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Free skin cancer screening offered on June 13

Free skin cancer screening offered on June 13

Skin cancer is one of the most preventable cancers – and one of the most treatable, if it’s detected early enough. Knowing the possible risk factors, such as fair skin, excessive sun exposure, or atypical moles, might help in recognizing the signs of the disease, and getting a professional screening is also always a good idea.

Each year, Stanford dermatologists offer a free screening for skin cancer; this year’s event is happening Saturday, June 13 from 8:00-11:30 AM at the Stanford General Dermatology Clinic in Redwood City. If you’re a local reader, plan to stop by.

Alex Giacomini is an English literature major at UC Berkeley and a writing and social media intern in the medical school’s Office of Communication and Public Affairs.  

Previously: The importance of sunscreen in preventing skin cancerSkin cancer images help people check skin more often and effectively, and Study shows link between indoor tanning and common skin cancer

Cancer, Dermatology, FDA, Health Policy, In the News, Public Health

Experts call on FDA for a “tanning prevention policy”

Experts call on FDA for a "tanning prevention policy"

6635416457_a62bfeb09d_zIndoor UV tanning beds are known carcinogens that are responsible for many cases of skin cancer, which is the most commonly diagnosed form of cancer in the U.S. A recently issued Call to Action to Prevent Skin Cancer from the U.S. Surgeon General states that “more than 400,000 cases of skin cancer [8% of the total], about 6,000 of which are melanomas, are estimated to be related to indoor tanning in the U.S. each year” while “nearly 1 out of every 3 young white women engages in indoor tanning each year,” making indoor tanning a serious public health issue.

In a JAMA opinion piece published yesterday, Darren Mays, PhD, MPH, from the Georgetown University Medical Center‘s Department of Oncology, and John Kraemer, JD, MPH, from Georgetown’s School of Nursing and Health Studies, argued that the FDA needs to step up its regulatory approach and restrict access to this technology – due to its limited therapeutic benefits and known damaging effects.

In 2011, California was the first state to ban access to indoor UV tanning beds to minors. The authors assert that “state-level policies restricting a minor’s access to indoor tanning devices are effectively reducing the prevalence of this cancer risk behavior among youth,” but argue that regulation at the federal level is in order:

Like tobacco products, a national regulatory framework designed to prevent and reduce indoor tanning could reduce public health burden and financial costs of skin cancer. …from a public health perspective the indoor tanning device regulations are not commensurate to those of other regulated products that are known carcinogens with very little or no therapeutic benefit.

However, the likelihood of this regulation taking place is questionable:

FDA did not leverage its authority last year to put a broader regulatory framework in place, which could have included a national minimum age requirement and stronger indoor tanning device warning labels… Critical factors seem to be aligning for such policy change to take place, but additional momentum is needed to promote change at a national scale. The US national political environment makes more expansive regulation by either FDA or Congress seem unlikely in the near future.

The authors concluded with a call for organizations other than governments to help build momentum on toward a “national indoor tanning prevention policy.” For example, they said, universities could implement “tan-free” campus policies similar to the “tobacco-free” campaign.

Previously: More evidence on the link between indoor tanning and cancers, Medical experts question the safety of spray-on tanning productsTime for teens to stop tanning?, Senator Ted Lieu weighs in on tanning bed legislation and A push to keep minors away from tanning beds
Photo by leyla.a

Dermatology, Research, Stanford News

Researchers identify genetic basis for rosacea

Researchers identify genetic basis for rosacea

roseceaRosacea causes skin on the face to redden and can result in acne-like bumps, but it isn’t just an aesthetic problem. Some rosacea patients experience itching, stinging and burning sensations on the affected skin, which can make sleeping, concentrating and social interactions challenging.

Finding out what causes rosacea could help scientists identify new treatments and understand its links to other known diseases – and Stanford researchers, in collaboration with the personal genomics and biotechnology company 23andMe, have now identified a genetic basis for the incurable but treatable inflammatory disease. Their work was published online March 12 in the Journal of Investigative Dermatology.

