Unless this is your first time to this blog (and if so, hi; take a look around and ignore the sarcasm long enough to realize I am actually a nice person), you know that I use a lot of pixels to chat about immunotherapy.
What you may not know (I honestly didn’t), is that apparently there’s a classification for melanomas that respond to immunotherapy. In a very strange version of the Hot or Not game, melanomas can either be hot – i.e. respond to immunotherapy to guide the immune system to destroy it – or cold (not) – i.e. immunotherapy provides little benefit. If your melanoma is hot, I suppose that’s good news in a way; although the best news would be if your melanoma was non-existent…
Anyway, the issue for melanoma patients and their doctors is that up to 50% of melanomas are cold. And I guess the even bigger issue is that there is currently not an effective test to prove one way or the other which type of melanoma you have. So the doctors administer immunotherapy and hope for the best. That can be very expensive in terms of time and money spent waiting to see if there’s any benefit or not.
So researchers at the University of Colorado Cancer Center are hoping that they might be able to solve the riddle of the “Hot or Not” question. According to a study presented at the American Association for Cancer Research Annual Meeting 2019 (that is a mouthful), they noted this intriguing finding: mutated tumors with genes that over-activate Nf-kB signaling pathways were more than three times likely to respond to anti-PD1 immunotherapy compared to tumors that didn’t have the Nf-kB signaling pathway activation genes.
Ok, in human terms it means that “hot” melanoma tumors have a tendency to have this mutation that makes the Nf-kB pathways get all crazy like pre-teens at a Bieber show (wait, is he relevant anymore? I’m not keeping up with what the kids are into these days). This might be a way for doctors to predict if your melanoma is hot or not, thereby more effectively determining if immunotherapy is the right treatment option for you.
You may be wondering, what the hell is a Nf-kB pathway anyway? Let’s break it down… Nf-kB stands for nuclear factor (Nf) kappa-light-chain-enhancer of activated B cells (kB). See, clear as mud, right? Now you’re thinking, what the hell does all that mean… Nf-kB is a protein complex, basically a boatload of proteins (does anyone remember that post about proteins – peptides are compounds made of amino acids, get enough amino acids together and a peptide becomes a protein). A protein complex like Nf-kB is a collection of proteins that work together to perform some action. It can get a lot more complicated than that explanation and you’re welcome to dive into the world of covalent bonds if you’d like but I got other stuff I want to do today…
So Nf-kB is a bunch of proteins that work together in your body (and pretty much every animal on the planet) to control DNA transcription, cytokine production and cell survival. If you’re coming down with a cold, Nf-kB is involved. If you’re stressed about an upcoming presentation or exam or meeting with your boss, Nf-kB is involved. If you’re growing new cells, Nf-kB is involved. Basically, Nf-kB is that person you know that gets all her work stuff done, exercises regularly, organizes the girls’ happy hour, and still manages to have a clean house. (I hate those people, seriously, don’t they know the joys of sloth?)
Nf-kB is heavily involved in your body’s immune response. And it’s classified as a “rapid-acting” transcription factor. This means that Nf-kB leaps into action at the first sign of immune trouble. Unfortunately Nf-kB is just like everything else in this imperfect world, it doesn’t always work correctly 100% of the time. Researchers have linked incorrect regulation of Nf-kB to cancer, autoimmune diseases, sepsis, and other undesirable outcomes.
Getting back to the University of Colorado Cancer Center study… If your Nf-kB pathway is overactivated, it may be a predictive tool for doctors to determine whether immunotherapy may work for you. There are some theories on why. One line of thinking is that if you have a tumor that is mutating like crazy, the difference between healthy tissue and the bad stuff is super easy for the immune system to spot and with a boost from immunotherapy, kill it off. Of course, the immune system is crazy complicated and it may be there are more subtle factors at play here.
