New Skin Cancer Drug Hailed As 'Greatest Advance Yet' By New England Journal Of Medicine

Vismodegib, a new skin cancer drug for patients with advanced basal cell carcinoma tested by TGen, Virginia G. Piper Cancer Center at Scottsdale Healthcare and Mayo Clinic, is hailed as "the greatest advance in therapy yet seen" for advanced basal cell carcinoma in an editorial in the New England Journal of Medicine.

Vismodegib (marketed under the name Erivedge) was administered for the first time in the world on Jan. 23, 2007 in a Phase I clinical trial at Virginia G. Piper Cancer Center Clinical Trials at Scottsdale Healthcare, a partnership with the Translational Genomics Research Institute (TGen).

This is the first drug tested under the Scottsdale Healthcare-TGen partnership to receive FDA approval, and is the first to receive FDA approval to treat inoperable basal cell carcinoma. Successful early trial results led to additional study sponsored by Genentech.

The successful Phase I study at Virginia G. Piper Cancer Center Clinical Trials at Scottsdale Healthcare, headed by Scottsdale Healthcare Chief Scientific Officer and TGen Physician-In-Chief Daniel Von Hoff, M.D, led to a broader study, published by the New England Journal of Medicine.

"The first patient put on this drug had advanced basal cell cancer, so we suspected that the tumor had the mutation this drug is targeted against," said Ramesh K. Ramanathan, M.D., Medical Director at Virginia G. Piper Cancer Center Clinical Trials and Clinical Professor and Deputy Director of the Clinical Translational Research Division at TGen. "And our partnership with Dr. Ronald Korn and his team who did advanced PET imaging helped to really demonstrate the drug's efficacy for Genentech to continue pursuing the additional study."

The follow-up study, a Phase 2 clinical trial of basal cell carcinoma (BCC), was headed by Dr. Aleksandar Sekulic, Assistant Professor of Dermatology for the Mayo Clinic in Arizona, and an Assistant Professor in TGen's Integrated Cancer Genomics Division.

This Phase 2 study provided the efficacy data for vismodegib that led to its approval by the U.S. Food and Drug Administration (FDA) on Jan. 30, 2012.

"As a result of a strong collaboration between the Valley institutions, clinical development of this new medication, from the first clinical trial to the FDA approval, was led by the Valley researchers," said Dr. Sekulic, M.D and Ph.D., whose study found that vismodegib shrank advanced basal cell carcinoma tumors in 43 percent of patients with locally advanced disease and in 30 percent of patients whose disease spread to other organs.

The drug blocks the Hedgehog signaling pathway and was approved for treatment of locally advanced and metastatic basal cell carcinomas. Additional research noted encouraging results for patients with inherited genetic susceptibility for development of large numbers of BCC tumors, known as basal cell nevus syndrome.

"The availability of vismodegib and similar medications will really change the way we treat the patients with advanced forms of BCC, who had very limited options to date. In addition, this drug will likely offer a life-changing treatment for patients with basal cell nevus syndrome. It is possible that the drug may also be of benefit in treatment of earlier stages of BCC, and this is currently being evaluated in several clinical trials," Dr. Sekulic said.

"It is a landmark day for patients with basal cell carcinoma and all those involved in their care," said the NEJM editorial. However the editors cautioned that additional study of Hedgehog pathway inhibitors like vismodegib warrant further study so a larger number of patients may benefit.

FDA approval in five years is a remarkable achievement because clinical trials typically progress through three phases and can take up to 15 years to successfully complete, according to Mark Slater, Ph.D., Vice President of Research at Scottsdale Healthcare.

Most instances of basal cell cancer can be effectively treated, but in some cases, the cancer cells spread and develop an aggressive form of the cancer that does not respond to standard surgical treatment.

"For a small percentage of patients, basal cell carcinoma can progress to inoperable life-threatening, locally advanced or metastatic tumors. Vismodegib, taken as a once a day pill, represents an opportunity to improve quality of life for these patients," said Dr. Glen Weiss, Director of Thoracic Oncology at Virginia G. Piper Cancer Center Clinical Trials and Clinical Associate Professor of TGen's Cancer and Cell Biology Division.

