Continuing Education Activity

Skin cancer encompasses a broad range of benign and malignant neoplasms that are common worldwide and more prevalent than many other cancer types. This condition involves the neoplastic proliferation of cells and tissues within the skin and can be associated with significant morbidity and mortality. UV radiation is a primary etiologic factor for most subtypes of skin cancer, including basal cell carcinoma, squamous cell carcinoma, and melanoma. These cancers may present with varying clinical features and often require evaluation through a skin biopsy and histopathological assessment to determine the specific type. This heterogeneous group of neoplasms may require a skin biopsy with histopathological evaluation and advanced therapies, including topical treatments, local non-topical therapies (eg, antineoplastic injections), systemic medications (eg, chemotherapy and immunotherapy), radiation therapy, and surgical or procedural interventions (eg, Mohs micrographic surgery and cryosurgery).

Risk factors, including UV exposure and genetic mutations, contribute to skin cancer development, thereby making preventive measures such as sunscreen use and minimizing UV exposure essential. In addition, early detection and tailored treatment are essential for optimal outcomes. This activity reviews the epidemiology, genetics, clinical presentation, and management of skin cancer and provides healthcare professionals with the knowledge and tools needed to improve patient care and outcomes. This activity also highlights the importance of collaboration among interprofessional healthcare providers to enhance patient care for this complex and prevalent condition.

Objectives:

• Identify early signs and symptoms of various skin cancer subtypes for timely diagnosis and treatment.
• Apply evidence-based guidelines for managing and treating skin cancer, including surgical and nonsurgical options.
• Select the appropriate diagnostic test, such as a skin biopsy, to identify skin lesions that may be skin cancer.
• Collaborate with interdisciplinary healthcare teams to ensure a comprehensive approach to the diagnosis and treatment of skin cancer.

Introduction

Skin neoplasms are one of the most common diagnoses among patient encounters.[1] Evaluating both benign and malignant neoplasms is vital, particularly due to the increasing incidence of skin cancers and complications associated with the condition.[2][3] Skin cancer has multiple etiologic factors, with UV radiation-induced DNA damage and oncogenesis being the most prominent. Preventive strategies, such as sunscreen application, are essential in reducing risk.[4] After evaluation by a trained healthcare provider, a biopsy is typically performed, and histopathological evaluation helps confirm the diagnosis and differentiate the type of skin cancer from other conditions.[5] Management of skin cancer may involve observation, topical therapies, local non-topical treatments (eg, antineoplastic medication injections), systemic regimens (eg, chemotherapy and immunotherapy), radiation therapy, and surgical or procedural interventions (eg, Mohs micrographic surgery and cryosurgery).

The skin's anatomical complexity allows skin cancer to arise from any of its cells or components. The proliferation of cells in skin cancer can be benign or malignant (see Image. Anatomy of the Human Skin). Please see StatPearls' companion resource, "Anatomy, Skin (Integument)," for more information on skin anatomy. In standard literature, malignant skin cancer is typically categorized into melanoma and nonmelanoma skin cancers, which usually refer to basal cell carcinoma or squamous cell carcinoma. However, this classification can be problematic, as skin cancer can originate from various cells and subdivisions of the skin.

Benign epidermal tumors may include epidermal nevi, pseudoepitheliomatous hyperplasia (eg, prurigo nodularis), and acanthomas (eg, seborrheic keratosis). Premalignant dysplasia, such as actinic keratosis and arsenical keratosis, may also be present. Malignant tumors of the epidermis include intraepidermal carcinoma (eg, Bowen disease), basal cell carcinoma, squamous cell carcinoma, and verrucous carcinoma. Please see StatPearls' companion resources, "Seborrheic Keratosis," "Clear Cell Acanthoma," "Cutaneous Horn," "Keratoacanthoma," "Cutaneous Melanoacanthoma," "Cutaneous Squamous Cell Carcinoma," "Intraepidermal Carcinoma," and "Basal Cell Carcinoma," for more information on common epidermal tumors.