So the research team looked at samples of melanoma they had from the Colorado Skin Cancer Biorepository, which totaled about 500 samples from 400 patients. They then asked which one of those patients had immunotherapy, looking to see if there was anything in the tumors that responded well to that particular type of treatment. Out of 52 people who got immunotherapy, only 21 had favorable responses to it. And out of those who got benefit from the immunotherapy, 67% had genetic differences associated with the Nf-kB signaling pathway.
As Carol Amato, senior professional research assistant at the University of Colorado Cancer Center said, “What we show is that cancers with alterations that over-activate the NF-kB may better benefit from immunotherapy.” And the really interesting thing is that due to a specific mutation in a negative regulator of Nf-kB (that is, a gene that basically put the brakes on Nf-kB action) called G34E – which in this study was only found in those tumors that responded well to immunotherapy – is that it didn’t matter if the tumor also had BRAF and/or NRAS mutations (which are common in melanoma tumors). In plain English, even if you have BRAF mutations which normally limit the effectiveness of treatments currently in use, looking at your activation of the Nf-kB pathway signaling may be a much better predictor of immunotherapy effectiveness than taking immunotherapy and crossing your fingers (and sadly, that is kinda current state right now).
While this study doesn’t really break new ground on curing melanoma, it does show the potential for a predictive tool for doctors to known whether anti-PD-1 immunotherapy will be effective for your specific instance of melanoma. And anything that can provide even a slightly better margin of error than a coin toss is an improvement.
Ok, as I was typing that title, I was thinking to myself, didn’t I got to high school with Clark Breslow? But actually, his first name is Nate. Hopefully he never needs to read a blog about melanoma, but if he does – what’s up dude? Still got your skateboard?
Anyway, for those of you that actually come to this blog to read about skin cancer stuff, in today’s post I’m going to review the two other melanoma staging models. If you can’t guess by the title of this post, one is called Clark and the other Breslow (and if you couldn’t guess, my brand of sarcasm is likely lost on you as well).
OK, let’s start with the news that the American Joint Committee on Cancer (AJCC) staging system no longer uses these staging classifications because the TNM model described in the last post has replaced them. BUT, some dermatologists or pathologists still refer to these numbers in their biopsy reports (mine did in 2014 even though the 2011 AJCC guidelines supposedly did away with Clark and Breslow). So this post may one day be as antiquated as instructions on how to use a rotary-dial telephone.
Both the Clark and Breslow scales measure how deeply the melanoma has penetrated the skin. So going back to the TNM staging, both of these scales measure a portion of the T element (reminder, T is for tumor and both thickness and ulceration are denoted by the combination of numbers and letters following the T).
The Clark scale looks at two things: one, how deeply the melanoma has grown into the skin; and two, which levels of the skin have been effected. Remember the quick anatomy lesson from the last post? Skin is the epidermis, dermis, and the fat layer (called the subcutaneous layer or hypodermis in the stock photo below – sorry for the weird colors, but do you know how hard it is to find a photo that gets as detailed on the skin layers as this one to help illustrate the Clark levels?).
There are five levels in the Clark scale:
Level 1 – melanoma in situ; meaning the melanoma cells are found only in the outer layer of skin, the epidermis
Level 2 – melanoma cells are in the papillary dermis, which is the layer directly under the epidermis
Level 3 – melanoma cells are through the entire papillary dermis and touching the reticular dermis, which is the next layer down
Level 4 – melanoma cells are through into the reticular dermis
Level 5 – melanoma cells have grown into the fat layer
I think you can see why the AJCC did away with the Clark scale. If you’re not extremely well versed on your fine-grained anatomy of the skin layers, the levels are pretty much meaningless – except for 5 because let’s face it, if cancer is staged from 1 being the least worst and 5 being the worst, you know if you have the highest number, things are not good.
So that leads us to the Breslow model. This one is pretty easy to understand in comparison to Clark. The pathologist measures the thickness or how deep the lesion has grown into the skin using a micrometer. You know how in the TNM model your T number depends on how many millimeters deep the lesion has grown? That’s pretty much your Breslow number. Your tumor is 3 mm deep? Your Breslow number is 3.