View drug information on Erivedge.

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NICE Denies Patient Access To Breakthrough Skin Cancer Pill

Negative draft decision for Zelboraf (vemurafenib) highlights challenges facing future value-based pricing implementation and UK access to medicines.

Roche is extremely disappointed with the preliminary decision that NICE is not planning to recommend Zelboraf (vemurafenib) to be available on the NHS for the treatment of BRAF mutation positive unresectable or metastatic melanoma.

While NICE recognises vemurafenib to be a 'step-change' in the management of advanced metastatic melanoma, acknowledges that it meets its end of life criteria and agrees it is a significant innovation for a disease with a high unmet clinical need, it still has made the decision to deny patients access through routine NHS channels. As these are the key factors that will constitute a value-based pricing system, this preliminary negative decision suggests that NICE methodology is not suitable for its introduction in 2014. NICE has now turned down nine out of the last ten end of life cancer drugs at final guidance stage.

The decision is all the more disappointing as since its launch in February 2012, vemurafenib has been widely used by clinicians through the cancer drugs fund, who have seen the benefit it can make to the lives of patients, in turn quickly making it the new standard of care for BRAF mutation positive metastatic melanoma. One of just two breakthrough treatments in the last 30 years in this disease area, vemurafenib is the first licenced personalised medicine to extend the lives of patients with BRAF V600 mutation positive unresectable or metastatic melanoma to over a year.

John Melville, Managing Director, Roche UK said, "Zelboraf ticks all the boxes when considering the types of medicines that value-based pricing aims to encourage pharmaceutical companies to develop, and in addition we strongly believe it is cost effective. NICE themselves acknowledge that Zelboraf is innovative and addresses an unmet need. The draft recommendation that results from the use of the existing NICE methodology highlights a need for change in order for value-based pricing to meet the Government's stated access to medicines objectives. Whilst patients can continue to access Zelboraf through the Cancer Drugs Fund, the fact the CDF was only intended as a bridge to value-based pricing, the outcome of this NICE decision causes me great concern in relation to long term patient availability.''

A key factor in NICE's recommendation was its assertion that there are uncertainties about the long term benefits of vemurafenib. This has occurred partly because Roche, on compassionate grounds and at the request of regulatory authorities, allowed patients who were not receiving vemurafenib on the trial to access the drug once its benefits became clear. Referred to as cross-over, this commonly happens in cancer clinical trials where true benefit is demonstrated by new medicines, despite the fact that cross-over can underplay the true long term benefits of the drug, as patients on both arms of the trial can end up receiving the treatment.

Roche feels it has been penalised for the decision to ethically ensure patients benefit from true advances in medicine. Additionally, Roche believes it is unsatisfactory that a treatment with acknowledged short term benefits to a group of patients with great need for an effective therapy should be rejected because of a lack of information on the impact of the drug five to 10 years after starting treatment. Although this information will emerge with time, it will be too late for most of those patients needing treatment today and who will, typically, live for less than a year with existing therapies.

Roche urges NICE to take into account its concerns about the methodology used to make its decision, and consider the views of clinical experts at centres of excellence.

Vemurafenib will continue to be available to patients in England via the Cancer Drugs Fund, although there is no similar access for patients in Wales, Scotland and Northern Ireland.

The most frequent grade 3 adverse events with vemurafenib were skin related and included cutaneous squamous cell carcinoma, a common skin cancer treated by local excision. Additionally, generally mild and reversible increases in liver enzymes (GGT, ALT, AST, alkaline phosphatase, and bilirubin) were observed in some patients. The most common adverse events reported with vemurafenib include arthralgia, fatigue, rash, photosensitivity reaction, nausea, alopecia and pruritus. Cutaneous Squamous Cell Carcinoma (CuSCC) was very commonly reported and was most commonly treated by local excision.

About Metastatic Melanoma and BRAF

Metastatic (or advanced) melanoma is the deadliest and most aggressive form of skin cancer. A person with advanced melanoma typically has a short life expectancy that is measured in months. There are an estimated 2,000 deaths annually in the UK from malignant melanoma, with young people disproportionately affected by the disease.12 Over the last 25 years, rates of malignant melanoma in Britain have risen faster than any other common cancer.12 If current trends continue, it is anticipated that there will be around 15,500 cases of malignant melanoma diagnosed per year within the next 15 years.12 Until recently there has been no major advance in treatment for 30 years and patients with advanced melanoma have had very few treatment options.