Pigmentary lesions include those with basal melanocytic proliferation (eg, solar lentigo), junctional or dermal melanocytic lesions (eg, Spitz nevus), dysplastic lesions (eg, dysplastic nevus), and malignant lesions (eg, melanoma, clear cell sarcoma). Please see StatPearls' companion resources, "Subungual Melanoma," "Lentigo Maligna Melanoma," "Metastatic Melanoma," "Dysplastic Nevi," "Atypical Mole," "Acral Lentiginous Melanoma," and "Congenital Melanocytic Nevi," for more information on pigmentary lesions relevant to skin cancer. 

Skin cancer may arise from cutaneous appendages, such as hair follicles (eg, desmoplastic trichoepithelioma), sebaceous glands (eg, sebaceous adenoma and sebaceous carcinoma), apocrine glands (eg, spiradenoma), and eccrine glands (eg, porocarcinoma). Please see StatPearls' companion resources, "Desmoplastic Trichoepithelioma," "Sebaceous Carcinoma," "Syringoma," "Spiradenoma," "Trichoblastoma and Trichoepithelioma," and "Cylindroma," for more information on tumors of cutaneous appendages.

Fibrous tissues of the skin can also proliferate, leading to skin cancer, such as dermatofibroma and its malignant counterpart, dermatofibrosarcoma protuberans. Please see StatPearls' companion resources, "Dermatofibrosarcoma Protuberans" and "Dermatofibroma," for more information on fibrous tumors. 

The presence of fat, muscle, cartilage, and bone can lead to skin cancers such as liposarcoma, leiomyosarcoma, chondroma, and osteosarcoma (although osteosarcoma may be considered metastatic by some). Please see StatPearls' companion resources, "Atypical Fibroxanthoma" and "Leiomyosarcoma," for more information on fat, muscle, cartilage, and bone tumors. 

Benign and malignant skin cancers can arise from neural tissue, such as Merkel cell carcinoma and schwannoma, or from vascular tissue, such as hemangioma and angiosarcoma. Please see StatPearls' companion resources, "Angiolymphoid Hyperplasia With Eosinophilia," "Angiosarcoma," "Merkel Cell Carcinoma of the Skin," "Neurothekeoma," "Hemangioma," "Cutaneous Vascular Malignancies," "Angiosarcoma," " Kaposi Sarcoma," and "Cutaneous Angiofibroma," for more information on common tumors of neural and vascular origin.

Infiltrative skin cancers can arise from various immune cells that reside in the skin, including mastocytoma, xanthoma, Langerhans cell histiocytosis, T-cell lymphoma, natural killer (NK)—cell lymphoma, and B-cell lymphoma. Please see StatPearls' companion resources "Sezary Syndrome," "Extranodal NK-Cell Lymphoma," "Peripheral T-Cell Lymphoma," "Dermatopathology Evaluation of Cysts," "Mastocytoma," "Mycosis Fungoides," and "Lymphomatoid Papulosis," for more information.

Etiology

The etiology of skin cancer varies depending on the type of cancer. UV radiation is a major etiologic factor for most nonmelanoma skin cancers, including squamous cell carcinoma and basal cell carcinoma, as well as melanoma.[6][7][8] Along with chemical carcinogens and wound-related changes, UV radiation is believed to damage DNA, which results in mutations in tumor suppressor genes (eg, p53) and genomic instability.[9][10][11] Most cutaneous squamous cell carcinomas (90%) exhibit UV-induced p53 gene mutations, leading to the uncontrolled proliferation of keratinocytes.[12] Mutations implicated in basal cell carcinoma include mutations in the PTCH gene and the p53 gene.[13] Mutations associated with melanoma include alterations in cyclin-dependent kinase inhibitor-2A (CDKN2A), melanocortin-1 receptor (MC1R), BRAF, and DNA repair enzymes, such as UV-specific endonuclease in xeroderma pigmentosum.[14]

