Results can also be transferred to humans

Findings initially gained from laboratory mice were also able to be reproduced by the team of researchers with human melanoma cells and various associated defense cells in the Petri dish. The melanoma cells likewise reacted to the messenger tumor necrosis factor-alpha with a loss of pigment cell characteristics and could then no longer be detected by pigment-cell-specific defense cells. "Detection by other defense cells which can search out specific genetic changes in the melanoma cells was not affected by this, however," stresses Prof. Dr. Thomas Wölfel, director of a working group involved in the study at the Medical Clinic III of the Mainz University Hospital.

Important findings for new treatment strategies

As soon as the tumor necrosis factor alpha no longer had an effect on the human and mouse melanoma cells, however, the cells regained their pigment-cell characteristics. Then they were also able to be detected and fought against by all immune defense cells once more. All of these findings yield important information for new treatment strategies. Thus in the future, defense cells against antigens of various categories and specificity should be used and at the same time, the inflammation utilized by the tumor cells should be therapeutically inhibited. "Our experimental model system will help us to develop optimally effective combination therapies as rapidly as possible," says Prof. Tüting. "However, it will still take several years until the clinical application of strategies of this type."

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Measures Needed To Curb Alarming Increase In Malignant Melanoma On The West Coast Of Sweden

Malignant melanoma is as much as 35% more common among people who live in Gothenburg and the region's coastal municipalities than those who live inland. Researchers at Sahlgrenska Academy, University of Gothenburg, Sweden, have found that the number of malignant melanoma cases in the Vastra Gotaland region has quadrupled since 1970.

Malignant melanoma has become increasingly common in the Western world over the past few decades. One of the biggest factors has been excessive and unprotected sunbathing despite widespread awareness of the health risks.

Melanoma takes a long time, sometimes several decades, to develop. For that reason, sunbathing habits from many years ago still affect a person's risk level.

According to a new study by researchers at Sahlgrenska Academy, University of Gothenburg, the number of melanoma cases in the Västra Götaland region has quadrupled among men and tripled among women since 1970.

"This represents a relative increase of more than 3% per year," says Magdalena Claeson, a researcher at Sahlgrenska Academy who participated in the study. "The increase in the region was considerably above average for the entire country."

The study found that 35% more men and 25% more women developed malignant melanoma in Gothenburg than in the inland municipalities. Fifteen per cent more women developed the disease in the coastal municipalities than inland.

One explanation is that inhabitants of Gothenburg and the coastal municipalities are exposed to the sun for more hours a day. A 2007 study conducted by the Swedish National Board of Health and Welfare found that inhabitants of Gothenburg and the coastal municipalities tend to take longer summer holidays in sunny countries and spend more time outdoors when abroad. Meanwhile, they are more likely to work indoors when they are in Sweden.

"The latest research suggests that melanoma is caused by this type of intermittent exposure to the sun," Magdalena Claeson says. "In other words, people get sunburned during their summer holiday and spend a lot of time indoors for the rest of the year."

The results have convinced the researchers that more preventive resources should be appropriated for the Västra Götaland region, particularly Gothenburg and the coastal municipalities.

"Among the measures likely to prove effective are educational initiatives among schoolchildren and sun protection information for people who travel abroad," Claeson says.

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Photosensitizing Antihypertensive Drugs May Increase Risk Of Lip Cancer

Long-term use of commonly used blood pressure medications that increase sensitivity to sunlight is associated with an increased risk of lip cancer in non-Hispanic whites, according to a Kaiser Permanente study that appears in the current online issue of Archives of Internal Medicine.

Funded by the National Cancer Institute, the study found that photosensitizing antihypertensive drugs such as nifedipine and hydrochlorothiazide were associated with cancer of the epithelial cells known as squamous cells - which are the main part of the outermost layer of the lips and skin.

Researchers compared 712 patients in Northern California with lip cancer to 22,904 people in a control group and found that the risk of squamous cell lip cancer was higher for those with long-term use of photosensitizing blood pressure medications.

"Lip cancer remains rare and an increased risk of developing it is generally outweighed by the benefits of these blood pressure drugs and other photosensitizing medications," said Gary Friedman, MD, an emeritus researcher at the Kaiser Permanente Northern California Division of Research and lead author of the study. "Physicians prescribing photosensitizing drugs should ascertain whether patients are at high risk of lip cancer by virtue of fair skin and long-term sun exposure and discuss lip protection with them. Although not yet confirmed by clinical trials, likely preventive measures are simple: a hat with sufficiently wide brim to shade the lips and lip sunscreens."

The risk of lip cancer appeared to increase with increasing duration of use of these drugs and was not explained by a history of cigarette smoking, also a known risk factor for lip cancer, according to investigators.

Photosensitizing drugs are believed to absorb energy from ultraviolet and/or visible light, causing the release of electrons. This leads to generation of reactive oxygen intermediates and free radicals which damage DNA and other components of skin and lip cells and produce an inflammatory response, Friedman said.