So while I might complain a bit about the complexity of the TNM model, it actually provides a hell of a lot of information within all of those letters and numbers.
In my previous post, I talked about the new changes to the guidelines for diagnosing and treating melanoma. One of the changes affects the definitions of melanoma stages. But I realized as I was talking about those changes that some people may not know what all of those letters and numbers mean.
To complicate matters further, there are actually a couple of different methods of staging. I’ll talk about those other methods in a later post, but this post is going to focus on what is referred to as TNM staging.
TNM means it defines the Tumor or lesion, Nodes that may be involved, and Metastasis (TNM). Let’s start with T – Tumor. There are actually two components to this element: the thickness of the tumor and ulceration. Thickness refers to how deeply the melanoma has grown into the skin. Ulceration means whether the skin is broken over over the tumor. So when the dermatologist asks you if that suspicious spot bleeds, she’s looking to answer that ulceration question. It used to be that ulceration was denoted by an “a” or “b” after the numbers. The updates have changed that slightly.
So, thickness… keep in mind that thickness here means: how deeply has the melanoma lesion penetrated the skin.
Quick anatomy lesson: your skin is made up of the epidermis, the dermis, and a fat layer (aka fascia).
The epidermis is the outermost layer of your skin and is between 0.5 and 1.5 mm thick. It is not just dead skin cells. The epidermis has immune cells working within it. But there are no nerves or blood vessels in this layer. This is the barrier that protects you from basically everything in the outside world.
The dermis is the next layer and it’s generally 1.5 – 3.0 mm below the surface. This layer has connective tissues and immune cells as well as a network of blood vessels and nerves. When you burn yourself, the burn has to hit the dermis for your body to register the pain. Same thing if you cut yourself. This layer is really about making your skin firm but elastic. It is also the place where the inflammatory processes occur, sending immune cells to combat microbes that somehow have made their way past the epidermis.
Below the dermis is a layer of fat that contains blood vessels but is mostly collagen. This layer is important in making sure that everything can move flexibly (among a whole bunch of other important things).
Ok, back to that T… As mentioned, the updated guidelines address how lesions should be categorized. I’m going to use the new guidelines to define the terms below:
Tis (I’ve sometimes seen this referred to as T0) – this means the melanoma cells are only found “in situ” or within the very top layer of skin. Basically, it’s surface-level melanoma in your epidermis.
T1a – a lesion is less than 0.8 mm deep and is not ulcerated
T1b – under the new guidelines, this can mean one of two things: any lesion, ulcerated or not, with a thickness between 0.8 and 1.0 mm OR any ulcerated lesion less than 0.8 mm thick
T2a – the lesion is greater than 1.0 mm up to 2.0 mm in depth and is not ulcerated; this melanoma is getting into your dermis level
T2b – same thickness as above but the tumor is ulcerated
T3a – the tumor thickness is greater than 2.0 mm up to 4.0 mm and is not ulcerated
T3b – an ulcerated lesion that is between 2.0 mm and 4.0 mm
T4a – any lesion with a thickness greater than 4.0 mm but does not have ulceration; this lesion has likely penetrated through both the epidermis and dermis layers and is hitting the fascia
T4b – an ulcerated tumor with a thickness greater than 4.0 mm
Summing up so far, we’ve looked at how deeply the melanoma has penetrated the skin and whether the lesion is ulcerated. Ulceration has been shown to be an indicator of how your melanoma is progressing; recent research indicates it may predict how your melanoma responds to using an immunotherapy called adjuvant interferon.
OK, moving along to the N. This denotes whether there are melanoma cells in nearby lymph nodes.
