Merix Pharmaceutical’s Releev Cold Sore Treatment in Convenience Stores
Merix Pharmaceutical Corp’s Releev 1 Day Cold Sore Symptom Treatment is now available in convenience stores, including 7-Eleven and soon in Circle K in the United States. Releev 1 Day Cold Sore Symptom Treatment had already been available in drugstores like Walgreens, CVS, and Rite Aid.
Releev contains Viracea, a proprietary botanical extract formula. Merix says its patented Echinacea Extract with the FDA-approved OTC antimicrobial antiseptic Benzalkonium Chloride is the fastest healing treatment for cold sores known. In a double-blind, placebo controlled, clinical trial, Viracea was found to heal cold sores in as little as one day, Merix reports. In laboratory testing, Viracea was found to be highly active against HSV-1 and HSV-2. releev.com
Revision Skincare Launches DEJ Eye Cream And DEJ Face Cream
Revision Skincare has created two comprehensive products, DEJ eye cream and DEJ face cream, utilizing Pathway Technology and Prebiotic Innovation to provide clinically-proven results and promote long-term skin health, the company says.
DEJ eye cream is intended to address the appearance of dark circles and puffiness around the eye area and is also uniquely formulated for the upper eyelid to improve the appearance of eyelid hooding, while also reducing the appearance of crow’s feet, sagging skin, and crepiness to create the look of more lifted, firmer, and smoother skin around the eye. Revision says the advanced, all-in-one eye treatment is clinically-proven to improve the visible signs of aging around the eye area including the eyelid in as little as four weeks.
DEJ face cream is an intensive, skin-renewing moisturizer with a lightweight feel that addresses visible signs of aging, including sagging and thinning skin, crepiness, fine lines and wrinkles, uneven skin tone, and redness. It is clinically shown to create the appearance of firmer, more lifted, and brighter skin, with results seen as early as four weeks, Revision says. RevisionSkincare.com
Neova Introduces Clinical Recovery Products
Neova SmartSkinCare is launching its Clinical Recovery range of products. The line of six new products is formulated to keep skin calm, soothed, hydrated, and protected following microdermabrasion, laser resurfacing, chemical peels, and laser hair removal treatments for increased rates of healing, optimal skin recovery, improved downtimes, and decreased risks of adverse side effects in post-procedure skin. The formulation contains a revolutionary Copper Peptide Complex based on more than 20 years of scientific research in cellular regeneration that is protected by seven active patents and is clinically shown to enhance healing of dermal wounds, tissue remodeling, and stimulate skin renewal, Neova says.
The six product range Copper Peptide Complex includes Clinical Recovery Cu3 Gentle Cleanser, Clinical Recovery Cu3 Recovery Spray Rehabilitating Mist, Clinical Recovery Cu3 Transforming Gel Recovery Mask, Clinical Recovery Cu3 Tissue Repair Recovery Cream, Clinical Recovery Cu3 Recovery Lotion Comfort Formula, and Clinical Recovery Cu3 Lip Repair.
NEOVA Clinical Recovery range is available at more than 2,500 dermatologist offices nationwide and online. neova.com
Flavor-free Toothpaste and New Concealer from Cleure
Dermatologists report toothpaste flavors containing the mint family as one of the top allergens that result in inflammation and rash around the outside and inside of the mouth, according to Cleure, which offers Cleure Flavor-Free Toothpaste, a flavorless natural toothpaste. Free of mint and other flavors that cause allergies, Cleure toothpaste is also free of additional harsh ingredients such as SLS, propylene glycol, fluoride, and others. It contains added dicalcium phosphate and xylitol to help reverse the initial stages of tooth decay and help with dry mouth. Cleure flavorless toothpaste is also beneficial for sensitive teeth.
The company also introduced a new concealer that it says doesn’t cause flare-ups or irritation. The sensitive skin-friendly Cleure Concealer is a mineral concealer. cleure.com
Therapeutics Focus: Skin Cancer
ACS CMO On Sunscreen Misuse
We are getting it all wrong when it comes to our reliance on sunscreen as the be all and end all protection from skin cancer, says Otis W. Brawley, MD, chief medical and scientific officer for the American Cancer Society in Atlanta.