I describe in a press release how Anne Lynn Chang, MD, lead author of the paper and an assistant professor of dermatology at Stanford, and her collaborators partnered with 23andMe on this work. 23andMe customers of European descent were asked via survey if they had ever been diagnosed with rosacea, and those who answered yes were grouped together while those who answered no were placed in a control group. And then:

The researchers compared the genomes of rosacea patients and controls and looked for differences in the DNA building blocks, called nucleotides, in people diagnosed with rosacea. Such differences, called single nucleotide polymorphisms, occur when one nucleotide, such as tyrosine, is substituted for another, such as cytosine. This kind of analysis is called a genome-wide association and, because the entire genome is searched, is an unbiased way to look for genetic links to disease.

Two areas of the genome were linked to having rosacea, and both areas were near genes involved in systemic inflammatory and autoimmune diseases, such as multiple sclerosis, diabetes, sarcoidosis and inflammatory bowel disease.

“The next step is to look more into these associations of rosacea with other diseases,” Chang told me, “and explore whether the inflammation in rosacea is a cutaneous sign of risk for other disease.”

Kimberlee D’Ardenne is a writing intern in the medical school’s Office of Communication and Public Affairs.

Previously: New study: Genes may affect skin youthfulness and When it comes to your genetic data, 23andMe’s Anne Wojcicki says: Just own it
Photo, altered from original, by Kristie Wells

Cancer, Dermatology, Research, Science

Common skin cancer evades treatment via specific mutations

Common skin cancer evades treatment via specific mutations

Anthony OroBasal cell carcinoma is the most common type of skin cancer. It is also one of the most treatable. But people with advanced cases of the disease often experience only a temporary response to the drug vismodegib, and their tumors recur within a few months as the cancer becomes resistant to the drug.

Now dermatologists Anthony Oro, MD, PhD; Jean Tang, MD, PhD; and Anne Chang, MD, have identified the specific mutations involved in the development of vismodegib resistance, and identified another treatment that may be successful even on vismodegib resistant tumors. They’ve recently published their findings in Cancer Cell (with an accompanying companion paper and commentary).

From our release:

Approximately 2 million new cases of basal cell carcinoma are diagnosed each year in the United States, making it the most common cancer in the country. About half of patients with advanced basal cell carcinomas will respond to vismodegib, which belongs to a class of drug compounds called Smoothened inhibitors. About 20 percent of these responders will go on to quickly develop resistance to the drug.

Basal cell carcinomas are uniquely dependent on the inappropriate activation of a cellular signaling cascade called the Hedgehog pathway. Blocking signaling along this pathway will stop the growth and spread of the cancer cells. The Hedgehog pathway plays a critical role in normal development. It’s also been found to be abnormally active in many other cancers, including pancreatic, colon, lung and breast cancers, as well as in a type of brain cancer called medulloblastoma.

The researchers found two classes of mutations in the Smoothened gene that inhibit vismodegib’s effectiveness by keeping the Smoothened protein active. Treating the cells with inhibitors that target a portion of the pathway downstream of Smoothened blocked the activation of the pathway even in cells with the mutations. These inhibitors, called Gli antagonists, could be an effective way to treat vismodegib-resistant tumors, the researchers said.

As Oro told me, “This research sheds new light on mechanisms of how tumors evolve to develop drug resistance, and has already helped us with personalized cancer genetics and therapy for our patients. It is now possible for us to identify those people who may benefit from a combination therapy even before they begin treatment.”

Previously: Studies show new drug may treat and prevent basal cell carcinoma, New skin cancer target identified by Stanford researchers and Another blow to the Hedgehog pathway? New hope for patients with drug-resistant cancers
Photo of Anthony Oro by Steve Fisch

Aging, Chronic Disease, Dermatology, Stanford News

Patching up diabetic ulcers

Patching up diabetic ulcers

Like the more than 29 million people in the U.S, my mother has diabetes. Her eldest sister and my maternal grandmother both died of complications of the disease, and her one surviving sister is coping with complications that will probably claim her life in a few years. I’ve got gestational diabetes (a temporary version of the disease that occurs during pregnancy), and due to that and my family history I’m likely to develop type-2 diabetes down the line, also. So I’m always very interested in hearing about research advances related to the disease.