Researchers ascertained prescriptions dispensed and cancer occurrence from August 1994 to February 2008. They identified 712 patients with lip cancer and 22,904 controls in the susceptible group of non-Hispanic whites. Researchers determined their use at least two years before diagnosis or control index date of the commonly prescribed diuretics, HCTZ and HCTZ combined with triamterene (HCTZ/TR), the angiotensin-converting enzyme inhibitor lisinopril, the calcium channel blocker nifedipine, and the beta adrenergic blocker atenolol, the only non-photosensitizer studied. Non- photosensitizing atenolol, when used alone, was not associated with increased risk. Findings for lisinopril were not as clear-cut as those for HCTZ, HCTZ/TR and nifedipine.

Researchers analyzed use of each drug both exclusively and regardless of use of others and focused on duration of use. The analysis controlled for smoking.

Researchers were not able to include basal cell and squamous cell cancers of the skin in this study because these diagnoses have not been recorded in their cancer registry. Also, researchers were not able to adjust for sun exposure, the most important lip cancer risk factor, along with relative lack of pigmentation of the lips. Risk of developing melanoma was not associated with these drugs. This form of skin cancer has been more strongly associated with intermittent sun exposures, especially those producing sunburn, than with chronic sun exposure, so timing of use of photosensitizing drugs could be an important consideration, explain the researchers.

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Skin Cancer Patients Should Be Screened Before Receiving Vemurafenib

Editor's Choice
Main Category: Melanoma / Skin Cancer
Also Included In: Cancer / Oncology;  Genetics
Article Date: 15 Aug 2012 - 10:00 PDT



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Skin Cancer: Potential New Treatment Target Identified For Melanoma

New research from Western University, Canada, has identified a potential new target for the treatment of melanoma, the deadliest of all skin cancers. Silvia Penuela and Dale Laird discovered a new channel-forming protein called Pannexin (Panx1) that is expressed in normal levels on the surface of healthy skin cells. But they found, in melanoma, Panx1 is over-produced to a pathological level. The researchers also discovered that if you reduce it or knock it down, the cell becomes more normal. The research is published in the August 17th issue of the Journal of Biological Chemistry.

Malignant melanoma only accounts for four per cent of all skin cancers and yet, it's responsible for 79% of skin cancer-related deaths. The World Health Organization says there are 200-thousand cases of melanoma diagnosed each year and 65 thousand melanoma-related deaths (2000 statistics).

"We think this over-production of Panx1, enables the melanoma to become very aggressive. The cells have these extra Panx1 channels and they can leave the primary tumor and invade other tissues," explains Laird, a Professor in the Department of Anatomy and Cell Biology, and Canada Research Chair in Gap Junctions and Disease. "And when you find a protein that is highly up-regulated in a disease cell such as a melanoma, the question becomes, is there therapeutic value in targeting a drug to that protein to reduce its production or block its function. Would that be an effective treatment?"

"We now want to correlate our discovery to patient samples using the human melanoma bank through our collaboration with Dr. Muriel Brackstone and other clinicians at the London Health Sciences Centre, to see if this is a cancer marker," says Penuela, a Postdoctoral Fellow working in the Laird lab. "So if a melanoma lesion has a lot of this protein, it might be a tool for prognosis, in saying this is more advanced, or going to be highly metastatic. And because it's on the skin, it would be more accessible for treatment." Penuela suggests potential treatment might be in the form of a topical medication to use on melanoma lesions.

The scientists also worked with David Litchfield and John Lewis and their teams at Schulich Medicine & Dentistry and the London Regional Cancer Program on this research. It was funded through the Canadian Institutes of Health Research. The Laird laboratory recently received a $200,000 Innovation Grant from the Canadian Cancer Society Research Institute to further its studies on Panx1.

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Understanding The Link Between Indoor Tanning And Skin Cancer

Editor's Choice
Main Category: Melanoma / Skin Cancer
Also Included In: Public Health;  Cancer / Oncology
Article Date: 20 Aug 2012 - 10:00 PDT



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Studying How Elesclomol Works Reveals New Molecular Target For Melanoma Treatment

A laboratory study led by UNC medical oncologist Stergios Moschos, MD, demonstrates how a new targeted drug, Elesclomol, blocks oxidative phosphorylation, which appears to play essential role in melanoma that has not been well-understood. Elesclomol (Synta Pharmaceuticals, Lexington, MA) was previously shown to have clinical benefit only in patients with normal serum lactate dehydrogenase (LDH), a laboratory test routinely used to assess activity of disease.

For more than 60 years, scientists have known that cancer cells undergo glycolysis, or metabolize glucose, at a much higher rate than normal cells. The observation, called the Warburg effect, demonstrated that the normal energy producing processes in the cell are disrupted in cancer cells, preventing them from using metabolic pathways in the cell's mitochondria (often called the cell's "power plants").

Recently, however, increasing evidence suggests that, in addition to glycolysis, other metabolic pathways may also play a role in cancer, with important therapeutic implications. A promising strategy for targeting cancer cells, while sparing normal cells, is to target these altered metabolic processes with drug therapies. Elesclomol has been shown to trigger cell death in metastatic melanoma cells, primarily by suppressing oxidative phosphorylation - the process that cells use to transform nutrients into energy.