The BRAF protein is a key component of the RAS-RAF pathway involved in normal cell growth and survival. Activating mutations in the BRAF gene cause this pathway to be overactive, which may lead to excessive growth and cancer. Mutations in the BRAF protein are found in about 50 percent of melanomas and it is estimated that approximately eight percent of all solid tumours contain BRAF mutations.

About vemurafenib

Vemurafenib is an oral medicine that is designed to selectively inhibit a cancer-causing mutated form of the BRAF protein. Vemurafenib is indicated in monotherapy for the treatment of adult patients with BRAF V600 mutation-positive unresectable or metastatic melanoma. It was co-developed under a 2006 licence and collaboration agreement between Roche and Plexxikon. A polymerase chain reaction-based companion diagnostic, the cobas® 4800 BRAF V600 Mutation Test, was co-developed by Roche Molecular Diagnostics and Plexxikon in parallel to identify people whose tumours carry the BRAF V600 mutation.

About clinical trials and patient cross-over

Clinical trials are designed to find out if a new treatment or procedure is safe, has side effects, works better than the currently used treatment and if it makes patients feel better.14 Cross-over in clinical trials occurs when patients are moved from the control arm of the trial, on to the treatment arm. In the case of vemurafenib, in the BRIM3 (phase III) clinical trial, some patients moved from receiving standard chemotherapy to vemurafenib, making it difficult to determine the clear impact of treatment. As such it is possible to underestimate the longer term benefit of the drug.

View drug information on Zelboraf.

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New American Chemical Society Video On Sunscreens

Just in time for summer, the American Chemical Society's (ACS') award-winning Bytesize Science video series is offering a new episode on the chemistry of the sunscreen products that millions of people will slather on their skin during the warm months ahead. The video, produced by the ACS Office of Public Affairs, is here:



The video explains that sun exposure can lead not only to sunburn and skin cancer, but premature aging that leaves the skin crinkled and wrinkled with unsightly "age spots." Fortunately, using sunscreen properly can help protect the skin all summer long. Unfortunately, only 1 out of 3 people use sunscreen regularly, according to a 2012 study in the ACS journal Environmental Science & Technology, as pointed out in the video.

It explains what happens to the sun's harmful UV rays after people apply sunscreen, and offers pointers on shopping for sunscreen products. For example, look for a three-letter acronym: SPF, or sun protection factor. This number tells how much protection from UV-B rays you get from the sunscreen. For example, an SPF 15 sunscreen delays the onset of a sunburn 15 times longer than no sunscreen at all.

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Biologists Find The Cause Of Pain In The Treatment Of Fair Skin Cancer

Pain caused by 2 different mechanisms

Apply the ointment, light on, light off - that's how easy it is to cure various forms of non-melanoma skin cancer. However, the majority of patients suffer severe pain during the so-called photodynamic therapy. Why the treatment with ointment and red light can be so painful has now been uncovered by researchers from the RUB. They identified the ion channels involved and signalling molecules secreted by the cancer cells. "The results may provide a starting point for suppressing the pain", says Dr. Ben Novak of the Department of Animal Physiology.

How the photodynamic therapy works

In contrast to normal cells, cancer cells are equipped with different enzymes and have a much higher metabolism. If you apply a molecule called aminolevulinic acid to the skin in the form of a gel, cancer cells take up considerably more of this substance than healthy cells. If aminolevulinic acid accumulates in the cells, the mitochondria - the power plants of the cells - form the molecule protoporphyrin IX. When irradiated with red light, protoporphyrin IX reacts with oxygen. This produces highly reactive oxygen species, free radicals, which destroy the cancer cells. Approximately ten minutes of red light irradiation is sufficient to successfully treat superficial forms of non-melanoma skin cancers such as actinic keratosis. Doctors also remove warts in this way.

