Need-to-know updates featured in articles, news briefs, podcasts, and videos keep everyone in the dermatology community in the vanguard of the effort to put a cure for melanoma within reach.

Melanoma Awareness Month

Acne Awareness Month

This online, on-demand virtual symposium brings together renowned experts in dermatology to discuss newer treatments for patients with psoriasis.

Maui Derm Tyk2 Psoriasis Archived Webcast

Patients with this rare and severe skin disorder may soon have a new therapeutic option.

Perspectives on Generalized Pustular Psoriasis

John Jesitus is a medical writer based in Westminster, CO.

A mouse model under development one day may unlock the role of adenomatous polyposis coli (APC) mutations in melanoma brain metastases. A $100,000 pilot award from the Melanoma Research Alliance (MRA), Washington, DC, will allow University of Minnesota researchers to lay groundwork for additional future funding.1

“What this means is, we can afford to do the initial development of the tools, model, and resources so that we can apply for multimillion dollar federal research funds. Without this award, we wouldn’t be able to do that,” said lead investigator James Robinson, PhD. He is assistant professor at The Hormel Institute, University of Minnesota in Austin, Minnesota.

Immune checkpoint inhibitors have revolutionized melanoma treatment, but few patients experience complete responses. Patients with mutations in the APC and beta-catenin genes suffer from a higher incidence of brain metastases than do patients without these mutations, which can alter cell growth, identity, movement, and death. However, Robinson said, it is unclear whether these mutations drive metastatic development, particularly to the brain, which remains a common point of checkpoint-inhibitor failure.

If one could identify patients with APC mutations sooner, he said, such patients may benefit from more aggressive treatment or mutation-specific treatment. Because APC mutations reside in the relatively well-understood Wnt signaling pathway, Robinson added, many drugs already in clinical trials or under investigation for other diseases could merit melanoma trials, depending on which mutations investigators choose to target.

The team has developed a unique mouse model for use in this research.2 In transgenic mouse models, tumors arise over time from multiple cells. Conversely, Robinson and colleagues use a chicken virus to produce melanoma from melanocytes. “We can put in different genetic alterations, such as these mutations we’re studying, or the typical mutations found in melanoma—for instance, BRAFV600E or deletion of PTEN—and study the whole melanoma from the point of initiation.” Once investigators have preliminary data from this project, they plan to screen melanoma samples nationally for the presence of these mutations and to ascertain whether and why these mutations are causing metastases.

“In human samples,” Robinson said, “you can look to see what actually happens in the patients with mutations. But it’s hard to do a direct, controlled experiment because there are obviously thousands of different changes that occur in tumors, and melanomas are the single most mutated human tumor. So it’s sometimes hard to see the woods for the trees.”

The mouse model allows researchers to ask direct questions such as such as how changing one base pair in a single gene impacts a melanoma tumor. “We’re going to look at all the immune components of the brain metastases in the primary tumors using state-of-the-art genomic techniques that allow you to interrogate different populations of tumor cells and normal cells within the tumor.” For example, antibody assays will allow investigators to differentiate the CD45 immune-cell component from the melanoma-cell component of the tumors.

Multiplexed ion beam imaging (MIBI) technology will enable investigators to screen up to 40 antigens simultaneously, using 40 antibodies at once in a paraffin-embedded tissue slice to explore whether immune changes or changes intrinsic to APC-mutated cancer cells themselves are driving metastases. “Are the cancer cells growing? Are they more motile, more invasive? Or do they survive in circulation to become metastatic cancer cells, as opposed to primary tumor cells? None of this is known.”

Working from a single paraffin block which may contain pieces of tumors sampled decades ago, the MIBI process will allow researchers to place a section of tumor on a slide, then use PCR DNA sequencing and, if necessary, whole genomic sequencing to determine what mutations and cell populations (such as CD4 and CD8 T cells and macrophages) are present. “The point of the pilot grant is to produce the model and pilot these technologies in a small number of samples so we can persuade the National Institutes of Health (NIH) to award sufficient funds to be able to do it on a national basis.”

With any study of this kind, Robinson said, key elements include securing samples from as many centers as possible and having the funding and ability to perform the actual screening, along with the mouse experiments. His team plans to begin applying for federal funding in October.