Moschos and his team demonstrated in the lab that metastatic melanoma cells exhibit a higher rate of glycolysis compared to their normal counterpart cells, termed melanocytes, which would be expected due to the Warburg effect.

"But we also found, surprisingly, that these cells have higher rates of oxidative phosphorylation - they are producing energy through more than one pathway, which explains a lot about how the drug works," says Dr. Moschos.

He notes that this drug has an interesting history. In a 600-patient phase III clinical trial conducted almost 4 years ago, Elesclomol had clinical benefit in the subgroup of patients with normal serum LDH. However, the FDA discontinued the trial, because the Elesclomol in combination with another chemotherapeutic drug may have negative effects in patients with high serum LDH, which is associated with poorer patient outcomes in metastatic melanoma. At the time, very little was known about Elesclomol's mechanism of action - blocking oxidative phosphorylation.

"Our inability to show how Elesclomol worked through measurement of biomarkers was the major driver to conduct this laboratory study," said Moschos, whose team took the clinical trial results back to the lab to try to figure out why the drug worked.

"Our results suggest that targeting oxidative phosphorylation in melanoma is a promising strategy for early metastatic disease, before melanoma cells switch their primary metabolic source to glycolysis, as Otto Warburg showed 60 years ago" said Dr. Moschos.

"Second, we were able to demonstrate a mechanism of resistance to Elesclomol, where long-term exposure to the drug leads to the selection of melanoma cells with high levels of glycolysis. This suggests that a two-pronged strategy aimed at blocking both metabolic pathways may be called for."

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Unique Adverse Events With Newly Approved Drug Reviewed By Melanoma Expert

An internationally recognized melanoma researcher at Moffitt Cancer Center and colleagues at the University of Kiel in Germany, including Axel Hauschild, M.D., and Katharina C. Kahler, M.D., have published an article in the Journal of Clinical Oncology that describes immune-related adverse events for patients receiving either tremelimumab or ipilimumab.

Both drugs are anti-CTLA-antibodies with similar mechanisms of action but manufactured by different companies. Ipilimumab is an immunoglobulin G1 with a plasma half-life of 12 to 14 days. Tremelimumab is an immunoglobulin G2 with a plasma half-life of 22 days. Both have been extensively tested in metastatic melanoma, and ipilimumab was approved in 2011 by the U.S. Food and Drug Administration for treating metastatic melanoma and other cancers.

"During treatment with ipilimumab and tremelimumab, a unique set of adverse events may occur called 'immune-related adverse events,' or irAEs," said study lead author Jeffrey S. Weber, M.D., Ph.D., director of Moffitt's Donald A. Adam Comprehensive Melanoma Research Center of Excellence. "These irAEs may include colitis, hepatitis, pancreatitis, lymphadenopathy, neuropathies and nephritis."

According to Weber, appropriate management of these side effects requires the cooperation of a multidisciplinary physician-led team that includes nurse practitioners and infusion nurses. He recommends that specialists, including gastroenterologists, endocrinologists, hepatologists, dermatologists and surgeons, receive education on managing these symptoms. Early recognition of irAEs and initiation of treatment are crucial, the researchers said.

In their review of studies on the drugs' adverse effects, the researchers also found that irAEs correlated with treatment response in some studies. The reduction in tumor burden came in four patterns after week 12 of treatment.

"Anti-CTLA-4 antibodies have shown patterns of anti-tumor response that are different from responses to conventional chemotherapy," explained Weber. "Because responses can occur slowly or be mixed, 12 weeks has been the time to first evaluation with ipilimumab."

Weber and his colleagues also reviewed the new set of response criteria that have been created - immune related response criteria, or irRC - to evaluate disease progression and benefit with immune checkpoint inhibitors such as ipilimumab. The irRC criteria have been compared with modified World Health Organization criteria in studies of patients receiving ipilimumab and can provide valuable information to oncologists as to when to stop or continue treatment with ipilimumab.

"In this study, we provide a detailed description of irAEs and recommendations for practicing oncologists who are managing them along with the unusual kinetics of response associated with ipilimumab therapy," Weber said.

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Intravenous Administration Of Green Tea Compound Shows Promise For Tackling Cancer

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A compound found in green tea could be a weapon in treatments for tackling cancer, according to newly-published research at the University of Strathclyde in Glasgow, Scotland.

The extract, known as epigallocatechin gallate, has been known to have preventative anti-cancer properties but fails to reach tumours when delivered by conventional intravenous administration.

However, in initial laboratory tests at the Universities of Strathclyde and Glasgow, researchers used an approach which allowed the treatment to be delivered specifically to the tumours after intravenous administration. Nearly two-thirds of the tumours it was delivered to either shrank or disappeared within one month and the treatment displayed no side effects to normal tissues.

The tests are thought to be the first time that this type of treatment has made cancerous tumours shrink or vanish.

In the tests, on two different types of skin cancer, 40% of both types of tumour vanished, while 30% of one and 20% of another shrank. A further 10% of one of the types were stabilised.

