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post Posted: Today, 02:34 AM
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Well known it is cumulative lifetime sun plus genetic factors causing risk.
What is MSH can modify gene expression?

If melanocortins exhibit DNA repair mechanisms, would this reverse or turn back the clock on some of this damage.
I gotta say I love the 6x per year implant (for me), but a daily melanocortin cream would be a home run if it works locally and effectively.
Throw out the sunscreen, Protect & Repair

How Much Sunshine Causes Melanoma? It’s in Your Genes

Australian researchers from QIMR Berghofer Medical Research Institute have shown that 22 different genes help to determine how much sun exposure a person needs to receive before developing melanoma.

For people at high genetic risk, sun exposure in childhood is a strong contributing factor while people at low genetic risk develop melanoma only after a lifetime of exposure to sunlight.

The study results have been published today in the British Journal of Dermatology.

Australia has the highest rates of skin cancer in the world. Each year more than 12,000 Australians are diagnosed with invasive melanoma, which is the most deadly form of the disease.

The head of QIMR Berghofer's Cancer Control Group and lead researcher, Professor David Whiteman, said the study used data from QSkin, the world's largest genetic study of skin cancer, to explore how genes and sun exposure affected a person's chances of developing melanomas.

"The study findings suggest that people with genes that predispose them to skin cancer only need modest levels of exposure to Australia's sunny climate to develop this disease," Professor Whiteman said.

"Our data show that people who are born and grow up in Australia have a 50 percent increased risk of melanomas, while those migrating to Australia as adults, who have the same genes, are less likely to develop the deadly disease.

"This confirms that sun damage up to the age of about 20 is particularly dangerous for people with a higher genetic risk because it's enough to trigger melanomas and they don't need long, cumulative exposure as well.

"It's important to point out though that people who don't carry the higher risk genes associated with skin cancer can still get melanomas –they just need to get a large enough dose of sunlight over their lifetime. These people will often have lots of sunspots as a result of that exposure."

QSkin study project manager, Catherine Olsen, said the researchers looked at genetic and behavioral factors in the data to work out melanoma risk.

"The QSkin data included information about place of birth, age at migration, sunburns and cumulative hours spent in the sun along with histories of squamous cell carcinoma, basal cell carcinoma and sunspots. It also included DNA information," Dr. Olsen said.

"We then followed those people from 2011 and learned about their melanoma diagnoses from the Cancer Registry, which allowed us to work out risks."

Dr. Olsen said the study results highlighted why more people should sign up to QIMR Berghofer's QSkin genetics study, which aims to better understand the role genes play in the disease.

"We want to dig deeper into what genes are involved in skin cancer, and that's why we want more recruits for QSkin," she said.

"More than 5000 people have recently signed up to provide DNA for the study but our goal is 20,000 Australians by this time next year.

"While this study provides an insight into the development of melanoma and may help in identifying people who would benefit from targeted sun protection messaging, more still needs to be done to understand this disease that affects more Australians than any other population in the world.

"As Australians gear up for another hot and sunny summer season, the reminder to avoid harmful sun exposure is timely."

Desert Rat
post Posted: Yesterday, 09:08 AM
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Singapore Vitiligo Trial: Very small trial: n=8 in the phase I randomized study of UV-B +/- afamel.), and n=13 in the single-arm (combination) open-label phase 2 part. It was submitted as a Letter to the Editor of the Journal of the Amer. Acad. of Derm. Afamelanotide (Scenesse) 16 mg implants, were administered every 28 days, six in total, in Fitzpatrick skin types IV thru VI (dark skin types) combined with narrow-band UV-B phototherapy. The pooled analysis included all 18 patients that received the combination therapy with p <0.05 by both the VASI and the Vitiligo European Task Force (VETF) vitiligo area measurements. The low recruitment was a result of possible “social anxiety” over the general skin darkening in non-vitiligo areas perceived as a negative in the Asian community. In that regard, the slight improvements in vitiligo-specific quality of life measurements for combination therapy patients were not statistically significant.


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post Posted: Yesterday, 08:34 AM
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To all the australiens
Have a great and happy Australian day !
And lets look forward to hopefully some good numbers coming Friday

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Dr Wally
post Posted: Jan 26 2020, 11:27 PM
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In Reply To: macgyver's post @ Jan 26 2020, 09:44 PM

Hey MacDaddy, you really are "off your rocker".

“” The discovery of the endogenous melanocortin agonists in the 1950s have resulted in sixty years of melanocortin ligand research.””

The never ending quest to have Afamelanotide (peptide) accepted for its potent ability to stimulate a natural photoprotective,cancer preventative, therapeutic “tan” was accomplished in 2019.

Regulator ignorance, bias, and stubborn resistance to Scenesse are the primary reasons behind this glacial journey. The evidence should be clear to all by now.
Patrick Mcloughl...
post Posted: Jan 26 2020, 10:34 PM
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Every stock has its story. However, this year one biotech caught the eyes of investors and opened their wallets. CUV stock rose by 150% over the past 12 months and with recent FDA approval success is imminent. Yeah Yeah we have all heard this before. So why is this biotech different? Click below and you will see why?

post Posted: Jan 26 2020, 09:44 PM
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In Reply To: sharelooker's post @ Jan 26 2020, 08:43 PM

They probably wanted to know which Fitzgerald skin classification Scenesse would be able to treat effectively. To me it seemed an exploratory trial more than anything, especially given the small number of patients. Those patients in Singapore may have ranged from Type 2 to Type 5 (Malays, Indonesians, Indians and Chinese), and with Vallaurix being established there along with Singaporean pharmaceutical expertise and business-friendly environment (not to mention PWs tax retreat), Clinuvel figured it was optimal to do the trial there.

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post Posted: Jan 26 2020, 08:43 PM
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In Reply To: sharelooker's post @ Jan 26 2020, 10:19 AM

A major limitation of this study was the low recruitment rate because of the darkening effect of SC which is culturally not acceptable in asia. I'm still wondering why they did this study. They should have know this problem.

Johnny H
post Posted: Jan 26 2020, 10:58 AM
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In Reply To: sharelooker's post @ Jan 26 2020, 10:19 AM

P value for a reduction in total body VASI score was <.001.

Clinuvel until my bowels release for the last time.

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post Posted: Jan 26 2020, 10:19 AM
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It seems, they've published the results of the recent vitiligo study in singapore.

Afamelanotide Implants and Narrow-band Ultraviolet B Phototherapy for the Treatment of Nonsegmental Vitiligo in Asians!

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post Posted: Jan 25 2020, 11:37 PM
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In Reply To: sharelooker's post @ Jan 24 2020, 11:32 PM

The take home message of this publication is that activation of MC1R by MT2 oder SC results in the ignition of multiple pathways in order to slow down or prevent melanoma growth. In XP where different XP-proteins are mutated and cannot do their job properly, other mechanisms like downregulation of COX II, upregulation of PTEN etc. can compensate it. Moreover there will be a protective tan.

In my opinion, it makes perfectly sense to test SC in XP.

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