Painful therapy

"The catch is: it's terribly painful", says Ben Novak. Forty percent of those treated experience pain during the light irradiation, which they assess on a scale of 0 to 10 (whereby 10 corresponds to an excruciating pain like a heart attack) as 7 to 8. Using injections, like at the dentist, it is possible to numb the nerves involved. "But that also always involves a risk", says the Bochum biologist. The scientists led by the RUB professor Dr. Hermann Lübbert have now solved the mystery as to why the treatment hurts at all.

Pain-sensitive cells in the skin are stimulated

The pain is generated by two mechanisms. In a cell culture experiment, the team showed that not only cancer cells but also pain-sensitive nerve cells in the skin take up aminolevulinic acid - and its derivative methyl aminolevulinic acid - from the ointment. Using calcium imaging, the animal physiologists followed the activity of nerve cells which they had treated with aminolevulinic acid and cells that were not exposed to the substance. Treated nerve cells fired when the researchers exposed them to light. In a living organism, this would mean that the cells would send a pain stimulus to the brain. Without the aminolevulinic acid, the pain-sensitive cells remained inactive under red light. In further experiments, the scientists showed that the activity of the nerve cells is caused by sodium channels and voltage-gated calcium channels in the cell membrane. "A drug that targets these channels would, conceivably, be able to suppress the pain - but that's still in the future", says Ben Novak.

Tumour cells alert nerve cells

Lübbert's team found that pain is generated in the nerve cells themselves, but also in another way. The affected tumour cells secrete a molecule - namely acetylcholine. "This is how they pass the message to other cells: something is wrong, my mitochondria are collapsing right now", Novak illustrates. Acetylcholine acts as a neurotransmitter in the nervous system, where it is harmless. "Previous studies have shown though, that it is very painful when it is injected into the skin". Some of the results have already been published. The researchers are currently preparing the data on the mechanisms of pain generation for publication. This attracted a great deal of interest at the 12th Congress of the European Society for Photodynamic Therapy in Dermatology (Euro-PDT) in Copenhagen in May 2012.

View drug information on Photodynamic Therapy.

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Gene Therapy Drugs Topically Delivered Via Commercial Moisturizers For Skin Disease Treatment

"Getting under your skin" takes on a brave new meaning thanks to Northwestern University research that could transform gene regulation.

A team led by a physician-scientist and a chemist - from the fields of dermatology and nanotechnology - is the first to demonstrate the use of commercial moisturizers to deliver gene regulation technology that has great potential for life-saving therapies for skin cancers.

The topical delivery of gene regulation technology to cells deep in the skin is extremely difficult because of the formidable defenses skin provides for the body. The Northwestern approach takes advantage of drugs consisting of novel spherical arrangements of nucleic acids. These structures, each about 1,000 times smaller than the diameter of a human hair, have the unique ability to recruit and bind to natural proteins that allow them to traverse the skin and enter cells.

Applied directly to the skin, the drug penetrates all of the skin's layers and can selectively target disease-causing genes while sparing normal genes. Once in cells, the drug simply flips the switch of the troublesome genes to "off."

A detailed study of a method that could dramatically redefine the field of gene regulation will be published online during the week of July 2 by the Proceedings of the National Academy of Sciences (PNAS).

Early targets of the novel treatment are melanoma and squamous cell carcinoma (two of the most common types of skin cancer), the common inflammatory skin disorder psoriasis, diabetic wound healing and a rare genetic skin disorder that has no effective treatment (epidermolytic ichthyosis). Other targets could even include wrinkles that come with aging skin.

"The technology developed by my collaborator Chad Mirkin and his lab is incredibly exciting because it can break through the skin barrier," said co-senior author Amy S. Paller, M.D., the Walter J. Hamlin Professor, chair of dermatology and professor of pediatrics at Northwestern University Feinberg School of Medicine. She also is director of Northwestern's Skin Disease Research Center.

"This allows us to treat a skin problem precisely where it is manifesting - on the skin," she said. "We can target our therapy to the drivers of disease, at a level so minute that it can distinguish mutant genes from normal genes. Risks are minimized, and side effects have not been seen to date in our human skin and mouse models."