One such advance: As reported today in the the Proceedings of the National Academy of Sciences, Stanford researchers have developed a new skin patch that delivers a drug to aid the healing of diabetic ulcers. Diabetic ulcers (or open wounds) are one of the most common complications of the disease, with an estimated 15 percent of diabetics developing them. They often occur on the feet and are the leading cause of diabetes-related amputations. The high level of blood sugar in diabetics’ blood impairs the body’s ability to grow new blood vessels, which slows down healing of the ulcers.

Deferoxamine, or DFO, is an FDA-approved drug that can help correct this problem, but it would be toxic if taken for as long as diabetics need it to heal their ulcers. So Stanford researchers developed a local application via a skin patch. In a press release, study authors Dominik Duscher, MD, a plastic and reconstructive surgery postdoctoral fellow, and surgeon Geoffrey Gurtner, MD, talked about the findings of their work in animal models:

Not only did the wounds in the mice heal more quickly, Duscher said, but the quality of the new skin was even better than the original. The researchers also used the DFO matrix on a mouse with diabetes to see if it would prevent ulcer formation — and it did. “We were very excited by the results,” Duscher said, “and we hope to start clinical trials soon to test this in humans.”

“This same technology is also effective in preventing pressure ulcers, which are a major source of morbidity and mortality in patients with neurologic injury or the elderly,” said Gurtner, who is also the Johnson & Johnson Distinguished Professor in Surgery II. “The actor Christopher Reeve actually died from a pressure ulcer and not his spinal cord injury, which really emphasizes the extremely limited therapeutic options for these patients.”

Luckily my mother hasn’t had to deal with diabetic ulcers, though when she gets small cuts or chaps on her skin, they do take forever to heal, so she’s super-vigilant about avoiding them. The possibility of preventing more serious ulcers with this patch is a development I’ll be following closely.

Previously: A primer on preventing or delaying type 2 diabetes and New medicine? A look at advances in wound healing

Aging, Dermatology, Public Health, Videos

Don’t skip the sunscreen in wintertime

Don’t skip the sunscreen in wintertime

When you’re spending time outdoors during the wintertime, it’s easy to justify skipping the sunscreen when the sun isn’t beating down on you mercilessly and you’re bundled up instead of sporting a swimsuit. But UV rays from the sun can penetrate clouds and snow can reflect sun onto your face, hands and any other exposed skin. So it’s important to remember to take sun safety precautions even on cold or overcast days, too.

This  Stanford Health Care video featuring dermatologist Justin Ko, MD, MBA, includes important tips for preventing skin cancer year-round. As I, like many others, prepare for a family trip to Tahoe to take advantage of the recent snow, Ko’s reminder about sun safety habits during the winter comes at a good time. For example, I suspect I’ve been skimping on sunscreen: Ko says you need a shot glass-full to completely cover your body. If you’re using a spray-on sunscreen, you need to spray for a full 60 seconds.

Watch the video to learn more information about how to identify possible cancerous moles and preventing high-risk exposures, like tanning beds.

Previously: Skin cancer linked to UV-caused mutation in new oncogene, say Stanford researchers, Humble anti-fungal pill appears to have a noble side-effect: treating skin cancer, Skin cancer images help people check skin more often and effectively, and The importance of sunscreen in preventing skin cancer

Biomed Bites, Cancer, Dermatology, Genetics, Research, Videos

Spotting broken DNA – in the DNA fix-it shop

Spotting broken DNA - in the DNA fix-it shop

It’s Thursday. And here’s this week’s Biomed Bites, a weekly feature that highlights some of Stanford’s most innovative research and introduces Scope readers to innovators in a variety of disciplines.

Neon green streaks across the screen. The phrases “End mismatched ligation” and “Repair of DNA double-strand breaks” flash at me. Did I stumble across an online, genetic fix-it shop? Sort of –  in that Stanford biochemist Gilbert Chu, MD, PhD, studies broken DNA and has a website to match.