The researchers encapsulated the green tea extract in vesicles that also carried transferrin, a plasma protein which transports iron through the blood. Receptors for transferrin are found in large amounts in many cancers.

Dr Christine Dufès, a senior lecturer at the Strathclyde Institute of Pharmacy and Biomedical Sciences, led the research. She said: "These are very encouraging results which we hope could pave the way for new and effective cancer treatments.

"When we used our method, the green tea extract reduced the size of many of the tumours every day, in some cases removing them altogether. By contrast, the extract had no effect at all when it was delivered by other means, as every one of these tumours continued to grow.

"This research could open doors to new treatments for what is still one of the biggest killer diseases in many countries."

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Cause skin cancer

Beating skin cancer in this country, is at times, a scary and perilous gamble. If the options are surgery or radiation, the light at the end of the tunnel might not look to bright. These things have prevalent risks involved, even when being done by seasoned professionals.

Well then what is it? Does sun exposure cause skin cancer?
Not necessarily. With an acidic body ph, high toxicity in the body, and a lack of nutrition, you are just asking for trouble.

What this disease looks like can vary. They can be in the form of discolored marks, blemishes, moles, or other abrasions. One also must realize that the sun isn't necessarily the cause and determining factor of whether or not you will have skin cancer.

The American Institute of Cancer Research in Washington has stated that,"In addition to limiting your sun exposure, eating certain foods may help reduce your risk", according to FitnessMagazine.com.

In a stunning study coming out of Italy chronicled inside the International Journal of Epidemiology, diet can be responsible for advancing your chances of avoiding these dangers.

Scientists have mentioned the diet of people in and near the Mediterranean tend to eat more plant based then people over on the western side of the world. This for example is what scientists are actually studying and discovering actually works to beat skin cancer and others.

The rays from the sun can transform your DNA. Before this can happen though, the dun damages skin cells that die and release free radicals. These in great numbers can help harbor safe and favorable environments for cancer growth.

In addition, a process called antiangiogensis can both fend off or help generate cancer cells if you know what you are doing. For the benefit of healing, the certain nutrients coming off of the plant based foods can act antagonistic towards cancer cells causing them to die. Certain monounsaturated fats such as olive oil also helps to release these antiangiogenic substances.

Beating skin cancer doesn't have to set the stage for death and disaster. You should be able to get as much sun exposure as you want and still avoid skin cancer. Your system has to be nutritionally adequate inside for you to avoid most dangers from these diseases. Like all cancer, the right diet can make or break your cancer fight. The reason why the secrets about how to beat skin cancer have been hidden are because the nature of the cure cannot be patented, thus it is not marketable or profitable. Anyone can beat this disease from the inside out. The trick to beating sking cancer isn't a trick at all, but historical fact.

Consider beating skin cancer a done deal. Get your sun and stay cancer free... The secret is diet...

CureYourCancerNaturally.blogspot.com

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Human Melanoma Stem Cells Identified

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Cancer stem cells are defined by three abilities: differentiation, self-renewal and their ability to seed a tumor. These stem cells resist chemotherapy and many researchers posit their role in relapse. A University of Colorado Cancer Center study recently published in the journal Stem Cells

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Lymph node metastasis

This is the deadliest form of skin cancer that develops in the melanocytes which are pigment cells present in the skin. Melanoma develops when unrepaired DNA damage caused by the sun's ultraviolet rays or tanning beds triggers a genetic defect or mutation. This mutation causes the skin cells to multiply rapidly forming malignant tumors. Melanoma can also form in the colored part of the eye and very rarely internal organs like the intestines.

Causes

Melanoma occurs when there are changes in pigment producing cells of the body called melanocytes. Melanocytes produce melanin which is responsible for skin and hair color. These changes disrupt the orderly manner in which skin cells form (new skin cells push older skin to the skin surface which die and fall off) and make the skin cells grow rapidly and out-of-order. The disorderly skin cell formation is what eventually develop into a mass of cancerous tissues. Melanocytes produce melanin which is responsible for skin and hair color. Melanoma often begins as a mole but it may also come in the form of a skin discoloration (red, pink, blue, purple or white).

Stages of melanoma

Melanoma has 5 stages. Staging is based on thickness of the lesion, depth of penetration and how far it has spread.

Stage 0 - This type of melanoma is confined to the epidermis. It has not yet reached the dermis

Stage I - This has two subclasses. It is characterized by the thickness of the tumor, presence and number of mitosis and status of any ulceration

Stage II - This has 3 subclasses. It is characterized by the tumor thickness and the status of ulceration. There is usually no distance or lymph node metastasis at this stage.

Stage III - This stage has 3 subclasses and its characterized by lymph node metastasis. There is no distant metastasis at this stage.

Stage IV - This has no subclasses. It is characterized by the location of distance met

Treatment

Treatment of melanomas depend on the stage of the cancer, your age and other medical condition. Usually early detection requires surgery to remove the cancer and surrounding tissue. The depth of the cancer is taken into consideration when removing the surrounding tissues. If the cancer has spread to the lymph nodes, they will be taken out. Surgery is normally the only type of treatment required for early melanomas.