Sunscreen wasn’t developed so we could all get a free pass to spend the day on the beach. “Ultraviolet (UV) A rays cause melanoma and UV B causes sunburns, and most sunscreens block more B than A,” he says.
This sets us up for melanoma. “People stay in the sun longer when the end result is that they don’t burn, but they are still getting high doses of UVA,” he explains. Sunscreens with higher SPFs may give an even greater false sense of protection, further increasing skin cancer risk by encouraging us to stay in the sun longer, he adds.
“Sunblock is a really a good thing if used appropriately, but like so many good things, when used inappropriately, it can cause harm.”
The best counsel is to stay out of the sun and wear protective clothing including a wide-brimmed hat and UV protective sleeves, he says. “If you can’t wear protective clothing, apply sunscreen on all exposed skin and get our of sun quickly,” Dr. Brawley adds.
Can New App Help Spot Skin Cancer?
Skinder, a dermatologist-developed app, may help medical students learn to spot skin cancer. Skinder works like the matchmaking app Tinder, but instead of considering pictures of potential dates, swiping right if they’re attractive or left if they’re not, users consider high-resolution pictures of lesions, swiping right if they’re benign or left if they’re cancerous. As users categorize each lesion, the app tells them if they’re right or wrong. At the end of the session the app scores their overall accuracy.
Michael Kolodney, MD, Chair of West Virginia University’s Department of Dermatology, developed the app to cultivate intuition in medical students. An initial study suggests Skinder may improve how accurately medical students diagnose melanomas. Study findings appear in JAMA Dermatology.
Thirty-six WVU medical students participated in Dr. Kolodney’s study of the app. None of them had completed a dermatology rotation yet. During the study, half of the participants spent an hour reviewing the “ABCD rule” for identifying melanomas. The other half of the participants spent an hour using the app to rapidly browse through images of lesions and categorize them as malignant or benign based solely on their appearance and without formally applying the ABCD rule.
When the medical students took a follow-up test to see how well they could visually diagnose melanomas, participants who used Skinder scored significantly better than their counterparts who focused on the ABCD rule.
“Dermatologists make their diagnoses based on just looking at a lesion and seeing what comes to mind. The reason medical students can’t do that is they have very limited exposure to dermatology,” says Dr. Kolodney in a news release. “The idea behind the app was to expose them to thousands of images in a short amount of time to develop this intuitive sense.”
Dr. Kolodney thinks the premise of Skinder could be useful in other fields that rely on visual diagnosis, such as radiology and ophthalmology. Eventually he wants to expand Skinder’s photo library and make the app available for free download.
Melanoma Research Alliance Seeks Proposals, Funding Available
The Melanoma Research Alliance (MRA) is soliciting proposals that address the gap in translational science. Successful proposals have the potential of applying important basic and preclinical discoveries to the near-term development of clinical trials and studies impacting melanoma detection, prevention, diagnosis, staging, and/or treatment.
Proposals for clinical studies testing well-defined and clearly articulated hypotheses are welcome and should be accompanied by a brief protocol synopsis and timeline with milestones. IRB approval is not required at the time of application but is required before initial payments are made. MRA (www.curemelanoma.org/assets/Uploads/MRA-2018-2019-RFP-FINAL.pdf) welcomes proposals in these areas:
- Prevention: Elucidation of environmental, epidemiological, and biological factors in melanomagenesis that lead to prevention strategies.
- Detection, Diagnosis, and Staging: Development of targeted screening methods and identification and validation of diagnostic and prognostic biomarkers.
- Treatment: Projects emphasizing the translation of scientific findings to new treatments for patients with melanoma. Examples include, but are not limited to, studies of melanoma immunotherapy, therapeutic applications based on molecular mechanisms involved in melanoma formation and/or progression, combination therapies, and development of novel biomarkers of response to therapy.
There are also Special Emphasis Areas for the 2018-2019 cycle, which are focused on current unmet clinical needs in melanoma.
Novel Epigenetic Mechanism May Cause Drug Resistance in Melanoma
New research sheds light on epigenetic reasons for drug resistance in melanoma, and identifies potential therapies that may prevent such resistance, according to a paper in Nature Communications.