N0 – no nearby lymph nodes contain melanoma cells
N1 – melanoma cells are in one lymph node
N2 – melanoma cells are found in 2 or 3 lymph nodes
N3 – 4 or more lymph nodes contain melanoma cells
The N section also contains letters – because what’s a little more complexity to a patient struggling to understand exactly what the diagnosis means, right? In order to severity:
Na – the melanoma in the lymph nodes can only be seen by a microscope or what is referred to as micrometastasis
Nb – obvious signs of melanoma in the lymph node – aka macrometastasis
Nc – the melanoma cells are also in areas of the skin very close to the primary location (what’s called satellite metastases) OR in the lymph channels in the skin (in transit metastases)
Obviously, Nc is not good because it shows that the melanoma cells are migrating away from the primary location of the lesion.
And M simply refers to whether the cancer has spread (i.e. metastasizing).
M0 – the cancer hasn’t spread anywhere else
M1 – the cancer has metastasized
Not to be left out, M1 gets letters too and these are not letters anyone wants to get in their inbox…
M1a – melanoma cells are in the skin somewhere else in the body OR melanoma cells are in lymph nodes far away from the initial lesion
M1b – melanoma cells are present in the lung
M1c – melanoma cells are in other organs OR the melanoma is causing your liver to create a high level of lactate dehyrogenase (high levels indicate tissue damage and/or whether a cancer treatment is working or not)
There you have it, TNM staging broken down. While your dermatologist should spend the time to review your pathology reports with you until you completely understand the implications, it is also a time when you are basically the “deer in the headlights”. Throwing a combination of letters/numbers/more letters at you when your brain is screaming, “What the hell is she talking about?? Am I going to die?” means that the message doesn’t always translate. Or even worse, family members start asking you “what does all this mean” and you’re really not in the mood to play doctor. So if your pathology report is TNM-based, you can just point them to this page…
I’ve had this tab open on my browser for some time, waiting for the day that my headache would subside enough for me to write. But seeing as I will likely have a permanent headache for the foreseeable future (and yes, I did go to a doctor and they told me basically that it was all in my head – har, har), I might as well write this post now.
The American Academy of Dermatology clinical guidelines on the management of primary cutaneous melanoma were last updated in 2011. For an old lady like me, 2011 seems like last week; but in reality, it’s eight years ago (half of today’s pop music I bitch about is made by people who were in elementary school eight years ago… heck, the majority of the Kardashians probably had their original lips and noses back then). And the world of science has advanced quite rapidly in those eight years.
The new guidelines incorporate recommendations from the American Joint Committee on Cancer (AJCC) on a variety of topics, including: staging definitions, biopsy and sentinel lymph node biopsy, pathology, and primary surgery.
Let’s first talk about biopsies as that is the procedure that takes all or a portion of the suspected lesion for lab testing. Obviously I had a biopsy performed that introduced me to the wonderful world of melanoma (I so wish we had a sarcasm font, that would make my life so much easier). The biopsy (actually the lab results from the biopsy, but whatever) allows a physician to definitely diagnose melanoma. It also determines the thickness of the lesion, which is an important consideration for staging (which I’ll talk about in a minute).
The new recommendations call for a complete biopsy of the lesion with up to 3mm margins around the entire spot. It also states that the biopsy should be deep enough to get underneath the base of the lesion. For my Loki, following these guidelines would have basically meant I would have had the excision at the same time as the biopsy. Which would have resulted in a considerable scar “just to see”. Fortunately, the guidelines do allow for partial or incomplete sampling based on the location. For nodular melanomas that grow in thickness or depth, a dermatologist may opt for a partial biopsy rather than digging deep into your tissues to make a diagnosis. But for those of you with superficial spreading melanoma (SSM), your biopsies may include a slightly bigger bullet hole in the future.