For advanced cases, the solution here is to shrink the tumor and make the patients as comfortable as possible. These may include;

Chemotherapy - These drugs can be given intravenously, in the form of a pill or where necessary both ways. Chemotherapy kills the cancer cells.

Radiation - These use high energy beams to relieve pain and discomfort caused by cancer that has spread.

Biological therapy - Medications like interferon or interleukin are used to boost your immune system to fight the disease.

Surgery - This is also done when the cancer has spread to relieve pain and discomfort

Read more at http://yourhealth-check.com/

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Study Of Malaysian Tribe Could Help Find East Asian Skin Color Genes

Genetic investigation of a Malaysian tribe may tell scientists why East Asians have light skin but lower skin cancer rates than Europeans, according to a team of international researchers. Understanding the differences could lead to a better way to protect people from skin cancer.

While the genetics of skin color is largely unknown, past research using zebrafish by Penn State College of Medicine's Keith Cheng, M.D., Ph.D., identified the gene in Europeans that differs from West Africans and contributes to a lighter skin color. Mutations in the genes SLC24A5 and SLC45A2 are largely responsible for European pigmentation, showing only single amino acid differences between Europeans and West Africans. Each version of a gene is called an allele.

While East Asians -- Chinese, Japanese and Korean -- also are light skinned, these European alleles are not present, suggesting that while both groups' lighter skin color evolved to allow for better creation of vitamin D in northern climates, they did so in a different way. This difference also affects skin cancer rates. Europeans have 10 to 20 times higher rates of melanoma than Africans. However, despite also having lighter skin, East Asians have the same melanoma rates as Africans. The reason for this difference can only be explained when the gene mutations for both groups are found.

"By finding the differences, we have the potential to find ways to make people with the European ancestry genes less susceptible to skin cancer," said Cheng, professor of pathology.

This is a challenge, because to find the unidentified mutations, researchers must study a population that includes a blend of original African ancestry and East Asian ancestry, with little European contribution.

The Senoi, one of three indigenous tribes from Peninsular Malaysia, meet this condition. The Senoi are believed to include ancestry of a dark-skinned tribe called the Negrito, and a regional Mongoloid population of Indo-China, such as the Proto-Malay. Since the skin color of the Senoi is darker than that of Northeast Asians, researchers will be able to focus on finding the primary genetic mutation of light skin color in Asians without seeing further skin lightening mutations.

Khai C. Ang, Ph.D., postdoctoral fellow in the Cheng lab, visited the Senoi, developed a positive relationship with them, and was able to collect 371 blood samples. Characterization of the Senoi's skin color was recently reported in PLoS ONE.

"As the world is becoming globalized, populations are becoming increasingly mixed," Ang said. "Time is running out and it will become increasingly difficult to establish how East Asian skin colors evolved."

The researchers will now map genes in the DNA using the collected samples to identify which might be responsible for the skin color of East Asians. In the Cheng lab, the candidate genes and mutations can then be tested in zebrafish for verification.

"Skin color has been tied to human welfare in modern history," Cheng said. "It is important for us as a species to realize that our skin color is determined by only a small number of minute changes in our DNA -- changes that have nothing to do with the value of human beings."

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Missing Pieces Of DNA Structure Is A Red Flag For Deadly Skin Cancer

Melanoma is the most dangerous type of skin cancer and is the leading cause of death from skin disease. Rates are steadily increasing, and although risk increases with age, melanoma is now frequently seen in young people.

But what if we could pinpoint when seemingly innocuous skin pigment cells mutate into melanoma? Researchers at Brigham and Women's Hospital (BWH) have achieved this. Teams led by Yujiang Geno Shi, PhD, from BWH's Department of Medicine, and George F. Murphy, MD, from BWH's Department of Pathology have discovered a new biomarker for the lethal disease. The findings offer novel opportunities for skin cancer diagnostics, treatment and prevention.

The study was published on September 14, 2012 in Cell.

"Dr. Shi and colleagues have discovered an exciting new connection between the loss of a specific chemical mark in the genome and the development of melanoma," said Anthony Carter, PhD, of the National Institutes of Health's National Institute of General Medical Sciences, which mainly funded the research. "This work is a prime example of how basic research on mechanisms of epigenetic regulation can yield clinically significant insights that hold great promise for diagnosing and treating cancer."

The researchers found that certain biochemical elements in the DNA of normal pigment-producing skin cells and benign mole cells are absent in melanoma cells. Loss of these methyl groups - known as 5-hmC - in skin cells serves as a key indicator for malignant melanoma. Loss corresponded to more advanced stages of melanoma as well as clinical outcome.

Strikingly, researchers were able to reverse melanoma growth in pre-clinical studies. When the researchers introduced enzymes responsible for 5-hmC formation to melanoma cells lacking the biochemical element, they saw that the cells stopped growing.

