Skin Cancer Prevention: Learn How to Detect It Early

Skin cancer is the most common type of cancer in the world. In 2021, around 6.6 million new cases of skin cancer were registered, with a consistent increase over the last 30 years. Therefore, when it comes to skin cancer prevention, it is important that the topic receives space for understanding its significance. 

 

Basal cell carcinoma is the most frequent, followed by squamous cell carcinoma. Melanoma accounts for about 1% of the cases, yet is responsible for most deaths from skin cancer [1]. In Brazil, skin cancer is also highly prevalent, representing 30% of all malignant tumors recorded in the country. Non-melanoma types correspond to about 31.6% of cancer cases diagnosed annually, while melanoma accounts for about 1% [2]. 

 

The risk is higher in regions with a predominance of people of European origin, such as the South and Southeast, where there are more cases per 100,000 inhabitants [3,4]. 

 

Due to its relevance in public health, skin cancer prevention and awareness campaigns, such as “Orange December”, have been increasingly reinforced in an attempt to reduce these numbers. 

 

In this content you will find very important information about the types of skin cancer, prevention methods, hereditary risk and diagnostic approaches. Check it out! 

What is skin cancer and why does prevention matter?

Skin cancer is a neoplasm that originates in the cells that make up the skin and, as already mentioned, is among the most diagnosed cancers in the world. It is mainly classified into melanoma and keratinocyte carcinomas, which include basal cell carcinoma and squamous cell carcinoma [5,6]. 

 

Melanoma represents a smaller proportion of cases, but has a more aggressive behaviour. Keratinocyte carcinomas are more frequent and generally have favourable evolution when diagnosed early [5,6]. 

 

Prevention of skin cancer plays a central role because most cases are related to exposure to ultraviolet (UV) radiation, a modifiable risk factor. 

 

Simple interventions – such as regular use of sunscreen, appropriate clothing and avoiding sun exposure during peak UV radiation hours – can significantly reduce incidence and mortality, as we will see below [5,6]. 

 

Who is at higher risk of developing skin cancer?

Although anyone can develop skin cancer, certain groups have higher vulnerability due to genetic, immunological and environmental characteristics: 

 

• Skin phototype: individuals with fair skin, light eyes and hair, who burn easily, are more prone to all types of skin cancer. This group has lower melanin, the pigment that offers natural protection from UV radiation effects [5,6].
• Family history: having first-degree relatives with melanoma or other types of skin carcinoma increases individual risk. The presence of multiple nevi (moles) or dysplastic nevi (with cellular alterations) intensifies the probability of disease development [5,6].
• Immunosuppression: immunosuppressed patients, such as those undergoing solid organ transplantation or living with HIV, have risk up to 100 times higher for squamous cell carcinoma compared to the general population. The suppression of immune surveillance facilitates proliferation of abnormal cells [5,6].
• Occupational exposure: professionals who spend long periods outdoors, such as farmers, fishermen and construction workers, have elevated risk, especially for squamous cell carcinoma, due to cumulative sun exposure [5,6]. 

 

It is important to highlight that the identification of these factors enables targeted preventive actions and screening strategies. Early recognition of suspicious lesions and population education are excellent tools for skin cancer control [5,6]. 

 

Types of skin cancer

The types of skin cancer differ according to the cells from which the tumour originates. The main forms are melanoma and keratinocyte carcinomas, the group that includes basal cell carcinoma and squamous cell carcinoma. Each of these subtypes presents distinct clinical characteristics, prognoses and growth patterns. Carcinomas usually evolve slowly and locally, while melanoma has lower incidence but more aggressive biological behaviour, with high potential for invasion and metastasis [5,6]. 

 

Sun exposure is the main trigger for all types, although the exposure pattern varies by subtype. In basal cell carcinoma, risk increases with intense and sporadic sun exposure from childhood; in squamous cell carcinoma, risk stems from chronic and cumulative exposure over the years; and in melanoma, both intermittent and continuous exposure show influence, in addition to genetic and immunological factors [5,6]. 

 

Melanoma: when is it dangerous

Cutaneous melanoma is the skin cancer that yields the highest mortality rate due to its ability to spread rapidly to other organs [6]. 