Ok, so the leads us to staging. As you probably know, cancer is broken into categories called stages (actually lots of medical conditions are broken out into stages). The stage of melanoma you are diagnosed with greatly impacts your plan of action. Stages can define the thickness (cleverly using a T + a number between 1 and 4 to describe, plus a letter), whether the lymph nodes are involved (which is signified by an N + a number between 1 and 4 plus some more letters), and whether the cancer has metastasized (options are M1 which can also have letters and M0 which doesn’t get letters). The diagnosis you get could be something like this: T3a / N1b / M1a. (In a post in the not too distant future, I’m going to break down further what all of that means. I was going to address here but I think it warrants its own post.)
Anyway, in the new guidelines Stages 1 and 2 got the most updates, specifically regarding that thickness elements. A T1 melanoma was defined as being a lesion that has a thickness less than 1 mm. Under the new guidelines, if you have a lesion that isn’t ulcerated and has a thickness less than 0.8 mm, you would be diagnosed with T1a. (By the way, ulcerated means, does the tumor have broken skin over the top of it and make it scabby or even bloody looking? The “a” and “b” in the diagnosis here denotes that.)
A T1b diagnosis would now mean any lesion, ulcerated or not, with a thickness between 0.8 and 1.0 mm OR an ulcerated lesion less than 0.8 mm thickness. So instead of the “a” and “b” signaling only ulceration in these thinner lesions, it would really mean thickness with or without ulceration.
For all other melanoma T stages, the classification would follow the standard “a” for no ulceration and “b” for ulceration. T2 would be classified if the thickness is greater than 1.0 up to 2.0 mm; T3 greater than 2.0 up to 4.0 mm; and T4 for any lesion with a thickness greater than 4.0 mm.
For someone used to the standard classification system, the only quibble I have is with the T1 staging because of the changes to the “a” and “b” designations for only that stage. I know it would probably cause even more confusion to add something else to the Ts (like T0.5 for those smaller than 0.8 mm with no ulceration), but still… There were no updates recommended for the N or M letters.
OK, onto pathology… these recommendations actually surprised me because in my naïveté, I assumed that these were standard operating procedures… anyway, it is now recommended that the pathologist looking at the biopsied tissue be given information about the patient – things like age, gender, location of the lesion, whether there is a previous history of melanoma, whether the lesion had changed, and such. I get not wanting to taint the pathologist’s independent opinion but I would have thought that the patient’s chart or something would be available to the pathologist anyway. Working in a vacuum without any of that information would make it more difficult to decide if something should get a bit more attention, don’t you think?
And finally, the surgical recommendations… obviously, surgery or excision is recommended after biopsy to ensure complete removal of the melanoma cells. You know that lovely phrase “the margins are clear”? That basically means that they looked at the patch of hopefully normal skin around the entire lesion and didn’t find melanoma cells. The new recommendations are concerned with those margins. So the greater in thickness your lesion, the bigger the margins should be. If you have a 1mm tumor, the recommended margin would be 1 cm (and yes, I meant to type 1 cm). Basically, up to 2cm of margin (i.e. clear skin around the lesion) should be taken during surgery or excision to remove the tumor. The minimum recommendation is 0.5 cm, but that’s only for melanoma in situ, which is only in the very top layer of skin. Oh, and the margins should be measured by the surgeon from the lesion or biopsy site, not from whatever was in the pathology report.
Ok, those are margins, but how deep will the excision or surgery go? The new recommended depth of excision is all the way to (but not including) the fascia, so basically pretty f’ing deep depending on the location of the tumor. (My excision went through the fascia as well because my Loki was a jerk and picked my knee to homestead.)
They also recommend that if you have to undergo a sentinel lymph node biopsy, that it should be done before the excision but at the same time as the procedure. So, sort of a 2-for-1 for the patient. Which makes sense that if you think your patient needs lymph nodes checked too, just do it all at once so the patient isn’t wasting time on getting the information needed to know the best course of treatment. I say it all the time here, but the earlier you catch and treat melanoma, the better the survival odds.