“The way that pilot grants work,” he said, “you usually expect not to get NIH funding the first time around.” Therefore, Robinson hopes that a February 2023 submission finds success. “If not, we have the other year of MRA funding, so we can continue to take this forward and apply in 2024 too.”

Robinson reports no relevant financial interests.

1. Melanoma Research Alliance. Melanoma Research Alliance announces $13 million in grants to advance melanoma prevention, detection & treatment.https://www.curemelanoma.org/assets/Uploads/MRA-Grant-Awards-2022.pdf. May 19, 2022. Accessed June 16, 2022.

2. Grigore F, Yang H, Hanson ND, VanBrocklin MW, Sarver AL, Robinson JP. BRAF inhibition in melanoma is associated with the dysregulation of histone methylation and histone methyltransferases. 

. 2020;22(9):376-389. doi:10.1016/j.neo.2020.06.006

Articles

A grant from the Melanoma Research Foundation powers the initial stages of the project.

Mouse Model May Shed Light on APC mutations in brain metastases

 What’s the difference between a biosimilar and a reference product?

They are just that. The reference product is usually the originator biologic, the one that did large-scale pivotal trials, often placebo-controlled or active comparator studies, competitor studies, or some type of standard of care. We’ve been using a lot of these molecules for decades. For example, etanercept and infliximab were approved in the late 1990s. Then the biosimilar product is a manufactured biologic process that, as you mentioned, doesn’t differ chemically or structurally in any important ways from the originator product, and then clinically has demonstrated very similar safety and efficacy.

 The only thing I’ll add is that I’d emphasize the point that the active part of the molecule of the biosimilar and the reference product are exactly the same. There may be a difference in folding. There may be a difference in glycosylation. That’s like the difference with a generic drug. A generic drug is a small-molecule chemical. It’s very easy to manufacture, and it’s identical to the brand product. The difference may be the excipients, or it may be a red pill vs a blue pill, but they’re exactly the same inside. It’s the same thing with the reference product and the biosimilar. The active moiety of the molecule is exactly the same, though there may be differences in things like folding and glycosylation.

Videos

Drs Roy M. Fleischmann and Joel M. Gelfand discuss differences between biosimilars and reference products.

Difference Between Biosimilars and Reference Product

, “A Game-Changer in Chronic Inflammation Management.” I’m Dr Roy Fleishmann, a clinical professor of medicine at the University of Texas Southwestern Medical Center, and co-medical director of Metroplex Clinical Research Center in Dallas, Texas. I’m joined by Dr Joel Gelfand, the vice chair of clinical research, the medical director of the dermatology clinical studies unit, the director for the psoriasis and phototherapy treatment center, and a professor of epidemiology in biostatistics and epidemiology at the University of Pennsylvania School of Medicine in Philadelphia, Pennsylvania. He’s also the James J. Leyden, MD, Endowed Professor in Clinical Investigation.

In this discussion, we’ll highlight the regulatory process to approve a biosimilar, highlight the use and impact of interchangeable biosimilars, and discuss how biosimilars can alter the treatment landscape in chronic conditions. Let’s begin.

Let’s start with a discussion. What is a biologic, and why are they very complex to manufacture? Unlike traditional DMARDs [disease-modifying antirheumatic drugs], which are small-molecule chemicals, biologics are produced by biotechnology and are genetically engineered to act like natural proteins in the immune system. Because they are proteins, they must be delivered by intravenous infusion or injection. If taken orally, they’ll be digested in the gastric system. They are highly specific and target a specific pathway of the immune system. Some may be monoclonal, chimeric, or humanized fusion antibodies, whereas others are receptors that have been fused to part of the immunoglobulin.

How is a biosimilar defined? A biosimilar is a biological product that’s approved based on the totality of evidence demonstrating that it’s designed similar to the approved biological product, or the originator or reference product, in terms of structure, function, quality, purity, potency, clinical efficacy, and safety.

What is the regulatory process or requirements to create a biosimilar? How is a biosimilarity study conducted? For the FDA and the EMA [European Medicines Agency], the goal of a biosimilar development program is to demonstrate biosimilarity between the proposed biosimilar product and the reference product, not to independently establish the safety and effectiveness of the proposed product. The manufacturing proposed by a similar product generates an array of data comparing the proposed product to the FDA-approved reference product to demonstrate biosimilarity. Comparative data are generated and evaluated in a stepwise fashion that begins the foundation with detailed analytical, structural, and functional characterizations and comparison of the products, moving on to animal studies if necessary and then to comparative clinical studies.