"It is difficult to repair the mutations in the actual DNA sequence that are believed to cause cancer," said Christine Lian, MD, a physician scientist in the Department of Pathology at BWH and one of the lead authors. "So having discovered that we can reverse tumor cell growth by potentially repairing a biochemical defect that exists-not within the sequence-but just outside of it on the DNA structure, provides a promising new melanoma treatment approach for the medical community to explore."

Because cancer is traditionally regarded as a genetic disease involving permanent defects that directly affects the DNA sequence, this new finding of a potentially reversible abnormality that surrounds the DNA (thus termed epigenetic) is a hot topic in cancer research, according to the researchers.

In the United States, melanoma is the fifth most common type of new cancer diagnosis in men and the seventh most common type in women. The National Cancer Institute estimates that in 2012 there will be 76,250 new cases and 9,180 deaths in the United States due to melanoma.

The Shi laboratory pioneers studies in both basic chromatin biology and translational epigenetic research at the Endocrine Division, BWH Department of Medicine, and collaborates with Dr. Murphy's laboratory that focuses on melanoma biology in the Program for Dermatopathology, BWH Department of Pathology. This pre-clinical study, which shows a key role for epigenetics in melanoma development and progression, also enlisted the support of an international team of investigators.

The findings will provide insight for future functional, pre-clinical studies of 5-hmC in cancer biology.

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Researchers Find Cause Of Chemotherapy Resistance In Melanoma

Researchers with UC Irvine's Chao Family Comprehensive Cancer Center have identified a major reason why melanoma is largely resistant to chemotherapy.

UCI dermatologist Dr. Anand Ganesan and colleagues found a genetic pathway in melanoma cells that inhibits the cellular mechanism for detecting DNA damage wrought by chemotherapy, thereby building up tolerance to cancer-killing drugs.

Targeting this pathway, comprising the genes RhoJ and Pak1, heralds a new approach to treating the deadly skin cancer, which claims nearly 10,000 U.S. lives each year. Study results appear online in Cancer Research, a journal of the American Association for Cancer Research.

"If we can find a way to turn off the pathway responsible for this resistance, melanoma tumors would suddenly become sensitive to therapies we've been using for the last 20 years," said Ganesan, assistant professor of dermatology and biological chemistry at UCI.

In pursuit of a cause for the chemo tolerance, he and his colleagues performed a genome-wide scan for genes controlling drug resistance in melanoma cells. Their search identified RhoJ, a gene normally involved in blood vessel growth. They saw that in response to drug-induced DNA damage in a melanoma cell, RhoJ activated another gene, Pak1, which initiated a molecular cascade suppressing the cell's ability to sense this damage - and blocking the apoptosis process.

"Normally, such drug-induced DNA damage would result in cell death," Ganesan said. "But this blunting of DNA damage response allows melanoma cells to mutate and proliferate. Being capable of rapid adaptation and change is a hallmark feature of this challenging form of cancer and makes it very difficult to treat."

On the heels of this discovery, he and colleagues have begun exploring methods to inhibit the genes responsible for this DNA damage tolerance. What they come up with could one day supplement chemotherapy treatments for melanoma, Ganesan added.

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Skin cancer screening

When was your last skin cancer screening? Do you have concerns about some of the moles on your body? Seeing a dermatologist is a great way to get the peace of mind you need when it comes to a variety of different conditions. Because this disease often affects people before there are any noticeable symptoms, diagnostic testing provides early detection. This means both patients and doctors have an opportunity to investigate treatment options as soon as possible to start getting a handle on the situation.

Checking at Home

You are the first person responsible for your own skin cancer screening. In the comfort of your own home, you can look over your body and take note of any moles that seem to be unusual. There are several specific things to look for, including an asymmetrical border or ragged edges. If any are larger than an eraser on a pencil or they are different colors, pay special attention. Finally, if any of the moles are starting to change in size, shape or color, it is time to set up a skin cancer screening with the doctor.

Make sure that you start from your head and work your way down, checking out all of your body. If you have any areas that you are concerned about, consider taking picture of them. Then, over the next several months you can see if there are any noticeable changes. Some patients, even after seeing a doctor, go home and take pictures to use as a reference.

Making an Appointment with a Professional

When it comes to skin cancer screening, if you have a concern, make an appointment. Even if you feel certain that nothing is wrong or you think you are overreacting, go ahead and see the dermatologist. In this situation, it is always better to be safe than sorry. Check with your health insurance to find a doctor covered by your plan, and schedule an appointment as soon as possible. Make sure that you mention to the receptionist that you want to have one or more moles looked at.

Your appointment usually begins with a visual inspection of the areas. Be sure to point out the moles that you have concerns about. Many doctors will go ahead with a full-body visual inspection to see if there are any other moles that are of concern. If the doctor believes that there could be a problem, a biopsy will be performed. This type of skin cancer screening will let the doctor know just how deeply the disease has penetrated, and he or she will be able to decide on the right treatment options.

Researcher Discovers Homing Device That Attracts Melanoma To The Brain

The process of metastasis, by which cancer cells travel from a tumor site and proliferate at other sites in the body, is a serious threat to cancer patients. According to the National Cancer Institute, most recurrences of cancer are metastases rather than "new" cancers.