So when should someone need to think about sentinel lymph node biopsies? If you have melanoma in situ or an unulcerated lesion with a depth less than 0.8 mm, you don’t need it and the doctor wouldn’t recommend it. Anything greater than a T1a, then it’s kinda up to the doctor to discuss it with you and decide whether it makes sense. And if you have a T1a but are cutting it close to that 0.8 mm depth and have some other high-risk factors, you might have your doctor recommend it. From the sounds of it, a lot more melanoma patients might be at least discussing sentinel lymph node biopsies with their doctors in the future.
There are other topics covered in the new guidelines but these are the ones that will have the most impact for the majority of melanoma patients.
A reader emailed to let me know that Adam Ant released some U.S. tour dates for later in the year. This correspondent was concerned that I wasn’t aware because I hadn’t posted anything yet about it. And seriously, I love the people who actually read this blog. You guys are awesome. Between your emails and the nice messages, you make up for me having to delete a bunch of random spam comments that idiots try to post on this blog. (Seriously, no one comes here looking for a good price on Adidas… stop it already.)
But yeah, I totally knew about the tour and already secured tickets to a few shows. Although I bought them the day after they went on pre-sale, I was already shut out of my favorite seats in the front row of the balcony. Seriously, who bought all of those tickets the second they went on pre-sale? Did someone actually read this blog and tell themselves that I obviously was onto a good thing and took it to an extreme? Can’t a procrastinating girl catch a break? And the scheduling of the tour stops really kinda hindered me from putting together a road trip that wouldn’t make me want to gouge my eyes out or more likely, ram other people off the road (I guess I would need to keep my eyes in their rightful places to accomplish that). While road trips can be fun, I have a max of 3 hours in the car per day before my road rage overtakes every single nice element of my personality – shut up, there are some. So it’ll be a different kind of midlife crisis concert tour for me than the previous ones.
In September, you’ll be subjected to my ramblings about the shows I attend. Thanks for making sure I was in the know! You guys are the best…
I used to go to San Francisco quite a bit back in the day for work. But about a year and a half ago, I changed roles in my company (and just recently had another role change). Upshot is that I hadn’t made the trek to the city by the bay (woah-ooh-ohh-ohhh-ohhh – the Journey song is now stuck in my head and if you’re of a certain age or enjoy what the kids call ancient rock, it might be stuck in yours too – sorry) in awhile. So, I’m really looking forward to this weekend because I’m heading out that way again.
I’m spending a few nights in the city itself and then a few more nights up in Napa. Let’s be honest, I love urban environments. I mean, I live in the middle of downtown Austin in a high rise, for god’s sake… And SF has so many areas to explore (although we all know my well-established dislike of some of the hills because of my “flat-lander” lung capacity). But I think I’m looking forward to Napa maybe a little bit more. Which is hilarious because while I’m all, “oh it’ll be so beautiful and nature-pretty and less hectic” – seriously, Wine Country can be a big old touristy crowded mess when the weather is beautiful. Heck, it might feel more crowded than the city.
But after a fairly drama-filled first quarter of 2019 followed by some “nose to the grindstone to prove that my new boss made the right decision to save me from the chopping block“, I’m planning on stepping away from work for a few days and instead guzzling some fine wine while hopefully gazing on some beautiful scenery. I haven’t had a travel update here at all yet this year (the horror!), so we’ll see if my cabernet-soaked jaunt serves up anything interesting to write about when I get back.
I really wanted to title this post “It’s a Laser Beam, Bozo” because Real Genius is one of my very all-time favorite movies with some obscure-but-quotable lines and one very hot Val Kilmer. But I didn’t want you to think I was calling you a bozo so you got the boring title instead.
Anyway, lasers can be employed for all kinds of really cool purposes – from eye surgery, to cutting steel, to making EDM concerts way more exciting, to being employed by evil henchmen in James Bond films for nefarious purposes. And researchers at the University of British Columbia in Canada have developed a potentially new and beneficial way a laser can be used.