A co-senior author of the paper, Mirkin is the George B. Rathmann Professor of Chemistry in the Weinberg College of Arts and Sciences and professor of medicine, chemical and biological engineering, biomedical engineering and materials science and engineering. He also is the director of Northwestern's International Institute for Nanotechnology.

Mirkin first developed the nanostructure platform used in this study in 1996 at Northwestern, and the FDA-cleared technology now is the basis of powerful commercialized medical diagnostic tools. This, however, is the first realization that the nanostructures naturally enter skin and that they can deliver a large payload of therapeutics.

"The field of medicine needs new constructs and strategies for treating disease," Mirkin said. "Many of the ways we treat disease are based on old methods and materials. Nanotechnology offers the ability to very rapidly create new structures with properties that are very different from conventional forms of matter. This collaborative study is a case in point."

The key is the nanostructure's spherical shape and nucleic acid density. Normal (linear) nucleic acids cannot get into cells, but these spherical nucleic acids can. Small interfering RNA (siRNA) surrounds a gold nanoparticle like a shell; the nucleic acids are highly oriented, densely packed and form a tiny sphere. The RNA's sequence is programmed to target the disease-causing gene.

"We now can go after a whole new set of diseases," Mirkin said. "Thanks to the Human Genome Project and all of the genomics research over the last two decades, we have an enormous number of known targets. And we can use the same tool for each, the spherical nucleic acid. We simply change the sequence to match the target gene. That's the power of gene regulation technology."

The nanostructures were developed in Mirkin's lab on the Evanston campus and then combined with a commercial moisturizer. Next, down in Paller's Chicago lab, the researchers applied the therapeutic ointment to the skin of mice and to human epidermis. The nanostructures were designed to target epidermal growth factor receptor (EGFR), a biomarker associated with a number of cancers.

In both cases, the drug broke through the epidermal layer and penetrated the skin very deeply, with cells taking up 100 percent of the nanostructures. They selectively knocked down the EGFR gene, decreasing the production of the problem proteins.

After a month of continued application of the ointment, there was no evidence of side effects, inappropriate triggering of the immune system or accumulation of the particles in organs. The treatment is skin specific and doesn't interfere with other cells.

Interdisciplinary research is a hallmark of Northwestern. Paller and Mirkin said their work highlights the power of physician-scientists and scientists and engineers from other fields coming together to address a difficult medical problem.

"This all happened because of our world-class presence in both cancer nanotechnology and skin disease research," Paller said. "In putting together the Skin Disease Research Center proposal, I reached out to Chad to see if his nanostructures might be applied to skin disease. We initially worked together through a pilot project of the center, and now the rest is history."

Northwestern has one of nine Centers of Cancer Nanotechnology Excellence funded by the National Cancer Institute and one of six Skin Disease Research Centers funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

"This study is a landmark achievement in the area of gene regulation - I believe our work has a chance to positively and irreversibly change the field," Mirkin said. "The skin is a very tough barrier to go through, which is why this effective gene knockdown has not been accomplished before. The power and elegance of this system are in its simplicity."

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Discovery Of Molecule In Immune System That Could Help Treat Melanoma

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Researchers from Brigham and Women's Hospital (BWH) have made a groundbreaking discovery that will shape the future of melanoma therapy. The team, led by Thomas S. Kupper, MD, chair of the BWH Department of Dermatology, and Rahul Purwar, PhD, found that high expression of a cell-signaling molecule, known as interleukin-9, in immune cells inhibits melanoma growth.

Their findings were published online in Nature Medicine.

After observing mice without genes responsible for development of an immune cell called T helper cell 17 (TH17), researchers found that these mice had significant resistance to melanoma tumor growth, suggesting that blockade of the TH17 cell pathway favored tumor inhibition. The researchers also noticed that the mice expressed high amounts of interleukin-9.

"These were unexpected results, which led us to examine a possible contribution of interleukin-9 to cancer growth suppression." said Purwar.

The researchers next treated melanoma-bearing mice with T helper cell 9 (TH9), an immune cell that produces interleukin-9. They saw that these mice also had a profound resistance to melanoma growth. This is the first reported finding showing an anti-tumor effect of TH9 cells.