 

This tumour may arise from a pre-existing mole or develop in an area of skin without apparent lesions. Clinical manifestations are varied, but generally involve changes in colour, shape or size in a pigmented lesion. Regular dermatological monitoring is the most effective way to recognise suspicious changes early [6]. 

 

Melanoma is considered dangerous precisely because of its rapid and silent progression. The absence of symptoms in early phases and the short interval between local growth and systemic dissemination make early diagnosis a key determinant for patient survival [6]. 

 

Carcinomas (basal cell and squamous cell)

Both basal cell carcinoma and squamous cell carcinoma derive from keratinocyte cells of the epidermis, but they present different clinical behaviours. Basal cell carcinoma is more common, accounting for around eight out of ten cases. It is characterised by slow growth, a nodular or ulcerated appearance and low risk of metastasis. Nevertheless, it can cause significant local damage when untreated, particularly in areas such as the face and neck [5]. 

 

On the other hand, squamous cell carcinoma is less frequent but more invasive. It may develop in chronically sun-exposed areas or on pre-existing lesions such as scars, ulcers and actinic keratoses. It has greater risk of lymphatic dissemination, especially in immunosuppressed individuals, older adults or those with long-standing skin disease [5]. 

 

Regarding prognosis, both types have high cure rates when treated early, generally by means of local surgical excision. However, squamous cell carcinoma requires closer monitoring, due to its potential for recurrence and regional metastasis [5]. 

 

Differences between sporadic melanoma and hereditary melanoma

Sporadic melanoma refers to the majority of cutaneous melanoma cases that occur as isolated events, without familial aggregation or multiple primary tumours. These cases are predominantly attributed to UV exposure and phenotypic factors such as fair phototype and presence of nevi, without identifiable genetic predisposition [7–9]. 

 

Hereditary melanoma corresponds to a minority of cases, estimated around 5% to 10% of melanomas, characterised by family aggregation (two or more first-degree relatives affected), multiple primary melanomas in the same individual, early onset (typically before 40–45 years) and, in some cases, association with other tumours such as pancreatic cancer [7–9]. 

 

Hereditary melanoma should be suspected in the following situations: 

• Family history of melanoma (≥2 first-degree relatives affected, especially in different generations);
• Multiple primary melanomas in the same individual, especially if the first diagnosis occurred at a young age (<45 years);
• Association of melanoma with other tumours, especially pancreatic cancer or neoplasms associated with genetic syndromes (e.g., mesothelioma, meningioma, uveal melanoma in carriers of BAP1 mutation);
• Presence of multiple atypical nevi (FAMMM syndrome) or high-risk phenotypic features. 

 

Main genes associated with hereditary risk

The main genes associated with hereditary melanoma risk are CDKN2A (the most common), CDK4, BAP1, MITF, POT1, TERT, ACD and, less frequently, BRCA2. The CDKN2A gene is related to the Familial Atypical Multiple Mole Melanoma syndrome (FAMMM), accounting for around 20–40% of familial melanoma cases. Germline mutation in CDKN2A confers high risk of multiple melanomas and is strongly associated with increased pancreatic cancer risk, in addition to other tumours such as breast and lung cancer in some families [10]. 

 

The CDK4 gene is less frequent, present in under 2–3% of families with hereditary melanoma, and is also associated with development of multiple melanomas, but the association with pancreatic cancer is less clear and less prevalent than in CDKN2A. 

 

Other genes, like BAP1, are linked to uveal melanoma, mesothelioma and renal carcinoma, while MITF (especially the p.E318K variant) increases risk of melanoma and renal carcinoma and may also be associated with pancreatic cancer [9,10]. 

 

The association between these genes and other tumours is better established for CDKN2A and pancreatic cancer, with cumulative risk estimated up to 17% for carriers by age 75 years. The presence of multiple melanomas in the same individual, early onset (<40–45 years) and family history of melanoma and/or pancreatic cancer are criteria for suspicion of genetic predisposition [11,12]. 

 

Importance of molecular analysis

Molecular analysis assists in identifying germline mutations in high-risk families for hereditary melanoma, as it enables precise risk stratification, preventive care guidance and personalised clinical decisions [14,15]. 