Lasers are machines that produce focused coherent light (no, it doesn’t talk but rather that the waves are lined up in perfect order with each crest of the wave matching up – it’s what makes the laser beam monochromatic i.e. all one color). If you remember from science class, light can be either in particle (called a photon) or wave form. When photons or light waves pass through an object, they scatter. Although the official explanation way more complicated, scattering is really why the sky is blue (tell that to the next annoying person who asks you why the sky is blue and bonus points if you name drop Rayleigh scattering).
Melanoma cells differ from regular skin cells in a few important ways – they are larger, denser, and more irregularly shaped. So the team at UBC took that concept and said, “hey, what if we bounced a laser beam off melanoma cells?” Well, actually they used a lot more jargon than that. But the concept of Polarimetry basically means using a non-destructive way to bounce light waves off something and measure the scattering of those waves.
Researchers designed a low-cost device based on these principles and then examined 69 skin lesions from patients at Vancouver General Hospital to see how the light waves change as they pass through a melanoma tumor. Using this knowledge, they showed that it was possible to develop an economical device (which they insist on calling a probe in the study and I simply can’t because “probe” make me think of insertions and aliens) that can be used for routine screening. Which is awesome because as we all know by now, the earlier you detect and treat melanoma, the better the outcome.
Maybe in a generation or so, doctors of all types could incorporate an inexpensive laser to detect early stage melanomas.
The biodiversity of this planet is in peril; in fact some biologists state we’re in the midst of an extinction event. The fact of the matter is the number of species on this planet is decreasing so rapidly that soon, all that will be left are humans, our livestock, mosquitoes, cockroaches, a billion strains of viruses, and ornamental lawn grasses.
And that would be an incredible loss for medicine because researchers have discovered a number of plants and animal species have the potential to aid in the fight against all kinds of diseases, including melanoma.
I wrote before that melanoma with BRAF mutations can be treated with BRAF-inhibitor drugs. But the problem with these types of drugs is that some patients’ melanoma cells develop resistance during the course of treatment.
With an eye towards developing novel approaches to treating melanoma, researchers from the University of California San Diego and the University of Sao Paolo who previously investigated a marine bacterium called Serinicoccus, turned their attention to a chemical it produces, known as Seriniquinone. Their research showed that Seriniquinone “demonstrated potent activity and selectivity toward melanoma cell lines”.
Backstory so the rest of the post makes sense… Dermcidin is a protein which encoded in the human DCD gene. Every time you sweat, you also secrete this protein. Dermcidin has been the focus of research for years as it has been shown to possess anti-microbial properties. Basically, it’s like your immune system’s way of killing any errant bacterial on your skin. And that should be awesome, right? Yay, protecting us from bacterial infection! But dermcidin has a darker side that researchers have recently uncovered. This protein has been associated with melanoma and breast cancer tumors. Scientists believe dermcidin may help cancer tumor cells proliferate and protect those cells from the immune system. That, as a former colleague of mine would say with understated gravitas, is suboptimal.
So getting back to Seriniquinone, the team from UC San Diego and University of Sao Paolo decided to see what this chemical would do against melanoma cells in a test tube. And their results were that not only did it induce cell death (which is exactly what you want melanoma cells to do – die and die quickly), but it also seems to be targeting dermcidin by binding with it. And as we know from previous science lessons here on the blog, when a protein is bound by another agent, it blocks the action of that protein. And in this case, Seriniquinone blocked the dermcidin from giving a boost to spreading those cancer cells.
Now obviously, something working in a test tube is not the exact same thing as something working in the human body. But it does provide a very intriguing avenue for developing therapies that can eventually be tested in animal and human subjects.
Who knows, maybe this exploration will lead to great advances against melanoma and it all comes from a somewhat rare marine bacterial species. Wouldn’t it be a shame if in the process of killing off the rhinos, the bees, and the sharks, we also ended up killing off the (potentially) beneficial Serinicoccus?