Multiple risk factors may synergistically interact with etiologic factors to accelerate skin cancer development, including age, sex, radiation exposure, environmental carcinogens, immune suppression, comorbid conditions, organ transplant history, family history, certain infections (eg, human papillomavirus), tanning bed use, vitamin levels, and occupational exposure.[15][16][17][4] Risk levels also vary within each category. For example, patients who receive thoracic cavity solid organ transplants (eg, heart) have a higher risk of skin cancer compared to those undergoing hematopoietic stem cell transplants, renal transplants, or other solid organ transplants.[18] 

Environmental carcinogens, such as arsenic and pollution, can accelerate DNA damage, increasing the risk of skin cancer.[19][20] Please see StatPearls' companion resource, "Overview of Environmental Skin Cancer Risks," for more information. Genetic predispositions also contribute to malignancies, as seen in conditions such as xeroderma pigmentosum, neurofibromatosis, and retinoblastoma.[21][22][23] Additionally, some skin cancers, such as Merkel cell carcinoma, are associated with infection, including the Merkel cell polyomavirus, which generally indicates a better prognosis in affected patients.[24] Although UV radiation is a significant factor in skin cancer development and progression, various other risk factors can accelerate this process on a case-by-case basis.

Table

What risk factors do many individuals regularly face in their day-to-day lives that may predispose them to skin cancer? How might you counsel individuals to reduce their exposure to environmental risk factors related to skin cancer?

Epidemiology

Skin cancers are more frequent than any other type of cancer worldwide and in the United States.[25][26][1] The economic burden of risk factors, such as indoor tanning, contributes to the rising incidence of skin cancer, resulting in an annual economic burden of at least 8.1 billion dollars in the United States.[27][28] The increasing number of people diagnosed with skin cancer highlights a significant health challenge, both in terms of patient well-being and healthcare expenditures.[29]

Skin cancer occurs in all races worldwide but is more common in individuals with lighter skin, likely due to the reduced photoprotective effects of epidermal melanin.[30] In individuals with lighter skin, approximately 75% to 80% of nonmelanoma skin cancers are basal cell carcinomas, whereas up to 25% are squamous cell carcinomas.[31][32] Heritable defects in DNA repair mechanisms, such as those seen in xeroderma pigmentosum and Muir-Torre syndrome, also increase the risk of cutaneous carcinomas in some patients.

Among skin cancers, melanoma has the highest disability-adjusted life year, basal cell carcinoma has the highest incidence rate, and squamous cell carcinoma has the highest prevalence.[1] The incidence of melanoma in the United States, from 1990 to 2019, increased to 17 per 100,000 individuals, and prevalence increased to 138 per 100,000 individuals. Meanwhile, nonmelanoma skin cancer had an incidence of 787 per 100,000 individuals and a prevalence of 359 per 100,000 individuals.[1] Males had a higher incidence, prevalence, and mortality rate than females from 1990 to 2019.[1] Although skin cancer occurs in all age groups, it is more common in older adults, likely due to increased cumulative UV light exposure.[33][34] Geographically, melanoma rates are higher in the northern half of the United States compared to the southern half, while nonmelanoma skin cancer incidence is highest in the southeastern, western, and northeastern regions of the country.[1]

Other malignancies, such as Merkel cell carcinoma or Kaposi sarcoma, have unique epidemiological information outside the scope of this resource. Merkel cell carcinoma is far more common in men and among individuals with lighter skin.[35] Kaposi sarcoma is more common in individuals with HIV.[36] Worldwide, skin cancer rates are highest in populations with significant UV light exposure and lighter skin tones, such as those in Europe and Australia.[37][38] 

Pathophysiology

The pathophysiology of skin cancer is not fully understood, but various etiological factors, with UV light being the most prominent, interact with risk factors that likely contribute to the development and neoplastic proliferation of skin cancer.[39] These proliferations may be benign or malignant; benign proliferation typically results from dysregulation, while malignant proliferation is driven by genetic and molecular alterations associated with UV radiation.[39]