Moreover, the researchers were able to detect TH9 cells in both normal human blood and skin, specifically in skin-resident memory T cells and memory T cells in peripheral blood mononuclear cells. In contrast, TH9 cells were either absent or present at very low levels in human melanoma. This new finding paves the way for future studies that will assess the role of interleukin-9 and TH9 cells in human cancer therapy.

"Immunotherapy of cancer is coming of age, and there have been exciting recent results in patients with melanoma treated with drugs that stimulate the immune system," said Kupper. "We hope that our results will also translate to the treatment of melanoma patients, but much work still needs to be done."

According to the researchers, other cell-signaling molecules have been used in treating melanoma; however, this study is the first to investigate the role of interleukin-9 in melanoma tumor immunity.

Melanoma is the most dangerous form of skin cancer. The National Cancer Institute estimates that in 2012, there will be more than 76,000 new cases of melanoma in the United States and 9,180 deaths. Melanoma is curable if recognized and treated early.

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Treatment Of Tumors Based On Differentiation Therapies, A Novel Strategy For The Treatment Of An Aggressive Type Of Skin Cancer

Skin squamous cell carcinoma (SCC) is a subtype of very aggressive skin cancers that usually develops in sunexposed body regions, but can also affect a large number of organs such as the bladder, esophagus, lungs etc. However, little is known about the biology of these cells, which consequently makes difficult the generation of new specific therapies; actually, the standard treatments are based on surgery and subsequent radiotherapy.

Researchers at the Spanish National Cancer Research Centre (CNIO) led by Erwin Wagner, vice-director of Basic Research and director of BBVA Foundation-CNIO Cancer Cell Biology Programme, have discovered a molecular mechanism that favours the disappearance and inhibition of SCC development. The authors propose that these mechanisms could be crucial for the development of targeted therapies that could potentially overcome drug resistance.

The study, which also involves the participation of medical researchers at the Medical University of Vienna, Austria, is published in the online edition of The Journal of Clinical Investigation.

"The guardian of the genome" p53, decreases cell division in favour of cell differentiation

Using in vitro models, mouse genetic models and human tumors, researchers have uncovered the molecular signals by which the p53 protein, also called "the guardian of the genome", prevents the formation of skin SCC tumors.

"We demonstrate for the first time that p53 promotes differentiation

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Uncommon BRAF Mutation In Melanoma Sensitive To MEK Inhibitor Drug Therapy

An uncommon mutation of the BRAF gene in melanoma patients has been found to respond to MEK inhibitor drugs, providing a rationale for routine screening and therapy in melanoma patients who harbor the BRAF L597 mutation.

The new study by co-first-authors Kimberly Brown Dahlman, Ph.D., Junfeng Xia, Ph.D., and Katherine Hutchinson, B.S., Vanderbilt-Ingram Cancer Center (VICC), Nashville, Tenn., was published online in Cancer Discovery. The research was led by co-senior authors William Pao, M.D., Ph.D., Jeffrey Sosman, M.D., and Zhongming Zhao, Ph.D., VICC, and Antoni Ribas, M.D., Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, Calif.

Mutations in BRAF V600E or KIT are common in about 40 percent to 50 percent of melanomas, and drugs that block or inhibit BRAF V600E were recently approved for treatment of melanoma patients with these mutations. However, there has been no effective treatment for patients with wildtype (WT) melanoma that is negative for these driver mutations.

To uncover other potentially targetable mutations, the investigators studied the tumor from a 75-year-old patient with an aggressive form of melanoma which was negative for the BRAF V600E mutation. They performed whole genome sequencing on the tumor, along with DNA from matched blood, and confirmed a mutation at BRAF L597.

To determine how many similar mutations might be overlooked by assessing only the BRAF V600 position, they analyzed the mutational status of 49 additional tumor samples negative for V600, as well as recurrent mutations in NRAS and KIT. Two of the tumors (4 percent) were found to have BRAF L597 mutations and a third tumor harbored a BRAF K601E mutation.