Mount Sinai researchers identified a novel epigenetic mechanism that causes resistance to the standard treatment in melanoma patients with mutations in the BRAF genes, which are found in about half of all melanomas. Researchers also found a biomarker for this drug resistance: a gene called IGFBP2, which is also associated with poor prognosis in melanoma patients.
Patients with high levels of IGFBP2 could benefit from combination therapies, which could be created in response to these findings, that inhibit BRAF mutations and IGFBP2-driven biological pathways as a multi-pronged approach to preventing drug resistance or reversing it once it has occurred, the study suggests. Other studies show the potential to find IGFBP2 via urine samples so the implications for detection and later treatment are large.
This research was funded by La Roche-Posay North American Foundation, American Skin Association, Pershing Square Sohn Cancer Research Alliance, and the U.S. Department of Defense.
Researchers Identify Cause of Aggressive SCCs in RDEB
Immune system-related enzymes contribute significantly to the development of aggressive and fatal squamous cell carcinomas early in the life of individuals with recessive dystrophic epidermolysis bullosa (RDEB), an international team of scientists led by researchers at the Sidney Kimmel Cancer Center–Jefferson Health finds. The discovery identifies new therapeutic strategies and reveals how chronic inflammation can spur cancer.
“We’re describing for the first time a mechanism that instigates tissue damage-driven cancers,” said senior author Andrew South, PhD, an associate Professor in the department of Dermatology and Cutaneous Biology at Jefferson.
Dr. South and colleagues wanted to figure out why squamous cell carcinoma (SCC) is so frequent in RDEB patients and what makes it so aggressive.
When the researchers examined the genetic sequences of RDEB patients’ tumors, they found a group of enzymes called apolipoprotein B editing complex (APOBEC) caused a large proportion of the cancer’s mutations. These proteins help our immune systems by editing nucleic acid messages in pathogens, and in us. When APOBEC enzymes edit our DNA’s messages, they increase the diversity of antibodies available to fight off infection. In RDEB patients, inflammation from continued tissue damage and the persistent threat of microbial infection ratchets up APOBEC expression, leading the enzymes to attack the patient’s DNA, which then creates cancer-causing mutations.
In fact, DNA changes from APOBEC account for 42 percent of mutations in an RDEB skin tumors. In most people with skin cancer, APOBEC is much less active, making up about only about two percent of the mutations in tumors. The finding means these APOBEC alterations distinguish RDEB skin cancer from the kind caused by sunlight. And since RDEB skin tumors develop in places with chronic wounds, the discovery further provides a mechanism for how inflammation and tissue damage spur cancer progression.
Dr. South and colleagues then looked at which genes turn off or on and by how much in RDEB skin tumors compared to SCCs in other tissues. When researchers grouped genes that perform similar biological functions, they discovered RDEB skin cancers share more in common with those that develop in the oral cavity than cancer that develops in the skin from UV exposure. The finding reveals RDEB skin cancer acts more like SCC of the oral cavity than the skin. Dr. South’s discovery suggests therapeutic approaches for oral cancer might be effective against RDEB skin cancers.
The research appears in the journal Science Translational Medicine.
As a result of the new work, the Department of Defense recently awarded Dr. South a grant for nearly $1.75 million USD to figure out what turns APOBEC enzymes on and to look for compounds that disable them.
Frequent BCC Linked to Other Cancers
Basal cell carcinoma may increase risk for the development of other cancers, including blood, breast, colon, and prostate cancers, according to a preliminary study by researchers at the Stanford University School of Medicine.
The researchers, who published their findings in JCI Insight, studied 61 people treated at Stanford Health Care for unusually frequent basal cell carcinomas—an average of 11 per patient over a 10-year period. They investigated whether these people may have mutations in 29 genes that code for DNA-damage-repair proteins.
They found that about 20 percent of the people with frequent basal cell carcinomas have a mutation in one of the genes responsible for repairing DNA damage, versus about three percent of the general population, a finding they described as “shockingly high.”
Furthermore, 21 of the 61 people reported a history of additional cancers, including blood cancer, melanoma, prostate cancer, breast cancer and colon cancer—a prevalence that suggests the frequent basal cell carcinoma patients are three times more likely than the general population to develop cancers.
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