Exposure to UV light from solar radiation is the most significant modifiable risk factor for developing both nonmelanoma skin cancer and melanoma.[40] UV radiation can be categorized into UV-A, UV-B, and UV-C based on their respective wavelengths—approximately 320 to 380 nm for UV-A, 280 to 320 nm for UV-B, and 100 to 280 nm for UV-C.[37] Sunlight is primarily composed of UV-A (~90%) and UV-B (~10%) radiation,[7] while UV-C rays are absorbed mainly by the atmosphere.[41]

UV-A, with its longer wavelength, penetrates the dermis and generates free radicals.[42] UV-B, with a shorter wavelength, penetrates to the level of the stratum basale of the epidermis, leading to the formation of pyrimidine dimers, such as thymidine dimers.[43][44] Both UV-A and UV-B contribute to carcinogenesis, with UV-A significantly impacting skin aging.[45] UV radiation causes cell injury and apoptosis and impairs DNA repair mechanisms, leading to DNA mutations.[46][47] Please see StatPearls' companion resource, "Biochemistry, DNA Repair," for more information on DNA damage from UV radiation. 

The development of cutaneous malignancy following DNA damage from solar radiation is multifactorial and influenced by genetic factors, Fitzpatrick skin type, and immunosuppressed status. Most (90%) cutaneous squamous cell carcinomas exhibit UV-induced p53 gene mutations, leading to uninhibited keratinocyte proliferation.[48] DNA mutations associated with basal cell carcinoma include mutations in the PTCH and p53 genes.[49] Melanoma-related DNA mutations include alterations in CDKN2A, MCR1, BRAF, and DNA repair enzymes, such as UV-specific endonuclease in xeroderma pigmentosum.[50][51] The complete list of genetic mutations and risk factors remains incomplete, but ongoing research continues to uncover new genes and targets involved in each subtype of skin cancer.[52][53][54]

Histopathology

The staging of skin cancer varies depending on the subtype and is beyond the scope of this resource. For example, histologic features of basal cell carcinoma include basophilic cells with minimal cytoplasm, and palisading or nests of cells may be observed. Necrosis and mitotic figures may also be evident (see Image. Basal Cell Carcinoma on Cheek—H&E Staining Showing Basaloid Islands). Histopathology showing intercellular bridges and pleomorphic nuclei, with or without nuclear molding, is consistent with squamous cell carcinoma. Keratin pearls may also be present but are not always observed (see Image. Squamous Cell Carcinoma). Please see StatPearls' companion resources, "Dermatopathology, Cutaneous Lymphomas" and "Melanoma Pathology," for more information on skin cancer histopathology.

History and Physical

A thorough skin examination is essential for identifying premalignant and malignant skin lesions, during which key symptoms (such as itching, bleeding, pain, and irritation) should be explored. Notably, it is essential to assess the location, texture, size, color, shape, borders, and any recent changes in suspicious lesions. Premalignant actinic keratoses often present as rough, gritty skin papules on an erythematous base.[55] Basal cell carcinomas usually appear as pink, pearly papules with telangiectasia (see Image. Basal Cell Carcinoma Presenting as Pink Papules on a Patient's Skin).[56] Squamous cell carcinomas are often pink, rough papules, patches, and plaques (see Image. Cutaneous Squamous Cell Carcinoma).[57] 

Melanomas are usually brown-to-black lesions with asymmetry, irregular borders, color variegation, and diameters greater than 6 mm (see Image. Ulcerated Acral Lentiginous Melanoma on Dorsal Toe). Please see StatPearls' companion resource, "Dermatoscopic Characteristics of Melanoma Versus Benign Lesions and Nonmelanoma Cancers," for more information. Any new or changing lesion that differs from other body nevi (often referred to as the "ugly duckling sign") should be considered suspicious.[58] A thorough full-body examination should be performed as soon as possible when a patient presents with a suspicious lesion, such as one consistent with melanoma.