Consequently, rather than generating the same full profile of nonclinical and clinical data as the reference product, a manufacturer that shows its proposed biosimilar product is highly similar to and has no clinically meaningful difference from the FDA-approved reference product may rely in part on the FDA’s previous determination of safety and effectiveness for the reference product for approval. Joel, what does this mean in English to the practicing rheumatologist or dermatologist?

Roy, that’s a nice overview of a complicated topic. The way clinicians need to think about it is that essentially a biosimilar product is just that. It isn’t identical, but the variation in the protein structure or glycosylation isn’t meaningfully different in any way. The chemical analysis done basically shows that any variation isn’t in the critical domains of where the biologics target the molecule, such as TNF [tumor necrosis factor].

There are a variety of ways that these therapies are studied. We could discuss that in more detail. Some studies look at only 1 disease. It might be only RA [rheumatoid arthritis]. Other studies may look at a multitude of diseases, such as psoriasis, RA, and inflammatory bowel disease. The agency is looking for a margin of what they say is noninferiority. Usually it’s about 15%, that the patients get the same outcome within 15% of one another. That would be a similar enough outcome. One biosimilar product shouldn’t necessarily have a better or worse outcome than the originator product.

 The FDA sets regulations to demonstrate biosimilarity. The biosimilar product application must include data demonstrating biosimilarity to the reference product, which usually includes data from the analytical studies, and as Joel said, demonstrated biologic properties similar to the reference product, notwithstanding minor difference in clinically inactive components. Then there are animal studies, including assessment of toxicity. Then, as Joel said, it could be a clinical study or studies sufficient to demonstrate the safety, purity, and potency of the proposed biosimilar product in 1 or more of the indications for which the reference product is licensed. This also typically includes assessing immunogenicity, pharmacokinetics, and in some cases pharmacodynamics. It also usually includes a comparative clinical study.

Roy M. Fleischmann, MD and Joel M. Gelfand, MD, MSCE, FAAD define the terms biologic and biosimilars and discuss how they are developed.

What are Biologics and Biosimilars, and How Are They Devolved?

The US Food and Drug Administration (FDA) has approved ustekinumab (Stellara; Janssen Pharmaceutical) for the treatment of active psoriatic arthritis (PsA) in pediatric patients. Ustekinumab is the first and only biologic that targets both cytokines interleukin (IL)-12 and IL-23.

 PsA is a rare disease that mimics adult PsA and affects 5%-8% of children and adolescents that suffer from chronic inflammatory arthritis. 

Since the first approval for adults with moderate to severe PsA in 2009, 2 out of the 4 indications for ustekinumab now include pediatric patients to further expand its treatment reach. Ustekinumab is a fully monoclonal antibody that selectively inhibits interleukin (IL)-12 and IL-23. Medical professionals recognize that both cytokines are important to calm down the overactive inflammatory response in many autoimmune diseases.

Ustekinumab is injected subcutaneously 4 times per year after 2 initial starter doses. The approval is based on pharmacokinetic (PK) data and the conclusion of the efficacy and safety of ustekinumab in multiple phase 3 studies in adult and pediatric patients with moderate to severe plaque psoriasis (PsO) (PSTELLAR, CADMUS, and CADMUS Jr) and adult patients with active PsA (PSUMMIT I and II). Data showed that PK exposure of ustekinumab in pediatric PsO patients with active PsA was consistent with phase 3 clinical trials of ustekinumab in pediatric PsO patients without active PsA, as well as with adult patients with moderate to severe PsO or adult patients with active PsA. Data on similar efficacy endpoints were similar in the pediatric PsO patients with active PsA.

Symptoms of pediatric PsA include joint inflammation and skin lesions. Overall, pediatric PsA is difficult to treat and needs a standardized treatment option. Some common adverse events of ustekinumab include nasal congestion, sore throat, runny nose, headache, itching, stomach pain, and joint pain.