 

Molecular analysis may be performed via multigene panels, which increase diagnostic yield in families without CDKN2A/CDK4 mutations, or via focused testing on high-penetrance genes, depending on clinical and family context. The identification of pathogenic variants allows confirmation of hereditary melanoma diagnosis and guidance of family screening [14,15]. 

 

Detection of germline mutations has direct impact on genetic counselling, enabling informing individual and family risk, discussing prevention strategies and indicating personalised screening. 

 

Carriers of mutations should have comprehensive dermatological exams, full-body photography and dermoscopy at reduced intervals (typically semi-annual or annual, according to risk and history), in addition to surveillance for other tumours such as pancreatic cancer in CDKN2A mutation carriers [14–16]. 

 

Pancreatic screening may include magnetic resonance imaging or endoscopic ultrasound, though the effectiveness of these strategies is still under evaluation. Molecular analysis also increases adherence to preventive follow-up and promotes behaviour change such as greater photoprotection use and skin self-examination [14–16]. 

 

Role of tumor genetic analysis (somatic)

Somatic genetic analysis of the tumor aids in the diagnosis and management of melanoma, allowing the identification of variants in genes such as BRAF, NRAS, and KIT, which define molecular subtypes and guide therapeutic decisions. 

 

Molecular classification of melanoma includes the groups BRAF-mutated, NRAS-mutated, KIT-mutated, NF1-mutated, and triple wild-type, each with distinct clinical and therapeutic implications [17–19]. 

 

Detection techniques include NGS (next-generation sequencing), ddPCR (droplet digital PCR), FISH, and multigene panels, capable of identifying low-frequency variants and multiple simultaneous alterations, increasing diagnostic sensitivity and enabling detailed tumor profiling. 

 

Correlation between mutations and clinical, histopathological, and dermoscopic characteristics is relevant: BRAF-mutated melanomas tend to present higher mitotic index and ulceration, whereas NRAS-mutated melanomas are more common in nodular and amelanotic types, often associated with poorer prognosis [17–19]. 

 

Molecular analysis contributes to the personalization of advanced melanoma treatment by enabling the selection of targeted therapies and immunotherapies according to the tumor’s genetic profile. Biomarkers such as tumor mutational burden (TMB), gene expression signatures, and presence of neoantigens help predict response to immunotherapy, with tumors exhibiting high TMB being more likely to respond to checkpoint inhibitors, for example [17–19]. 

 

In summary, somatic genetic analysis of the tumor is essential for accurate diagnosis, prognostic stratification, and rational therapy selection in advanced melanoma, promoting personalized medicine and optimizing clinical outcomes. 

 

Warning signs on the skin

Skin cancer symptoms typically manifest as spots, moles, or sores that appear or change over time. Alterations in size, shape, color, texture, or local sensation (such as itching, pain, or bleeding) should always raise concern [20]. 

 

For melanoma, early identification depends on observing subtle changes in pigmented lesions. For non-melanoma carcinomas, persistent, scaly, or non-healing lesions are common. Both doctors and patients should monitor any visible or sensory change on the skin, especially in individuals with a family history of the disease, fair phototype, or frequent sun exposure [20]. 

 

ABCDE rule for melanoma

The ABCDE rule is a widely recommended clinical and educational method to recognize suspicious melanoma spots early. It helps differentiate benign moles from potentially malignant lesions, facilitating early diagnosis [20,21]. 

 

Table: Checklist – How to identify suspicious signs (ABCDE rule) [20,21] 

 

Criterion	Description	Alert Indication
A – Asymmetry	One half of the lesion differs from the other	Uneven mole
B – Border	Irregular, notched, or poorly defined edges	Non-uniform contours
C – Color	Presence of multiple shades (brown, black, reddish, white, or blue)	Color variation within the same lesion
D – Diameter	Usually larger than 6 mm (about the size of a pencil eraser)	Lesion ≥ 6 mm
E – Evolution	Recent changes in size, color, shape, or symptoms (itching, pain, bleeding)	Mole that changes over time

 

In addition, attention should be given to the “ugly duckling sign,” describing a lesion that stands out from other moles on the body due to its appearance and coloration [20,21]. 