Virtually all types of cancer can spread to other parts of the body, including the brain. Once metastatic melanoma cells are entrenched in the brain, patients typically have only a few months to live.

Now Prof. Isaac Witz and his team at Tel Aviv University's Department of Cell Research and Immunology are delving deeper into what attracts metastatic melanoma cells to the brain, and how they survive and prosper in this environment. Their experiments have discovered that melanoma cells produce receptors for two chemokines - a family of small proteins secreted by cells - present in the brain tissue. These receptors may act as a homing device, drawing the cancerous cells to the brain.

"These interactions between the chemokines in the brain and the melanoma cell receptors could be potential targets for new therapies," Prof. Witz says. "With medications that suppress these molecules, you could hope to interfere with this specific migration." Published in the International Journal of Cancer, this research is supported by the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.

A dangerous attraction

Although metastasis is a well-understood process, researchers are still trying to uncover the underlying mechanisms of why cancer cells begin to migrate in the first place. It is also crucial to understand what allows them to sustain themselves, divide, and propagate once they have arrived at their new location.

To better understand metastacized melanoma cells in the brain, the researchers cultured brain tissue in the lab, then analyzed all of the materials that were expressed by the cells. They identified certain chemokine receptors in brain-metastasizing melanoma cells and corresponding chemokines in the brain tissue which could ultimately be responsible for the cancer cells' being "attracted" to the brain. If a certain chemokine is released from the brain, and the melanoma cells have the appropriate receptors, a chemical attraction will take place where the melanoma cells would be drawn to wherever the chemokine is.

Duplicating nature

The researchers have also developed a method to compare metastatic and non-metastatic cells with identical genetic backgrounds. Though they are derived from the same cancer, some of these cells become metastatic, while others do not. "This is a good way for us to concentrate on the genes that are specific to metastatic cells. Because we have these two types of cellular variants, where only one goes to the brain and metastasizes, it's an important tool" for future research, explains Prof. Witz.

The researchers have found that mice that are inoculated with non-metastatic cells do end up with melanoma cells in the brain, but they are dormant and do not generate overt metastasis. The key is to discover why these originally identical cells differ - why the non-metastatic cells don't develop in the same way.

Understanding the process will help scientists to "duplicate what nature does, and prevent these cells from becoming metastatic," says Prof. Witz. "If there already is metastasis, it is too late - so what we want to do is to prevent development by understanding the mechanism that keeps the non-metastatic cells dormant."

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Drug Trials Seek Combinations Effective For Melanoma

Promising new data from trials aimed at delaying resistance to BRAF inhibitors

Promising new data on drug combinations to treat metastatic melanoma were presented at the ESMO 2012 Congress of the European Society for Medical Oncology in Vienna.

The phase I and II trials focus on combining drugs to slow the development of resistance to drugs that inhibit BRAF, a gene that is mutated in about half of melanomas. Earlier trials with drugs that target BRAF generated excitement for their ability to quickly shrink melanoma tumors in suitable patients. But for many patients the benefits proved short-lived, as the cancer cells develop resistance to the drugs.

"These studies exemplify an important landmark of some tumors, which has emerged from recent laboratory research: the presence of specific mutations, such as the BRAF mutation in metastatic melanoma which exposes an Achilles' heel--MEK in this case," said Prof Yossef Yarden from the Weizmann Institute of Science, Israel. "In-depth understanding of cancers and their mutations is expected to reveal more of these deadly weaknesses in cancer, which we can exploit using new drugs and drug combinations."

Phase II of the BRAF inhibitor dabrafenib alone vs combination with MEK1/2 inhibitor trametinib

Dr Georgina Long from Westmead Hospital and the Melanoma Institute Australia and colleagues report that combining the new drugs dabrafenib and trametinib provided a clinically meaningful improvement in progression-free survival, response rate and duration of response in 162 patients with melanoma that had BRAF V600 mutations.

Patients in the study received either dabrafenib 150mg twice daily; twice-daily dabrafenib plus once-daily 1mg trametinib; or twice daily dabrafenib plus once-daily 2mg trametinib. The combination prolonged progresion free survival over single-drug therapy from 5.8 months to 9.4 months, which represents a 60% improvement. Among patients who received both drugs at the higher dose, 41% had not progressed 12 months after treatment began, compared to 9% in the monotherapy arm of the study.

"The combination therapy of the BRAF inhibitor dabrafenib and the MEK inhibitor trametinib prolongs the progression-free survival in patients with V600 BRAF mutation-positive metastatic melanoma compared with dabrafenic monotherapy," Dr Long said. "Importantly, the combination also decreases the rate of the cutaneous toxicities compared with dabrafenib monotherapy, particularly the oncogenic cutaneous toxicity of squamous cell carcinoma."

Phase IB study of vemurafenib in combination with the MEK inhibitor, GDC-0973

A Phase I study in 44 patients shows that the combination of the MEK inhibitor GDC-0973 and vemurafenib can be delivered safely, Dr Rene Gonzalez of the University of Colorado Cancer Center, Denver, and colleagues report.