BRAF L597 and K601 are adjacent to V600. Since V600 mutants are sensitive to both BRAF and MEK inhibitor drugs, the investigators tested whether the BRAF inhibitor drug vemurafenib and a MEK inhibitor drug could inhibit cell proliferation signals induced by these mutants in cell lines. The MEK inhibitor led to a dramatic shut down of signaling, suggesting that tumors harboring BRAF L597 and K601 mutations might benefit from treatment with MEK inhibitors.

Confirming this hypothesis, a 69-year-old patient with metastatic melanoma harboring a BRAF L597S mutation experienced significant disease shrinkage after two cycles on therapy with a MEK inhibitor drug called TAK-733, currently in Phase I clinical trials. The patient was disease progression-free after more than 24 weeks.

The authors believe these data demonstrate that BRAF L597 mutations have clinical significance in melanoma. Further study is needed to confirm these findings.

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Take 23 Nude Pictures Of Yourself And This iPhone App Will Tell You If You Have Cancer

TheA National Cancer Institute estimates that there will beA 2 million new diagnoses of skin cancer in the U.S. alone this year, including nearly 80,000 cases ofA melanoma.

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Use Your Naked Photos to Track Skin Cancer

After your summer tan begins to fade and you worry about all the damage you may have done to your skin, wouldn't it be great if you could check out your skin for potential skin cancer without trekking to your doctor? Now there's an app for that. 

UMSkinCheck Keeps a Temporal Record of Users Skin for Surveillance of Dermatologic Cancers

Skin cancer is an unusual cancer in that it often hides in plain sight, looking like pimples, warts, and other benign growths.A A regular full body photo-exam professionally done at a clinic can be useful as a screening tool for early cancer detection, but it's time consuming, can be expensive, and may not appeal to people who don't like to undress ... (more)

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Skin Cancer Checks Using Digital Imaging

Skin cancer checks with digital imaging can be undertaken by a trained nurse or doctor using a special digital dermoscopic camera and skin mapping software. Digital dermoscopy uses high magnification and high light intensity to illuminate the sub-surface features of skin lesions that cannot be detected with the naked eye. It is particularly suited to the identification of melanoma, although it has some application in diagnosing non-melanoma lesions such as basal cell carcinomas. Digital imaging can provide advantages in the form of remote diagnosis, early skin cancer detection, and preventative medicine.

Diagnostic Accuracy

While relatively good diagnostic accuracy can be obtained with traditional dermoscopic methods, digital dermoscopy can enhance the accuracy of skin cancer detection. During a digital skin check, images are taken of all lesions meeting certain that may indicate malignancy. Typically, a conventional photographic image of a lesion is taken, followed by a high resolution dermoscopic image. Data pertaining to a lesion, such as itchiness or perceived growth, may also be recorded. By linking these details together in an electronic record, digital dermoscopy can aid medical practitioners in skin cancer detection and help to reduce the need for unnecessary excision of benign lesions. This method may also reduce the need for medical practitioners to perform biopsies.

Advantages of Digital Record Keeping

One of the key benefits of digital dermoscopy is that once an initial digital record has been made, it can be compared against images made during subsequent consults. This enables medical practitioners to detect changes in the skin at an early stage and to treat skin cancers before they become problematic. This is especially useful for patients who have a lot of moles (50 moles or more), or a large number of atypical moles (5 moles or more), as it can be difficult for doctors to track changes with such large numbers. It is also useful for patients with a high-risk of melanoma skin cancer, as many melanomas arise out of previously unmarked skin and can do so comparatively rapidly. Patients that undergo digital imaging are usually checked on a periodic basis at least once a year.

Applications in Telemedicine

Digital images may be reviewed on-site by a doctor or dermatologist, but are often used in telemedicine, where a doctor or dermatologist reviews the images off-site. This can be of use for patients in remote areas who don't have access to specialist doctors. After diagnosing each lesion, a dermatologist or specialist doctor would forward a report to a local general practitioner identifying lesions of concern and detailing any recommended treatment. Digital dermoscopy can also assist medical clinics that have a high volume of patients, as it allows a nurse or general practitioner to perform the time consuming work of image taking, while a specialist doctor or dermatologist undertakes diagnosis at a later time. By focusing on diagnosis, the specialist can review the images of a high number of patients in a short amount of time.