Basal cell and squamous cell carcinomas are commonly found on parts of the head and neck that accumulate the most UV radiation over a lifetime, such as the nose, ears, and upper lip. Melanomas can occur anywhere on the body, with the most frequent locations being the backs and shoulders of men and the lower limbs of women.[59] Studies comparing melanoma risk per unit skin area have shown that the face is the highest-risk area for melanoma.[60] However, the presentation of skin cancer can vary across different body types and skin colors, so a thorough examination with dermoscopy and further diagnostic workup may be necessary if the clinical history and examination are insufficient or equivocal.

Evaluation

Patients at risk for cutaneous malignancy are typically evaluated by a medical professional with a full-body skin examination. While most primary care providers can conduct this exam, specialists with advanced dermatology training may assist with dermoscopy, allowing for a more detailed inspection of suspicious lesions. Please see StatPearls' companion resources, "Dermatoscopic Characteristics of Melanoma Versus Benign Lesions and Nonmelanoma Cancers" and "Dermoscopy Overview and Extradiagnostic Applications," for more information on skin cancer evaluation with dermoscopy.

Most concerning lesions identified during a physical examination will undergo an office procedure called a skin biopsy, typically a shave or punch biopsy. This is performed under local anesthesia during an outpatient visit. The specimen is then sent to a trained dermatopathologist for interpretation. If the pathologist confirms a diagnosis of cutaneous malignancy, further intervention is typically required based on the pathological diagnosis and clinical context. In some cases, laboratory tests may be necessary to prognosticate or assess the extent of the disease. For example, patients with suspected Kaposi sarcoma should undergo an HIV test.

A shave or punch biopsy is typically sufficient for most nonmelanoma skin cancers, provided it reaches an adequate depth to analyze the tissue pattern and possible perineural invasion. For melanoma, however, complete excisional removal is recommended. In the case of dermatofibrosarcoma protuberans, a deep incisional biopsy is necessary. For many lymphomas, such as cutaneous T-cell lymphoma, a broad-shave biopsy is preferred over a punch biopsy. Meanwhile, for cutaneous B-cell lymphoma, a deep incisional biopsy is preferred.[5] Imaging may be required to assess bony invasion, such as with squamous cell carcinoma. Following specific tumor guidelines is important, such as those provided by the National Comprehensive Cancer Network (NCCN), as these are frequently updated to reflect the latest research.

Treatment / Management

Treatment of precancerous lesions and cutaneous malignancies should be individualized to achieve the best clinical outcome for each patient. When presented as isolated lesions, precancerous actinic keratoses can be treated with lesion-directed therapies, such as cryotherapy.[61] In cases where patients have numerous lesions or diffuse actinic damage, field-directed therapies may be more appropriate than treating each lesion individually.[61] These therapies can include topical agents, such as 5-fluorouracil, imiquimod, and ingenol mebutate, or photodynamic therapy, which involves sensitizing the skin with a topical agent before treatment.[62]

Initial preemptive efforts should aim to reduce the patient's risk of developing cutaneous malignancies. This includes optimizing immunosuppressant regimens in solid organ transplant patients, such as switching to sirolimus, establishing appropriate surveillance schedules for patients receiving immunomodulatory therapies, and adequately treating precancerous lesions.[63] 

Many superficial basal cell and squamous cell carcinomas can be treated with topical or local therapies, depending on provider preference. However, the standard approach is surgical treatment using destructive methods such as electrodesiccation and curettage or surgical excision. Larger cancers or those in functionally or cosmetically sensitive areas (eg, head and neck) may qualify for micrographic dermatologic surgery or other forms of peripheral and deep margin assessment, such as Mohs micrographic surgery, according to the Appropriate Use Criteria.[64][65][66] 