Johnson JPC of J&J. Stelara (Ustekinumab) approved by the US food and drug administration to treat pediatric patients with active psoriatic arthritis. Accessed August 1, 2022. 

https://www.prnewswire.com/news-releases/stelara-ustekinumab-approved-by-the-us-food-and-drug-administration-to-treat-pediatric-patients-with-active-psoriatic-arthritis-301596940.html

Janssen Pharmaceutical Companies of Johnson & Johnson announced the approval of ustekinumab as a new treatment option for patients aged 6 years or older with active psoriatic arthritis.

Ustekinumab Approved by the FDA for Pediatric Patients with Psoriatic  Arthritis

 provides a dermatologist's skin care routine for eczema and 

 dissects the misinformation associated with clean beauty and 

A Dermatologist’s Eczema-Approved Skincare Routine

Experts Swear by These Hyaluronic Acid Serums for Hydrated, Supple Skin

Clean Beauty Has a Misinformation Problem

Here’s Every State That Has Passed the Crown Act

13 Reasons Why You Need A Skincare Fridge

Space Explorer Dr. Sian Proctor Shares Her Beauty Routine

This week's edition of the Mainstream Patient features stories about skin care for eczema, clean beauty misinformation, the Crown Act, skin care in space, and more.

The Mainstream Patient: August 1 

Dustin Portela, DO, a board-certified dermatologist and dermatologic surgeon at Treasure Valley Dermatology in Boise, Idaho.

Dustin Portela, DO, a board-certified dermatologist and dermatologic surgeon at Treasure Valley Dermatology in Boise, Idaho, visits the La Roche-Posay Thermal Treatment Center in France to discuss beneficial eczema treatments. 

Opinions expressed are that of Portela and do not express the views or opinions of Dermatology Times®.

In this week’s Pointers with Dr Portela, the 208SkinDoc travels to the La Roche-Posay Thermal Treatment Center. 

Pointers with Dr Portela: 5 Treatments That Fix Eczema at the La Roche-Posay Thermal Treatment Center

I’m going to put you 2 on the spot. I’m going to ask you, Omar, to give me the synopsis of the mechanism of action [MOA] of biologics. Angela, I’m going to give you the same question for JAK [Janus kinase] inhibitors. Omar, you go first. I’m the average Joe patient who comes in, or I’m the average Joe dermatologist at 1 of your lectures. How would you describe the MOA of the biologics?

When it comes to the biologics, and when it comes to atopic dermatitis, we’ve identified that in the immune system, in its simplest form, there’s a Th1 and a Th2 phenotype of patients. The Th1 phenotype is more psoriasis related, with cytokines associated with psoriasis. The Th2 phenotype has cytokines associated with atopic dermatitis. When diving deeper into these different cytokines that are producing the inflammation we see with eczema, we see IL-4, IL-13, TSLP, and IL-31. I’ve grown up with pharmaceutical industries creating medications to targets, which has then allowed me to better appreciate the immune system. IL-4 and IL-13 are specifically involved in different factors of eczema, whether it’s B-cell class switching or antimicrobial peptides, increasing the risk of staph infections in our atopic patients. Beyond that, beyond producing the inflammation, these IL-4 and IL-13 are also involved in barrier disruption. When we target these cytokines with biologics like dupilumab, tralokinumab, and future biologics that come to the market, we can minimize the immune system’s response to these cytokines and their downstream effect. That’s essentially how we’re minimizing the phenotype of these atopic patients and how it translates into clinical practice.

That’s excellent. It brings into the light the targeting of the immune mechanisms and where things are at, in terms of blanketing vs going after the process.

Angela, I’ll give you the same charge for the JAK inhibitors. Feel free to include the topical ruxolitinib also. I didn’t mean to overlook that. I want to hear your progression of how we’ve gone form crisaborole and tacrolimus to topical ruxolitinib and obviously how the 12-year-old upadacitinib indication is helpful. Give us the nuts and bolts with some of those descriptors.

