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What Is Skin Cancer?
Skin cancer -- abnormal cell changes in the outer layer of skin -- is by far the most common cancer in the world. It can usually be cured, but the disease is a major health concern because it affects so many people. About half of fair-skinned people who live to age 65 will have at least one skin cancer. Most can be prevented by protecting your skin from the sun and ultraviolet rays.
Every malignant skin tumor will, over time, show up on the skin's surface. That makes this the only type of cancer that is almost always found in its early, curable stages.
Skin cancers fall into two major categories: melanoma and nonmelanoma.
The most common skin cancers, basal cell carcinoma and squamous cell carcinoma, are nonmelanoma skin cancers and rarely life-threatening. They grow slowly, seldom spread beyond the skin, are easily found, and usually are cured. Basal cell carcinoma, which accounts for nearly 3 out of 4 skin cancers, is the slowest growing. Squamous cell carcinoma is somewhat more aggressive and more inclined to spread.
A rare nonmelanoma skin cancer is Kaposi's sarcoma, notable for its purple growths. It's related to a weak immune system and can be more serious. People with AIDS and the elderly tend to get it.
Some noncancerous skin growths could become cancerous. The most common are actinic keratoses -- crusty, reddish patches on sun-exposed skin that may scratch off but grow back.
The other type of skin cancer, melanoma, is a potentially aggressive, life-threatening cancer. It can start in dark skin tissue, such as a mole or birthmark, as well as in normally pigmented skin. For men, it generally shows up first on your head, neck, or between your shoulders and hips. Women tend to get it on their arms and legs. You may also find it on the palm of your hand, on the sole of your foot, under a fingernail or toenail, in mucus linings (in your mouth, vagina, or anus, for example), and even in your eye.
Melanoma is usually curable if found and treated early. But it grows faster than other types of skin cancer, and it can spread beyond your skin to other parts of the body, including your bones and brain. Then it's very hard to treat and is difficult to cure.
Spending too much time in the sun is the main cause of skin cancer. Sunlight has ultraviolet (UV) rays that can change the DNA in skin cells in ways that lead to cancer. Sunlamps, tanning booths, and X-rays also make these UV rays that damage skin.
Basal cell carcinoma and squamous cell carcinoma have been linked to ongoing sun exposure, typically in fair-skinned people who spend a lot of time outside. Melanoma has been linked with blistering sunburns; just one during childhood seems to double your risk for melanoma later in life.
Regularly working around certain chemicals and other things known to cause cancer may raise the odds of getting a nonmelanoma skin cancer, including:
Skin cancer tends to affect people of light skin color because they're born with the least amount of protective melanin in their skin. The odds are highest if you're:
People with many freckles or moles, particularly odd-looking ones, may be vulnerable to melanoma. It's possible for dark-skinned people to get skin cancer, but it's rare and usually on lighter areas of their body, such as the soles of the feet or under fingernails or toenails.
Where you live also plays a role. Places with intense sunshine, such as Arizona and Hawaii, have a larger share of people with skin cancer. It's more common in places where fair-skinned people moved from less sunny areas, like Australia, which was settled largely by fair-skinned people of Irish and English descent.
About 3 times more men than women get skin cancer. It's more likely when you're older. Most people diagnosed are between ages 45 and 54, although more younger people are now being affected. If you or any close relatives have had skin cancer, your chances go up.
Finding and treating skin cancer quickly is considered a cure. The type of skin cancer you have and how much it has spread, as well as your other health issues, will help your doctor decide how to treat it.
They may use one or more different ways to remove, kill, or stop the cancer cells from growing:
If the usual treatment doesn't work or it's difficult for you, you may be able to find a clinical trial. These test new ways to treat cancers that could be more effective or have lesser side effects.
Once you've had a skin cancer, like basal cell carcinoma, squamous cell carcinoma, and melanoma, and squamous cell carcinoma, there's a good chance that you'll develop a new skin cancer within a few years, so you'll need to get your skin checked regularly to catch it early.
New Information On The Most Important Early Stage Of Embryonic Development
A new discovery by researchers challenges our current understanding of gastrulation, the most important stage of early embryonic development.
When the zygote, or fertilized egg, starts to develop, the forming inner cell mass, a cluster of cells that will eventually develop into the individual, retains its pluripotent stem cell potential for the first few weeks. In other words, every cell in this cluster has the ability to form an entire new individual and all of the hundreds of different cell types that the human body needs. The potential of stem cell therapies is based on this pluripotency of early embryonic stem cells.
Gastrulation is a crucial stage in embryonic development where this pluripotency is lost and the germ layers of the embryo (ectoderm, mesoderm and endoderm) and the three body axes of the developing body (anterior and posterior, dorsal and ventral, left and right) are formed. In fact, gastrulation is often referred to as the most important stage of life, with a large share of early miscarriages resulting from unsuccessful gastrulation.