Chu describes his research in the video above: “We started out in the lab trying to understand and recognize DNA that’s been damaged by ultraviolet radiation, which causes skin cancer. This led to the discovery of a protein that turned out to be missing in patients with a very rare disease called xeroderma pigmentosum.”

XP afflicts about 1 in 1,000,000 people in the United States. Without the protein Chu mentioned, mutations and damage accumulates in sufferers DNA, causes cancers and extreme sensitivity to the sun.

Chu’s team has also developed methods that allow other researchers to examine the expression of genes across an entire genome and to determine which cancer patients might be harmed by treatment with ionizing radiation.

“The reason I got interested in this research is that as a member of the Department of Medicine, I am an oncologist and I’m very interested in trying to help cancer patients,” Chu said.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving forward biomedical innovation here.

Previously: Skin cancer linked to UV-caused mutation in new oncogene, say Stanford researchers, Radiation therapy may attact circulating cancer cells, according to new Stanford study and How ultraviolet radiation changes the protective functions of human skin

Dermatology, Research, Science, Stanford News, Stem Cells

The politics of destruction: Short-lived RNA helps stem cells turn on a dime

The politics of destruction: Short-lived RNA helps stem cells turn on a dime

Many stem cells live a life of monotony, biding their time until they’re needed to repair tissue damage or propel the growth of a developing embryo. But when the time is right, they must spring into action without hesitation. Like Clark Kent in a phone booth, they fling aside their former identity to become the needed skin, muscle, bone or other cell types.

Now researchers at Stanford, Harvard and the University of California-Los Angeles have learned that embryonic stem cells in mice and humans chemically tag RNA messages encoding key stem-cell genes. The tags tell the cell not to let the messages linger, but to degrade them quickly. Getting rid of those messages allows the cells to respond more nimbly to their new marching orders. As dermatology professor Howard Chang, MD, PhD, explained to me in an email:

Until now, we’ve not fully understood how RNA messages within the cell dissipate. In many cases, it was thought to be somewhat random. This research shows that embryonic stem cells actively tag RNA messages that they may later need to forget. In the absence of this mechanism, the stem cells are never able to forget they are stem cells. They are stuck and cannot become brain, heart or gut, for example.

Chang, who is a Howard Hughes Medical Institute investigator and a member of the Stanford Cancer Institute, is a co-senior author of a paper describing the research, which was published today in Cell Stem Cell. He shares senior authorship with Yi Xing, PhD, an associate professor of microbiology, immunology and molecular genetics at UCLA, and Cosmas Giallourakis, MD, an assistant professor of medicine at Harvard. Lead authorship is shared by postdoctoral scholars Pedro Batista, PhD, of Stanford, and Jinkai Wang, PhD, of UCLA; and by senior research fellow Benoit Molinie, PhD, of Harvard.

Messenger RNAs are used to convey information from the genes in a cell’s nucleus to protein-making factories in the cytoplasm. They carry the instructions necessary to assemble the hundreds of thousands of individual proteins that do the work of the cell. When, where and how long each protein is made is a carefully orchestrated process that controls the fate of the cell. For example, embryonic stem cells, which can become any cell in the body, maintain their “stemness” through the ongoing production of proteins known to confer pluripotency, a term used to describe how these cells can become any cell in the body.

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Dermatology, Stanford News

From the newsstands to exam rooms: My chat with Stanford dermatologist Laurel Geraghty

From the newsstands to exam rooms: My chat with Stanford dermatologist Laurel Geraghty

Laurel G

First thing to know about Laurel Geraghty, MD: She can geek out with the best of them. Don’t be fooled by her fashionable clothes or her graceful manner: Geraghty can riff on mole types and describe the symptoms of psoriasis with passion. Geraghty had to suppress her science savvy as an editor at Glamour magazine, although there were plenty of other perks – including weekend jaunts to Las Vegas or the Caribbean and “working” celebrity-packed Manhattan fashion shows.