The first thing is understanding the JAK-STAT [signal transducer and activator of transcription] pathway and how the interleukins that bind to those, where you don’t have the JAK inhibitors, upmodulate and regulate some of the phenotype we see in atopic dermatitis. You see the lichenification, you see the itching, and you see that whole itch-scratch cycle. What’s beautiful about these JAK inhibitors is they go in and block that pathway. They pretty much prevent the formation of those cytokines at the nuclear level. That all trickles down. What makes the JAK inhibitors so different is that they block the whole process, and that’s why you see some of those adverse effects, because several of the more nonspecific ones inhibit the B-cell and T-cell proliferation. That’s why we see some of the hematopoietic adverse effects. I find them incredibly exciting, and it all comes down to that JAK-STAT pathway and production in the nucleus.

That fits right into 1 of my favorite analogies: turning off the faucet vs mopping up the mess, because you’re stopping the process in its tracks to some degree. That’s something you can talk to parents about. You tell them we’re going to try to prevent what’s coming. Even though you don’t want to put it into a context of prevention and a cure, you want to say we’re trying to stop the process rather than just the result.

Based on that, Angela, is there anything about any of the topicals or the systemic agents we talked about that would be a barrier in talking about with different racial groups or different ethnic groups? We touched on that, but now we’ve put the MOA in there.

You mentioned filaggrin. You mentioned some of the other issues that go along with this. Is there anything else that we should be focusing on? Omar, I’ll ask you the same thing: is there anything else we’re missing?

 For some of the newer ones, the biggest is this idea that you definitely have to do lab checks. What I liked about dupilumab was what you just basically said: there are some potential adverse effects but no labs. The minute you start telling people we may have to check your lipids—we’re going to make sure you don’t have TB [tuberculosis], we have to check your liver—that can throw people off. Those are harder conversations to have. When I talk to patients or when I’m doing decision trees in my mind about which 1 to select, these are often patients I know well. Frankly, I’m influenced by which person is going to be more put off by an injection every so often vs a pill—daily, no injection, but some labs. With those conversations, even if I think 1 may work better, the potential side effects are definitely things I have to think about.

That’s pretty encompassing. Playing defense is what we do pretty much all day, so it would be nice to get past that and get some things through. Omar, how would you take on that same question?

This discussion is important because it’s allowing us to know, as Angela referred to earlier, that not every person is the same. People ask me all the time, “What’s the first medication you use, and why?” I tell everyone there’s no first-medication algorithm; every person is different. I’m not a vending machine, right? If a patient comes in with atopic dermatitis, I don’t just put in A6 and you get the first medication, and then if that medication fails, you get the second medication. That’s not the world that we live in. Everyone is built differently. Every situation is different. A lot of things go into it. There are patient preferences and cultural biases that we talked about. There are genetic susceptibilities that patients will do better with 1 medication vs the other.

By having this discussion about skin-of-color patients, we increase our knowledge and our education to target patients into better treatment. Unfortunately, at this moment in time, we can’t be so specific to say what medication brown patients will respond to, White patients will respond to, or Black patients will respond to. That doesn’t exist; however, we’re working to that goal. What I want my patients to know when I choose a medication for them is my comfort level with that medicine in patients I’ve used it on—what I’ve grown to see in my patients through a multitude of skin types, and what they should expect to see. When they understand that in a very communicative way, they can appreciate what I think is going to happen and then we go from there. It gets back to better communication, which plays a large role.

That’s a good example. It reminds me a lot of how we talk to people with darker skin types about sunscreen. Everyone has a preconceived notion:” I don’t need to do that. I’m already dark.” That doesn’t mean a thing. We don’t want to take apples and oranges away from the discussion of anyone who’s lighter or darker. It’s more about getting to the process. Let’s think about the fundamentals and get what’s under the hood with all that. I go back to that analogy about the cost of not treating patients. You have to talk to them about the cost of not treating all facets of your disease, whether it’s the moisturizing, the anti-itching, and everything else that goes with it.

Drs Noor and Lamb discuss mechanisms of action of biologics and JAK inhibitors and the importance of patient communication while selecting AD treatments.

Mechanism of Action and AD Treatment Selection in Patients With Skin of Color

Angela, I want to ask you about your approach with kids. How much different will it be compared with what we do with adults? Obviously, the 2 JAK [Janus kinase] inhibitors out are for 12- and 18-year-olds. Upadacitinib is 12, abrocitinib is 18, dupilumab is now 6 months, and tralokinumab is still 18. But then we go back to the basics, like crisaborole, tacrolimus, or even steroids. Is there going to be much of a difference in the way we approach kids compared with what we’ve had with adults until now?