Please see StatPearls' companion resources, "Mohs Micrographic Surgery Appropriate Use Criteria (AUC) Guidelines," "Mohs Micrographic Surgery," "Mohs Micrographic Surgery Evaluation and Treatment of Microcystic Adnexal Carcinoma," "Mohs Micrographic Surgery of Uncommon Tumors (Angiosarcoma, Eccrine, Paget, and Merkel Cell)," "Mohs Micrographic Surgery Management of Melanoma and Melanoma In Situ," and "Mohs Micrographic Surgery Evaluation and Treatment of Dermatofibrosarcoma Protuberans," for more information.

Patients with aggressive or recurrent basal cell carcinoma who are not good surgical candidates may be treated with radiation therapy, systemic medications (eg, vismodegib), or novel therapies such as oncolytic viruses.[67][68][69][70][71] Please see StatPearls' companion resource, "Vismodegib," for more information. Other malignancies, such as melanoma, are typically treated with surgical excision or other unique systemic therapies. Late-stage unresponsive malignancies may require chemotherapy or immunotherapy.[72][73]

Differential Diagnosis

Skin neoplasms can be either benign or malignant, with each type of skin cancer presenting in a variety of ways. Due to this diversity, the differential diagnosis includes all lesions that may appear as macules, patches, papules, plaques, or nodules. In rare cases, they may also present as vesicles, bullae, or pustules. The differential diagnoses should consider relevant vascular, infectious, neoplastic (eg, metastases to the skin from other organs), inflammatory, traumatic, metabolic, mechanical, allergic, autoimmune, and iatrogenic lesions.

Common lesions to distinguish from true skin cancer include:

• Psoriasis
• Atopic dermatitis
• Tinea corporis (or other body area)
• Acne vulgaris
• Warts
• Lupus erythematosus
• Actinic keratosis
• Metastatic skin tumors
• Sebaceous hyperplasia
• Nevus
• Benign melanocytic lesions
• Dysplastic nevi [74][75][76][77][78]

Cysts should also be considered in the differential diagnosis of skin cancer. Please see StatPearls' companion resource, "Dermatopathology Evaluation of Cysts," for more information.

Staging

The staging of skin cancer is specific to each subtype of skin cancer and is beyond the scope of this resource. Please see StatPearls' companion resource, "Clinical Guidelines for the Staging, Diagnosis, and Management of Cutaneous Malignant Melanoma," for more information on the staging, diagnosis, and management of cutaneous malignant melanoma.

Prognosis

Most skin cancers, particularly nonmelanoma types such as basal cell and squamous cell carcinomas, have a good prognosis with curative management.[79][80][81] However, prognosis can vary widely depending on the subtype. For example, Merkel cell carcinoma has an unfavorable prognosis, with survival rates often less than 20%.[82][83][84] The prognosis generally depends on specific risk factors and treatment options for each malignancy. Detailed prognosis for each subtype is beyond the scope of this resource.

Complications

Skin cancer can lead to several complications, many of which can be prevented with early detection and management. However, the complications vary based on the subtype of skin cancer. General complications include:

• Further invasion of the cancer locally, either peripherally or deeply, causing tissue damage and symptoms such as pain.[85]
• Metastasis of skin cancer to other areas of the body, including the brain, lungs, lymph nodes, or skin.[86]
• Infection of skin cancer, particularly in ulcerated lesions.[87]
• Scarring and tissue destruction from the cancer or its surrounding skin, which could lead to temporary or permanent physical debility or disfigurement.[88]
• Unpleasant patient-reported symptoms, such as pain, itching, bleeding, or discomfort in the area of the skin cancer.[89][90]
• Recurrence of skin cancer, even after treatment.[91]
• Psychiatric conditions associated with skin cancer, such as depression or anxiety.[92]
• Psychological complications, such as distress or fear.[93]
• Effects of treatments, such as adverse drug events.[94]
• Impaired immune function.[95]