 

Suspicious non-melanoma lesions: when to be concerned

Not all suspicious skin cancer lesions are darkly pigmented. Non-melanoma carcinomas, which include basal cell carcinoma and squamous cell carcinoma, have distinct characteristics and are often mistaken for common wounds [22]. 

 

• Basal cell carcinoma: typically appears as a pearly or translucent papule or nodule, sometimes with visible small blood vessels (telangiectasias). Central ulceration, crusts, and spontaneous bleeding may also occur. Although growth is slow, it can invade nearby tissues if untreated [22].
• Squamous cell carcinoma: often presents as a firm, red, scaly lesion that may evolve into an ulcer with raised, irregular edges. Persistent crusting and rapid growth are common, especially in sun-exposed areas such as the face, scalp, ears, and backs of hands [22].

 

Other signs warranting medical evaluation include: 

• Wounds that do not heal after several weeks [22];
• Thickened or erythematous plaques in photo-exposed areas (actinic keratosis or Bowen’s disease) [22];
• Lesions showing hardening, ulceration, or recurrent bleeding [22]. 

 

Any persistent skin change should be examined by a dermatologist. Biopsy is the procedure indicated to confirm diagnosis and determine appropriate treatment. Early recognition of suspicious lesions, melanoma or not, is crucial to increase the chances of cure and reduce clinical complications [22]. 

 

Diagnosis and tests

Skin cancer diagnosis begins with clinical observation of spots, moles, or sores that change over time, have irregular borders, color changes, progressive growth, or impaired healing. 

 

Detection is initially performed by a dermatologist, who visually evaluates lesions and decides on the need for complementary exams [20]. 

 

Key tools include dermoscopy and biopsy, considered essential for diagnostic confirmation. Imaging and laboratory tests are reserved for specific cases, when tumor dissemination or lymph node involvement is suspected [20]. 

 

Dermoscopy and biopsy: how confirmation is achieved

Dermoscopy is a non-invasive office procedure that allows detailed observation of skin structures. Using a dermatoscope, which magnifies and illuminates the skin, the physician can visualize color and vascular patterns invisible to the naked eye [20]. 

 

This examination significantly increases clinical diagnostic accuracy, enabling the dermatologist to distinguish benign from malignant lesions and reduce unnecessary biopsies. Professionals experienced in dermoscopy achieve the best results, particularly in melanoma and cutaneous carcinomas [20]. 

 

If malignancy is suspected, a biopsy is performed, removing a fragment of the lesion for histopathological analysis. This procedure is the gold standard for confirming all types of skin cancer. The collected material is examined in the laboratory, where cellular characteristics are assessed to confirm or rule out the diagnosis [20]. 

 

Imaging and laboratory tests: when indicated

Imaging and laboratory tests are not part of the initial evaluation of skin cancer but are indicated in specific cases, usually with invasive melanoma or high-risk lesions [20]. 

 

After diagnosis confirmation by biopsy, the physician may request: 

• Regional lymph node ultrasound to assess possible dissemination [20];
• CT scan or MRI if metastases in internal organs are suspected [20];
• PET-CT in advanced disease for systemic screening [20]. 

 

Overall, skin cancer diagnosis relies on detailed clinical evaluation, dermoscopy, and biopsy. Decisions regarding complementary exams should always be guided by the dermatologist, based on lesion type, extent, and stage [20]. 

 

Daily skin cancer prevention

Prevention focuses on reducing exposure to ultraviolet (UV) radiation, the main risk factor. Daily use of sunscreen, protective clothing, and planning outdoor activities are simple, effective measures. UV radiation is present even on cloudy days and can reflect off surfaces like water, sand, and concrete, increasing unnoticed exposure [20]. 

 

Sunscreen: SPF, amount, and reapplication

Sunscreen should have SPF ≥ 30 and UVA/UVB protection. The recommended amount is about 30 mL (one shot glass) to cover all exposed areas, including ears, neck, feet, backs of hands, and lips (with SPF ≥ 30). Apply 15 minutes before sun exposure and reapply every 2 hours or after sweating, bathing, or swimming. Continuous use is essential to prevent burns, premature aging, and skin cancer [20]. 