I’ll be honest, especially with this new armamentarium, I won’t change necessarily my approach, except for the parents. Parents are the biggest barrier. The only thing I might have to get around is, do I think this person has severe enough penetration of disease that I want to have that conversation with a parent of a 12-year-old or a 6-month-old to say, “Let’s maybe try an oral. Let’s try an injection.” That’s an easier conversation to have with an adult who’s treating themselves than it is to have with a parent if someone has a burden of disease where topical medications are appropriate. You mentioned several. I have almost no difference in how I manage those patients. But when we’re talking about severe disease—high EASI [Eczema Area and Severity Index] scores or IGA [Investigator Global Assessment]—those are the folks with a child about whom I have to think twice before having that conversation, or if I think I can get them where they need to be with the topicals.

It’s interesting because 1 thing we tend to forget is the moderate patient. The severe patient makes all the headlines, but it’s that moderate 10% to 20% that we would otherwise be giving prednisone to or throwing steroids at. We forget about that patient. I joke sometimes that it’s the patient who’s at the traffic stop and scratching, or the 1 sitting in their cubicle, who can’t think about anything but their itching. But the moderate patient is probably still walking and talking. Omar, this is not just with treating kids, but in getting over the hump, is anything a driving factor? Who’s a shot patient? Who’s a pill patient? Should we always be treating from the top down, is there anything that’s a driving force behind that?

My No. 1 criterion is that I want to get you better. I tell every patient that my goal is to get you better, but I also want you to be on the least amount of medication to stay better. Because of that, we’re looking at efficacy, but we’re also looking at that safety profile. For that moderate patient sitting in the car, I like to give a scenario: it’s a beautiful summer day, you’re in the pool in the morning, you go for lunch, you’re eating a burger, you’re sitting there for 2 hours, maybe you have a beer. Suddenly, you just start shifting in your seat, your swimming trunks get a little itchy, and you’re shifting. For some of our patients, that’s the best that they feel in their entire life. Flip that around, we’re in New York City. Imagine shifting in your seat like that when you’re in a boardroom discussing a $44 billion sale of Twitter. If you’re shifting and uncomfortable, you can’t focus. In this world, in the United States, you have to be on your game 100% of the time. If you’re not, then we need to fix that. For a patient like that, even though they may not technically fall into the right bucket for body surface area, that’s a shot patient because I want to improve your itch. I want you to be on a medication that’s easy for you to use, where you’re injecting it twice a month, in an adult. I want to see the improvement. From a safety profile, I want to feel comfortable prescribing it to you.

Those are great examples. I have a lot of patients in the Navy and Marine Corps, and it’s exactly that. You’re in your uniform on duty, and the last thing you need is something else.

Drs Lamb, Noor, and Bhatia discuss their approach to selecting treatment in light of recent AD approvals.

Approaching Treatment Selection in AD

Marketing a practice wasn’t likely part of your medical education, but being able to market yourself is an important part of running any business. Beyond traditional advertising there are other ways you can market your practice and connect with your patients, potential patients, and colleagues.

You may be on Facebook, LinkedIn, or Instagram, but is your practice? Also, if you have social accounts are you sharing them on your website or advertising them in your practice?

You can set up company pages that describe your practice, they also connect all your employees. You ought to at least set up the page, add your logo and basic information. It’s also a great place to share videos, articles or other information for potential patients. Need examples of what to do? Check out 

You can have a company page on Facebook as well. It’s a great place to share photos of company events, community service, or employee milestones. It also allows you to connect with patients and employees in a more casual environment. Also, if you’re looking to bring in new patients, look at Facebook promotion options. You can target your audience and spend as little or as much as you like to reach more people. Check out 

Facebook and most of the other platforms offer options for paid promotion of your posts if you are wanting to target your posts to a particular audience.

