Hello, this paper needs to be
– 300-500 words for the intro that engages the rea

Hello, this paper needs to be
– 300-500 words for the intro that engages the reader, and any sources are allowed to hook the reader. 
– 4 – 5 primary sources from 2023 and 2024 with 4 – 5 different treatments on Melanoma treatments, this will be one treatment per primary source explaining what they were testing and the results
– 200-300 words summary explaining where this can go next. 
I started something below but, feel free to build on it I do want to talk more about the different treatments available and it is a cancer course so it needs more specific pathways explained. Also, to be sure the sources are APA format and primary NO REVIEWS PLease because we are essentially created the review. 
Dr.
T
Advancing Cancer Treatments for
Melanoma
Introduction
Cancer used to be known as the
disease of old age, but now our beauty standards are causing it to affect a
much larger population. Not only is it old people developing cancer due to
telomer degradation and cell proliferation, but young girls wanting to be subjectively
beautiful will knowingly harm themselves to reach this desired tan they see
through social media. Sometimes they are uneducated on the gravity of these
risks caused by these indoor tanning beds, but most likely they are lying to
themselves with optimism bias. Meaning that they know it is a risk, but they
believe melanoma also known as skin cancer will only happen to other people and
never themselves. Tanning beds use ultraviolet radiation to stimulate the skin
into producing more melatonin by damaging the cells and increasing
melanogenesis. Melanogenesis is the production of melanin. When ultraviolet
radiation comes in from the sun it generates reactive oxygen species within the
skin. These are highly reactive molecules that contain oxygen and can damage
the cellular structure through oxidative damage. Specifically, the damage is to
the DNA of the melanocytes which are embedded in the epidermis and contain
melanosomes which synthesize melanin. This damage to the melanocytes causes a
cellular defense mechanism to be initiated known as melanogenesis.
Melanogenesis is the synthesis of melanin. The melanocytes express a gene for a
G–protein coupled receptor called Melanocortin–Receptor 1 (MCR1) which is
activated by a Melanocyte-Stimulating Hormone. This hormone triggers an
increase of receptors and enzymes like tyrosinase which is an enzyme in charge
of converting the amino acid tyrosine into dihydroxyphenylalanine.
Dihydroxyphenylalanine then gets further converted into dopaquinone, this
intermediate leads to the biosynthesis of melanin of different color pigments
including black, brown, red and yellow. These pigments ultimately produced by
tyrosine called melanin is the defense mechanism our body produces to protect
us from ultraviolet radiation by absorbing light across a range of wavelengths.
This absorption protects our skin, from ultraviolet radiation but, it leads to
increased cell proliferation, DNA cell damage, and trigger programmed cell
death apoptosis which is when we get sunburned.
When cells are damaged it triggers a
damage repair pathway with p53 transcription factor which is normally
downregulated by the MDM2 protein through a positive feedback loop. The DNA
damage activates ChK2, ATR, ATM kinases to phosphorylate p53 and MDM2. When a
p53 is phosphorylated its able to bind to DNA and activate the gene that
regulate the cell cycle, including DNA repair and apoptosis. One gene will code
for p21 which when produced in high concentrations will pause the cell cycle
and prevent the cell from moving past the R point and into cell division phase.
The p21 protein is a cyclin dependent kinase inhibitor (CDK). An active CDK is
needed to move past the R point and transition from the G1 phase to the S
phase, by inhibiting the CDK the cell can repair the damage. The first step to
repair is the p53 being activated within the myocytes which were damaged by UV
radiation. An increased level of MSH (myocytes stimulating hormone) is produced
which bind to MC1R receptors causing cAMP to activate kinase A, which then
phosphorylates the transcription factor CREB. CREB is responsible for
upregulating expression of microphalmia-associated transcription factor (MITF).
MITF is activated by Mitogen-activated protein kinase (MAPK). cAMP and MAPK
trigger pathways resulting in tyrosine synthesis which is then converted by
enzyme tyrosinase to as mentioned earlier to melanin. 
The
leading cause of melanoma skin cancer is exposure of the sun’s ultraviolet
rays. It’s estimated that 7.8 million young people were engaging in indoor
tanning beds. Additionally, we see this perspective of tan beauty and encourage
a tan complexion on women.
References
Siegel, R. L., Giaquinto, A. N., & Jemal,
A. (2024). Cancer statistics, 2024. CA: a cancer journal for clinicians, 74(1),
12–49. https://doi.org/10.3322/caac.21820