 

Clothing, hats, and UV-protective eyewear 

Wearing long-sleeve clothing with UPF ≥ 30, wide-brimmed hats (minimum 7.5 cm), and UV400 sunglasses protects frequently exposed areas. Caps with neck flaps are useful for prolonged outdoor activities. Combined use of clothing and sunscreen offers the most effective protection [20]. 

 

Peak risk hours and UV index

Between 10 a.m. and 4 p.m., solar radiation is strongest. When the Ultraviolet Index (UVI) exceeds 6, skin damage risk is high, even during short exposure. Monitoring the UVI via weather apps and seeking shade during these hours complements photoprotection [20]. 

 

Occupational prevention: PPE, shade breaks, and workplace policies

Outdoor workers should use UV-protective PPE, including UPF ≥ 30 clothing, hats, sunglasses, and sunscreen. Shade breaks, schedule adjustments to avoid peak radiation, and educational programs on sun risk are important. These actions reduce cutaneous carcinoma incidence and demonstrate employer commitment to employee health [20]. 

 

What tests does SYNLAB offer for skin cancer investigation?

Among the diagnostic tests offered for skin cancer are: 

 

• FISH panel on tissue samples to detect chromosomal alterations and genetic rearrangements associated with melanocytic lesions, helping differentiate benign from malignant lesions, e.g., for genes and regions: CCND1(BCL1)(11q13), RREB(6p25)/MYB(6q23)/CEP6.
• MLPA panel for CDKN2A, CDKN2B, and CDK4 genes, identifying deletions, duplications, and variants associated with hereditary melanoma predisposition and tumor progression.
• Candidate gene sequencing panels for evaluating somatic and germline mutations in multiple genes of interest (BAP1, BRCA2, CDK4, CDKN2A, MC1R, MITF, POT1, PTEN, RB1, TERT, TP53), providing a detailed genetic profile and assisting in prognosis and therapeutic planning.

 

With state-of-the-art technology and a highly qualified team, SYNLAB partners with healthcare professionals, offering complete and precise diagnostic solutions for skin cancer management. 

 

Get to Know SYNLAB – A Leader in Medical Diagnostic Services!

Accurate and up-to-date testing is essential for precise diagnoses and better treatment guidance. SYNLAB is here to help. 

 

We offer diagnostic solutions with rigorous quality control to the companies, patients, and healthcare providers we serve. Present in Brazil for over 10 years, we operate in 36 countries across three continents and are leaders in diagnostic services in Europe. 

 

Contact the SYNLAB team to learn about our available tests. 

 

Frequently Asked Questions (FAQ)

Here, we answer the most common questions about skin cancer. 

 

What is the best way to prevent skin cancer?

The main form of skin cancer prevention is daily photoprotection, avoiding sun exposure between 10 a.m. and 4 p.m., and using sunscreen with SPF ≥ 30, reapplying it every two hours. 

 

What are the 3 main types of skin cancer?

The three main types of skin cancer are: basal cell carcinoma (BCC) – the most common and slow-growing type; squamous cell carcinoma (SCC) – more invasive and with a higher risk of metastasis and melanoma – the least frequent but most aggressive type, with a high potential for spreading. 

 

What are the early signs of melanoma?

The first signs of melanoma follow the ABCDE rule, which evaluates suspicious moles based on:

 

A – Asymmetry: one half is different from the other; B – Border: irregular or blurred edges; C – Color: variation in shades (brown, black, red, blue, or white); D – Diameter: greater than 6 mm; E – Evolution: changes in size, color, shape, or new symptoms (itching, pain, bleeding). 

 

How is skin cancer detected? What test identifies it?

Diagnosis is made by a dermatologist through clinical examination and dermoscopy, a technique that allows detailed visualization of skin structures invisible to the naked eye.

A biopsy confirms the diagnosis through histopathological analysis of the lesion.

High-precision molecular tests can also help characterize the tumor’s genetic profile and assist in prognosis and treatment planning. 

 

Is skin cancer curable? When is it dangerous?

Yes. Most cases have a high cure rate when diagnosed early.
However, melanoma is the most dangerous type due to its risk of metastasis.