Now, she’s a second-year dermatology resident at Stanford, married and the mother of a 3-year-old and a 5-year-old. In a recent interview, I chatted with Geraghty about her career change, future plans, skin cancer, acne, and even tattoos. About the latter, she told me:

Tattoos can be safe if done by a reputable professional using new and sterilized equipment. There is a risk of transmitting communicable diseases, including hepatitis, if needles are re-used or are not sterilized. There are a variety of different itchy, red, skin reactions that people can get from tattoo ink, especially red ink, which contains mercury sulfide, and that can be hard to deal with when it happens.

But tattoos don’t have to be forever. Skin lasers can break down tattoo ink within the skin, though the treatments can be painful and expensive. Some say the laser removal is more painful than getting the tattoo. Red tattoo ink is by far the most difficult color to remove and has the highest risk of causing a skin reaction, so avoiding red may be a good choice

And for Geraghty herself? No tattoos. “When I went away to college, my mother told me she would not pay my tuition if I ever came home with a tattoo. So I never did.”

Previously: Skin cancer linked to UV-caused mutation in new oncogene, say Stanford researchers, Ask Stanford Med: A focus on on scleroderma, New study: Genes may affect skin youthfulness
Photo by Norbert von der Groeben

Cancer, Dermatology, Research, Science, Stanford News

Skin cancer linked to UV-caused mutation in new oncogene, say Stanford researchers

Skin cancer linked to UV-caused mutation in new oncogene, say Stanford researchers

sunbathingA link between the UV rays in sunshine and the development of skin cancer is nothing new. We’ve all (hopefully) known about the damage sun exposure can wreak on the DNA of unprotected cells. But it’s not been known exactly how it causes cancers like squamous cell carcinoma or melanoma. Now, Stanford dermatologists Paul Khavari, MD, PhD and Carolyn Lee, MD, PhD have identified a UV-induced mutation in a protein active during cell division as the likely driver in tens of thousands of cases of skin cancer. Although the protein hasn’t been previously associated with cancer, the work of Khavari and Lee suggests it may actually be the most-commonly mutated oncogene in humans.

Their work was published yesterday in Nature Genetics. As we describe in our release:

Lee and Khavari made the discovery while investigating the genetic causes of cutaneous squamous cell carcinoma. They compared the DNA sequences of genes from the tumor cells with those of normal skin and looked for mutations that occurred only in the tumors. They found 336 candidate genes for further study, including some familiar culprits. The top two most commonly mutated genes were CDKN2A and TP53, which were already known to be associated with squamous cell carcinoma.

The third most commonly mutated gene, KNSTRN, was a surprise. It encodes a protein that helps to form the kinetochore — a structure that serves as a kind of handle used to pull pairs of newly replicated chromosomes to either end of the cell during cell division. Sequestering the DNA at either end of the cell allows the cell to split along the middle to form two daughter cells, each with the proper complement of chromosomes.

If the chromosomes don’t separate correctly, the daughter cells will have abnormal amounts of DNA. These cells with extra or missing chromosomes are known as aneuploid, and they are often severely dysfunctional. They tend to misread cellular cues and to behave erratically. Aneuploidy is a critical early step toward the development of many types of cancer.

The mutation in KNSTRN is a type known to be specifically associated with exposure to UV light. Khavari and Lee found the mutation in pre-cancerous skin samples from patients, but not in any samples of normal skin. This suggests the mutation occurs early, and may be the driving force, in the development of skin cancers. As Khavari, chair of the Department of Dermatology and dermatology service chief at the Veterans Affairs Palo Alto Health Care System, explained in the release:

Mutations at this UV hotspot are not found in any of the other cancers we investigated. They occur only in skin cancers… Essentially, one ultraviolet-mediated mutation in this region promotes aneuploidy and subsequent tumorigenesis. It is critical to protect the skin from the sun.

Previously: Master regulator for skin development identified by Stanford researchers and My pet tumor – Stanford researchers grow 3D tumor in lab from normal cells
Photo by Michael Coghlin

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