Researchers from the University of Helsinki and the National Institutes of Health (NIH) in the United States found that the ectoderm, one of the germ layers, does not lose its pluripotency in gastrulation after all. It also answers the long-standing question posed by developmental biologists on how the neural crest, which originates from the ectoderm during embryonic development, has such an exceptionally high stem cell potential. The study is published in the journal Nature Communications.
Following gastrulation, the neural crest develops into a large number of cells that form various parts of the body. To name a few, tissues derived from the neural crest include pigment cells in the skin, the entire peripheral nervous system, the bones of the face and neck, parts of the heart, and several hormone-producing cell types—in practice, cell types whose differentiation from a single germ layer should be impossible.
"Our findings shed new light on the chain of events in early embryonic development. The findings indicate that the expression stage of stem cell genes needed for the production of pluripotent stem cells continues throughout the ectoderm almost until the completion of the neural tube, a precursor to the central nervous system.
"The findings also indicate a much higher plasticity in the cell fate determination process that occurs in the ectoderm than previously thought," says Dr. Laura Kerosuo, principal investigator of the research group, a former Academy researcher at the University of Helsinki, and currently the Chief of the Neural Crest Development and Disease Unit at the NIH.
A high-resolution imaging technique, capable of analyzing individual cells, helped the researchers uncover the findings.
Previously, the research group developed this technique for the simultaneous analysis of the expression of several genes, which they modified further for this study to enable them to monitor the location of individual stem cells in the ectoderm at different stages of development following gastrulation.
"With this precise and effective technique, cell profiles can be identified on site in the original tissue. The technique can be applied to any question, such as comparing sick and healthy tissue," says Doctoral Researcher Ceren Pajanoja from the University of Helsinki.
Neurocristopathies, or disorders originating from the neural crest, account for roughly one-quarter of all congenital developmental disorders. The new knowledge gained from this study helps to reveal the pathogenetic mechanisms of neurocristopathies and identify the gene defects that cause them already in early pregnancy. The study can also help in developing alternative therapies that could in the future be applied to the fetus during pregnancy.
Cancers originating from the neural crest include melanoma and neuroblastoma, an often fatal disease in infants, which Dr. Kerosuo's research group is also investigating from the perspective of neural crest development.
"It has only recently been realized how important it is to understand the normal development of the original tissue to find out what went wrong when the cancer was activated," she says.
In addition, techniques for the differentiation of neural crest derived tissues from stem cells hold great promise for usage for future tissue replacement therapies.
More information: Ceren Pajanoja et al, Maintenance of pluripotency-like signature in the entire ectoderm leads to neural crest stem cell potential, Nature Communications (2023). DOI: 10.1038/s41467-023-41384-6
Citation: New information on the most important early stage of embryonic development (2023, September 27) retrieved 1 October 2023 from https://phys.Org/news/2023-09-important-early-stage-embryonic.Html
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Early Intervention Impacting CKD Treatment Pathways
Clinical and financial considerations surrounding screening and early intervention for CKD are discussed by key opinion leaders.
Ryan Haumschild, PharmD, MS, MBA: When you're thinking about this, Dr Green…how can early intervention in patients with heart failure or type 2 diabetes…prevent or slow the progression of CKD [chronic kidney disease]? And what have you really seen in your practice?
Jennifer B. Green, MD: Well, that's a great question. Before I dive into that, can I just make a couple of comments about some of what's been discussed already in the program? So I thank Dr Anderson for bringing up [the] idea that managing cardiorenal risk is a shared responsibility. I think management of risk is often treated as a hot potato, right? It's kind of tossed to the next doctor that the individual is…going to see. And we need to stop and take the time to understand our patient's risk and recommend either the interventions designed to treat ourselves or to engage the other providers directly who will be responsible for that aspect of care. And we've talked a lot about urine albumin-creatinine measurements. I would like to remind everyone who is listening that this is not a new recommendation. This is not a new test for people with type 2 diabetes. That has been a recommendation that they have that test performed and at least annually for decades. So this is nothing new. It's just not happening. So we really failed to appreciate the risk posed to many of our patients with type 2 diabetes. And I'm a little bit more diabetes centric, so I will mention that a good bit of the time, but you brought up early intervention. So of course, identification of risk is part of early identification of risk and the implementation of strategies to mitigate that risk. When I think about early intervention, I think about it in 2 ways. There's early in the sense of early in the course of the disease, but there's also early in a person's life span. So those are 2 different concepts. And we need to be very cognizant of the fact that in this country, people are developing type 2 diabetes or these other complications at very young ages. And there [are] very compelling data that [have] been published that show if you are a young person—and when I say young, I'm talking about 40s who has type 2 diabetes—and you have also either kidney disease or cardiovascular disease or both, the adverse effect on your life expectancy is very, very substantial. If you have these problems early in life—don't forget about people who are young with these conditions. There's a misconception that they are not at great risk. In fact, their risk is greatest over their lifetime, and they need to be identified as at risk and treated appropriately. So that's an opportunity. The reason we want to think about early intervention, particularly when it comes to kidney disease and kidney function, is that, at a certain point in adulthood, your eGFR [estimated glomerular filtration rate], your kidney function just starts to steadily decline. And you can only modify that so much if you are a person who has diabetes or already has kidney disease or has heart disease. And in particular, if you have a lot of albumin in your urine, you're on the fast track, and your eGFR decline over time will be far greater. So what we want to do is identify people early in that process where they haven't gotten very far down that fast track toward, for example, needing dialysis, so we can intervene at that time and keep their eGFR, for example, as high as it can be for as long as it can be.