Treatment is most effective when the disease is detected in its early stages, reinforcing the importance of regular dermatological evaluations. 

 

Does skin cancer require chemotherapy?

Chemotherapy is not the standard treatment in most cases. It may be used in advanced stages or when metastases are present, particularly in melanoma.

In specific cases, targeted therapies and immunotherapies are used according to the tumor’s genetic profile. 

 

What are the recommended occupational prevention measures?

For workers exposed to sunlight, occupational prevention includes: the use of personal protective equipment (PPE) with UV protection, such as clothing with UPF ≥ 30, wide-brimmed hats with neck protection, UV-filter sunglasses, and sunscreen provided by the employer. Additional measures include taking breaks in shaded areas, adjusting work hours to avoid peak radiation times, and educational programs about sun exposure risks. 

 

References

[1] Zhou L, Zhong Y, Han L, Xie Y, Wan M. Global, regional, and national trends in the burden of melanoma and non-melanoma skin cancer: insights from the global burden of disease study 1990-2021. Sci Rep. 2025 Feb 18;15(1):5996. doi: 10.1038/s41598-025-90485-3

 

 

[2] Silva AA. Outdoor Exposure to Solar Ultraviolet Radiation and Legislation in Brazil. Health Phys. 2016 Jun;110(6):623-6. doi: 10.1097/HP.0000000000000489

 

 

[3] Vazquez Vde L, Silva TB, Vieira Mde A, de Oliveira AT, Lisboa MV, de Andrade DA, Fregnani JH, Carneseca EC. Melanoma characteristics in Brazil: demographics, treatment, and survival analysis. BMC Res Notes. 2015 Jan 16;8:4. doi: 10.1186/s13104-015-0972-8

 

 

[4] de Melo AC, Wainstein AJA, Buzaid AC, Thuler LCS. Melanoma signature in Brazil: epidemiology, incidence, mortality, and trend lessons from a continental mixed population country in the past 15 years. Melanoma Res. 2018 Dec;28(6):629-636. doi: 10.1097/CMR.0000000000000511

 

 

[5] Nehal KS, Bichakjian CK. Update on Keratinocyte Carcinomas. N Engl J Med. 2018 Jul 26;379(4):363-374. doi: 10.1056/NEJMra1708701

 

 

[6] Schadendorf D, van Akkooi ACJ, Berking C, Griewank KG, Gutzmer R, Hauschild A, Stang A, Roesch A, Ugurel S. Melanoma. Lancet. 2018 Sep 15;392(10151):971-984. doi: 10.1016/S0140-6736(18)31559-9. Erratum in: Lancet. 2019 Feb 23;393(10173):746. doi: 10.1016/S0140-6736(19)30361-7

 

 

[7] Long GV, Swetter SM, Menzies AM, Gershenwald JE, Scolyer RA. Cutaneous melanoma. Lancet. 2023 Aug 5;402(10400):485-502. doi: 10.1016/S0140-6736(23)00821-8. Epub 2023 Jul 24. Erratum in: Lancet. 2023 Aug 5;402(10400):450. doi: 10.1016/S0140-6736(23)01581-7

 

 

[8] Scarano C, Veneruso I, D’Argenio V. Genetic Landscape of Familial Melanoma. Genes (Basel). 2025 Jul 23;16(8):857. doi: 10.3390/genes16080857

 

 

[9] Soura E, Eliades PJ, Shannon K, Stratigos AJ, Tsao H. Hereditary melanoma: Update on syndromes and management: Genetics of familial atypical multiple mole melanoma syndrome. J Am Acad Dermatol. 2016 Mar;74(3):395-407; quiz 408-10. doi: 10.1016/j.jaad.2015.08.038

 

 

[10] Read J, Wadt KA, Hayward NK. Melanoma genetics. J Med Genet. 2016 Jan;53(1):1-14. doi: 10.1136/jmedgenet-2015-103150

 

 