If sharing what you do through images and video makes sense, Instagram and TikTok or other photo and video sharing apps may be worth spending time on. Instagram and TikTok are usually less formal and may utilize casual videos with helpful information or just be for fun. Check out what 

YouTube is great for longer form videos or as a repository for all of your video content. For example, in our business we share physician spotlights on different elements of working locum tenens. Others that have good YouTube pages are 

As a physician you are an expert in your field. You may have written research papers or submitted to medical journals, but have you looked for other ways to share your expertise? Company blogs are a great place to share information on what your practice is doing, your latest service offerings, or medical topics that would be relevant to your patients. Sharing that expertise through blogs is another way to bring attention to your practice and establish your credibility. Check out 

 for great examples of healthcare focused blogs.

Not interested in writing a regular blog but still have thoughts you want to share. Many online healthcare publications accept submissions on a variety of clinical and non-clinical topics. Check first with the sites you regularly read and then expand out looking for sites that match the audience you are trying to reach. Also, professional specialty organizations often have opportunities for their members to submit articles, so that is another place to check.

Lisa Grabl is president of CompHealth, the nation’s largest provider of locum tenens physicians and founder of the traveling physician industry. She joined CompHealth in 2001 as a sales consultant and served in a variety of management roles prior to being named president in 2017. Lisa is passionate about building lasting relationships and helping her team members reach their highest potential.

This article was published by our sister publication Medical Economics.

Harnessing digital marketing tools can help your medical practice grow.

Marketing Tips for Your Medical Practice

Phase 3 results of the Fluorescent Light Activated Synthetic Hypericin (FLASH) study

 demonstrated significant reductions in cutaneous T-Cell lymphoma (CTCL) lesion sizes with synthetic hypericin (HyBryte; Soligenix) treatment. These findings provide hope for a new treatment to patients diagnosed with the life-altering disease. As a chronic type of cancer that severely impacts patients’ quality of life, there is an unmet need for a well-tolerated and safe treatment option. The FLASH study is the largest double-blind, randomized, placebo-controlled clinical trial for CTCL to date.

The study data also showed that the treatment response continued to improve over 6-week treatment cycles. The main end point of the study evaluated the Composite Assessment of Index Lesion Severity (CAILS) of three specific lesions and the success was determined as ≥50% reduction in CAILS score relative to baseline. Patients reported that their lesions continued to reduce throughout the treatment cycle. After the first 6-week treatment cycle, 16% of patients had a response (p=0.04 versus patients with 6 weeks of placebo treatment). The response rate continued to increase to 49% through 18 weeks of treatment (p<0.0001 versus patients with 6-week hypericin or placebo treatment).

Synthetic hypericin is a novel photodynamic therapy that uses safe, visible light for activation. The drug is topically applied to skin lesions and activated with visible light 16-24 hours after. The US Food and Drug Administration has granted orphan drug and fast track designations for the groundbreaking treatment.

Data throughout the study indicated that synthetic hypericin was safe and well-tolerated, while current treatment options for CTCL have significant safety concerns and black-box warnings. Synthetic hypericin will offer safer long-term options to patients. CTCL is a class of non-Hodgkin's lymphoma (NHL), a cancer of the white blood cells. Unlike other NIHLs, CTCL is caused by an expansion of malignant T-cell lymphocytes which normally migrate to the skin. There is currently no cure for CTCL.

Kim EJ, Mangold AR, DeSimone JA, et al. Efficacy and Safety of Topical Hypericin Photodynamic Therapy for Early-Stage Cutaneous T-Cell Lymphoma (Mycosis Fungoides): The FLASH Phase 3 Randomized Clinical Trial. JAMA Dermatol. Published online July 20, 2022. doi:10.1001/jamadermatol.2022.2749

Hybryte cutaneous t-cell lymphoma (CTCL) treatment. Soligenix. Accessed July 29, 2022. https://www.soligenix.com/pipeline-programs/hybryte-for-cutaneous-t-cell-lymphoma-ctcl/

Soligenix announces positive phase 3 results from FLASH study for the use of synthetic hypericin to reduce cutaneous T-cell lymphoma lesions.  

Pointers with Dr Portela: 5 Treatments That Fix Eczema at the La Roche-Posay Thermal Treatment Center

Mechanism of Action and AD Treatment Selection in Patients With Skin of Color

Approaching Treatment Selection in AD

Marketing Tips for Your Medical Practice

Study Reveals Successful Results for Treatment of Cutaneous T-Cell Lymphoma

Perspectives on Generalized Pustular Psoriasis