"BRAF inhibition has resulted in high response rates and improved survival in patients with BRAF mutated melanoma," Dr Gonzalez said. "One of several mechanisms of resistance has been reactivation of the MAPK pathway. Preclinical models show that combined inhibition of BRAF and MEK can delay the acqusition of resistance compared to BRAF inhibitor monotherapy. Inhibition of the pathway downstream from BRAF with the MEK inhibitor GDC-0973 could theoretically overcome or delay this resistance mechanism and improve outcomes."

The study was not designed to evalate efficacy. "While early data in a small number of patients did show tumor reduction, it would be premature to comment on efficacy based on these preliminary results and further research is warranted," Dr Gonzalez said.

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Ultraviolet light source

The experience of sunburn can be a very efficient (i.e. painful) reminder to heed adequate protection on future occasions. However more importantly, it should be a reminder of the long-term effects of sun exposure on our bodies and health – which can include aging of the skin and skin cancer.

In order to more fully understand these consequences, let’s take a look at exactly what sunburn is, its symptoms and its effect on the body.

Sunburn results when the amount of exposure to the sun, or other ultraviolet light source (e.g. tanning lamps and welding arcs etc.), exceeds the ability of the body's protective pigment, melanin, to protect the skin. Melanin content varies greatly, but in general darker skinned people have more melanin than lighter skinned. (Although fairer skinned people are generally more prone to getting sunburn than darker skinned people, this certainly does not exclude the latter from risk.)

Sunburn destroys cells in the outer layer of the skin, damaging tiny blood vessels underneath. Burns deeper into the skin’s layers also damage elastic fibers in the skin, which over time and with repeated sun overexposure, can result in the appearance of yellowish, wrinkled skin.

The damage to skin cells from UV exposure (either sunlight or tanning lamps etc.) can also include damage to their DNA. It’s this repeated DNA damage, which can lead to a cell becoming cancerous. With the incidence of skin cancer rising dangerously in many parts of the world, and with its ability to develop and establish itself in the body ‘long’ before external signs are detected, -- paying attention to this aspect of sun exposure and sunburn should certainly not be ignored if we are serious about preserving our health.

Now while it may be easier to ignore the effects of sunburn occurring at a cellular level, ignoring the external symptoms of sunburn in the days immediately following such exposure is entirely another matter.

While sunburn is usually not immediately obvious, skin discoloration (ranging from slightly pink to severely red or even purplish) will initially appear from 1 – 24 hours after exposure. Although pain is usually worst 6 – 48 hours afterward, the burn can continue to develop for 24 – 72 hours after the incident. Where there is skin peeling, this generally occurs 3 – 8 days after the burn occurs.

While minor sunburns typically cause nothing more than warm/hot skin, slight redness, and tenderness to the affected area, -- in more serious cases, extreme redness, swelling and blistering can occur. These blisters filled with fluid may itch and eventually break. This can then cause peeling of the skin, exposing an even tenderer layer of skin underneath.

Severe sunburn can cause very red, blistered skin but can also be accompanied by fever, chills, nausea (in some cases vomiting), and dehydration. In instances of extreme sunburn where the pain is debilitating, medical treatment may be required.

While the immediate effects of sunburn can certainly be painful and cause discomfort, the real deterrent to UV overexposure should be the potential damage to your long-term health – including the risk of premature aging of the skin along with skin cancer.

Don’t let sunburn and sun overexposure kill your chances of enjoying youthful skin, and a healthy body. Remember, the easiest way to treat sunburn will always be to avoid it in the first place!

Angela Perin is editor of the 'Safe Tan Ezine', which features practical articles and tips on Beauty, Fitness, Nutrition and more. To discover the Ultimate Experience in Natural Sunless Tanning, visit http://www.safetan.com.au

Article Source: ArticlesAlley.com

Use Of Interstitial Fluid Pressure Via Noninvasive Measurement, A...

Main Category: Cervical Cancer / HPV Vaccine Also Included In: MRI / PET / Ultrasound ; Melanoma / Skin Cancer ; Cancer / Oncology Article Date: 02 Oct 2012 - 1:00 PDT Researchers validated a method of noninvasive imaging that provides valuable information about interstitial fluid pressure of solid tumors and may aid in the identification of ... (more)

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Celgene's Abraxane meets main goal in melanoma trial

Celgene Corp said on Tuesday that in a late-stage clinical trial, patients with metastatic melanoma who took its drug Abraxane lived for a longer period without getting worse than those who received the chemotherapy dacarbazine.

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Resistance In Melanoma Patients Delayed By Combination Of Targeted Treatment Drugs

Combined treatment with two drugs targeting different points in the same growth-factor pathway delayed the development of treatment resistance in patients with BRAF-positive metastatic malignant melanoma .

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Indoor Tanning Causes Common Skin Cancers, Study Finds

Indoor tanning, already associated with an increased risk for the deadliest type of skin cancer, appears to increase the likelihood for other skin cancers as well.

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