[11] Potrony M, Puig-Butillé JA, Aguilera P, Badenas C, Carrera C, Malvehy J, Puig S. Increased prevalence of lung, breast, and pancreatic cancers in addition to melanoma risk in families bearing the cyclin-dependent kinase inhibitor 2A mutation: implications for genetic counseling. J Am Acad Dermatol. 2014 Nov;71(5):888-95. doi: 10.1016/j.jaad.2014.06.036

 

 

[12] Horn IP, Marks DL, Koenig AN, Hogenson TL, Almada LL, Goldstein LE, Romecin Duran PA, Vera R, Vrabel AM, Cui G, Rabe KG, Bamlet WR, Mer G, Sicotte H, Zhang C, Li H, Petersen GM, Fernandez-Zapico ME. A rare germline CDKN2A variant (47T>G; p16-L16R) predisposes carriers to pancreatic cancer by reducing cell cycle inhibition. J Biol Chem. 2021 Jan-Jun;296:100634. doi: 10.1016/j.jbc.2021.100634

 

 

[13] Ribeiro Moura Brasil Arnaut J, Dos Santos Guimarães I, Evangelista Dos Santos AC, de Moraes Lino da Silva F, Machado JR, de Melo AC. Molecular landscape of Hereditary Melanoma. Crit Rev Oncol Hematol. 2021 Aug;164:103425. doi: 10.1016/j.critrevonc.2021.103425

 

 

[14] Swetter SM, Tsao H, Bichakjian CK, Curiel-Lewandrowski C, Elder DE, Gershenwald JE, Guild V, Grant-Kels JM, Halpern AC, Johnson TM, Sober AJ, Thompson JA, Wisco OJ, Wyatt S, Hu S, Lamina T. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2019 Jan;80(1):208-250. doi: 10.1016/j.jaad.2018.08.055

 

 

[15] Ribeiro Moura Brasil Arnaut J, Dos Santos Guimarães I, Evangelista Dos Santos AC, de Moraes Lino da Silva F, Machado JR, de Melo AC. Molecular landscape of Hereditary Melanoma. Crit Rev Oncol Hematol. 2021 Aug;164:103425. doi: 10.1016/j.critrevonc.2021.103425

 

 

[16] Pauley K, Khan A, Kohlmann W, Jeter J. Considerations for Germline Testing in Melanoma: Updates in Behavioral Change and Pancreatic Surveillance for Carriers of CDKN2A Pathogenic Variants. Front Oncol. 2022 Mar 16;12:837057. doi: 10.3389/fonc.2022.837057

 

 

[17] Curti BD, Faries MB. Recent Advances in the Treatment of Melanoma. N Engl J Med. 2021 Jun 10;384(23):2229-2240. doi: 10.1056/NEJMra2034861

 

 

[18] Bai X, Flaherty KT. Targeted and immunotherapies in BRAF mutant melanoma: where we stand and what to expect. Br J Dermatol. 2021 Aug;185(2):253-262. doi: 10.1111/bjd.19394

 

 

[19] Kim HJ, Kim YH. Molecular Frontiers in Melanoma: Pathogenesis, Diagnosis, and Therapeutic Advances. Int J Mol Sci. 2024 Mar 4;25(5):2984. doi: 10.3390/ijms25052984

 

 

[20] US Preventive Services Task Force; Mangione CM, Barry MJ, Nicholson WK, Chelmow D, Coker TR, Davis EM, Donahue KE, Jaén CR, Kubik M, Li L, Ogedegbe G, Rao G, Ruiz JM, Stevermer J, Tsevat J, Underwood SM, Wong JB. Screening for Skin Cancer: US Preventive Services Task Force Recommendation Statement. JAMA. 2023 Apr 18;329(15):1290-1295. doi: 10.1001/jama.2023.4342

 

 

[21] Abbasi NR, Shaw HM, Rigel DS, Friedman RJ, McCarthy WH, Osman I, Kopf AW, Polsky D. Early diagnosis of cutaneous melanoma: revisiting the ABCD criteria. JAMA. 2004 Dec 8;292(22):2771-6. doi: 10.1001/jama.292.22.2771

 

 

[22] Madan V, Lear JT, Szeimies RM. Non-melanoma skin cancer. Lancet. 2010 Feb 20;375(9715):673-85. doi: 10.1016/S0140-6736(09)61196-X