Ryan Haumschild, PharmD, MS, MBA: You know, I think we hear so much advocacy from the provider for early intervention. And I appreciate the passion because it's the right thing to do for the patient. And so many times the question comes up: How do providers and payers incentivize early screening intervention? So, Dr Cohen, I'd like to pose that question to you and maybe [ask]: Can payers incentivize CKD screening through population health programs or maybe even internal quality measures?
Ken Cohen, MD: They can. Payers to a limited extent. I think this is more impactful when you look at our current health care landscape. We continue to have physicians who are practicing in small solo or small group practices and then many others who are practicing in more sophisticated care models where there is a population health infrastructure, where there are care managers. And we have been able to demonstrate that the quality of screening differs in those 2 models and that when patients are cared for in a sophisticated care model, they actually have higher screening rates, sometimes as much as twice as high…. And if you take that 1 step further, we've been able to show that when patients are cared for in models where the physician organization or the hospital physician organization is accountable for total cost of care, there is another quantum increase in outcomes. We published a study in JAMA Open Network last year, my colleagues and I, that showed, for example, there was a 10% lower rate of stroke and heart attack in Medicare patients who were treated in a 2-sided risk model compared with fee-for-service Medicare. So shifting that responsibility, both clinically and financially, to a physician organization creates a compelling indication to move upstream and begin to risk-stratify and try to get earlier into the disease process. We've modeled, for example, home uACR [urine albumin-creatinine ratio] programs where we send patients kits for free and have them do their screening at home, take it out of the PCPs' [primary care physicians'] hands. Our PCPs are incredibly busy. And anything that you can do with population health management through either care management or direct patient access that will make the PCP's burden less, it's likely to improve ultimate screening results. We've even piloted doing home serum creatinine testing. We now have kits with micro capillary tubes that patients can acquire the sample on their own and just mail in and do both uACR and eGFR just through home testing. So that's one way. The other way is to look at your population health management infrastructure and create incentives. And those incentives can either be intrinsic or extrinsic. Physicians, NPs [nurse practitioners], and PAs [physician assistants] are very competitive by nature. And transparently reporting results of screening is a very potent change agent, and nobody likes to be at the bottom of those lists. So that concept of transparent reporting is important. And on top of that, you can leverage financial incentives as well. So for clinicians who are up-to-date in screening—and it isn't just diabetes, but creatinine clearance, uACR, breast and colorectal cancer screening, immunization rates—you can create comprehensive incentive models that encourage screening that significantly impact screening results.
Ryan Haumschild, PharmD, MS, MBA:I like that you gave us a couple of ideas focusing on value-based care, dual-sided risk with total cost of care, but even the competitiveness, I know in our organization, we like sports, but we really like competitive publishing. And so the more we can get the data out there and show the difference we're making, I think that goes really far…. So I appreciate that perspective. And just kind of wrapping up this section, Dr Anderson, I want to pose to you: How can payers educate local providers about some of the screening guidelines and encourage them? As we heard from Dr Green, these aren't new recommendations. These are things that have been around. How can we create more education and focus on these recommendations so that patients are screened earlier?
John E. Anderson, MD: Well, I think he said something great. You can have some incentives for financial based improvement if you're doing the proper screening. But I think it's also about just educating the providers in the primary care system. I mean, getting a urinalysis happens in a primary care office 10 times a day. So getting a urine sample for a uACR is not a burden. There's no burden of acquisition. We're pretty good at getting eGFRs, but I think for so long, the primary care community has avoided microalbumin screening because they've seen no value in it, and it's a whole new day of education. So I think programs like these—any provider-based network that has incentives—I know that HEDIS [Healthcare Effectiveness Data and Information Set] is going to have incentives for getting this done. I know that some of the pathology laboratories are now wanting to do just a kidney panel, and if you order a kidney panel, you get the eGFR, the BNP [brain natriuretic peptide], and you get the uACR together. So it's tied in a bundle. But for so long in the primary care world, we have watched our patients with chronic kidney disease get worse and worse and worse. And we've had nothing to offer them. If they get to the progression of CKD—because we know that most of these patients will die of a cardiovascular event before they get to end-stage kidney disease—we now have something to do, which should excite the primary care community. We have something to offer our patients we haven't had for years. But it's also a little bit of a stick. You need to do these, and you are going to be judged and financially rewarded based upon whether you're doing the right thing for your patients.
Transcript is AI-generated and edited for clarity and readability.
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