Early evaluation and management of skin cancer are crucial to prevent potential complications. For example, recurrence rates of skin cancer vary widely depending on the subtype. Basal cell carcinoma has a rare recurrence rate after treatment with micrographic dermatologic surgery.[96] In contrast, mucinous carcinoma of the skin, which can be either primary or metastatic from other areas (eg, colon and breast), has a local recurrence rate estimated to be between 20% and 40%. Recurrence is most commonly associated with the tumor's size.[97] The interprofessional team's coordination throughout a patient's care continuum is essential in communicating skin cancer prevention, early detection of skin cancer, tailored treatment, and early detection of complications. 

Enhancing Healthcare Team Outcomes

Patients with skin cancer are at high risk for morbidity and mortality associated with the disease. Early identification and management are critical in reducing these risks. The care of skin cancer patients requires a collaborative approach among healthcare professionals to ensure patient-centered care and optimize outcomes. Dermatologists, primary care physicians, pathologists, surgeons, advanced practitioners, nurses, pharmacists, and other healthcare providers involved in patient care should have the necessary clinical skills and knowledge to accurately diagnose and manage skin cancer. This includes expertise in recognizing the varied clinical presentations and understanding the nuances of diagnostic techniques such as biopsies and histopathology.

Healthcare teams can improve early detection and, in some cases, the eradication of skin cancer through collaboration. Patient and caregiver education on risk factors, medication adherence, treatments, and prevention (eg, sun protection) is crucial to reduce morbidity associated with skin cancer.[98] Please see StatPearls' companion resource, "Skin Cancer Prevention," for more information on skin cancer prevention. A strategic approach is essential, incorporating evidence-based strategies to optimize treatment plans and minimize adverse effects. Ethical considerations should guide decision-making, ensuring informed consent and respecting patient autonomy in treatment choices.

Each healthcare professional must understand their responsibilities and contribute their unique expertise to the patient's care plan, fostering a collaborative, multidisciplinary approach. Effective interprofessional communication is crucial, facilitating seamless information exchange and collaborative decision-making among healthcare team members. Care coordination is pivotal in ensuring that the patient's journey from diagnosis to treatment and follow-up is well-managed, minimizing errors and enhancing patient safety. By embracing these principles—skill, strategy, ethics, responsibilities, interprofessional communication, and care coordination—healthcare professionals can deliver patient-centered care, ultimately improving patient outcomes and enhancing team performance in the management of skin cancer.

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References

1.

Aggarwal P, Knabel P, Fleischer AB. United States burden of melanoma and non-melanoma skin cancer from 1990 to 2019. J Am Acad Dermatol. 2021 Aug;85(2):388-395. [PubMed: 33852922]

2.

Rogers HW, Weinstock MA, Feldman SR, Coldiron BM. Incidence Estimate of Nonmelanoma Skin Cancer (Keratinocyte Carcinomas) in the U.S. Population, 2012. JAMA Dermatol. 2015 Oct;151(10):1081-6. [PubMed: 25928283]

3.

Glazer AM, Winkelmann RR, Farberg AS, Rigel DS. Analysis of Trends in US Melanoma Incidence and Mortality. JAMA Dermatol. 2017 Feb 01;153(2):225-226. [PubMed: 28002545]

4.

Haddad S, Weise JJ, Wagenpfeil S, Vogt T, Reichrath J. Malignant Melanoma: Vitamin D Status as a Risk and Prognostic Factor - Meta-analyses and Systematic Review. Anticancer Res. 2025 Jan;45(1):27-37. [PubMed: 39740829]

5.

Elston DM, Stratman EJ, Miller SJ. Skin biopsy: Biopsy issues in specific diseases. J Am Acad Dermatol. 2016 Jan;74(1):1-16; quiz 17-8. [PubMed: 26702794]

6.

Kaplan B, von Dannecker R, Arbiser JL. The Carcinogenesis of the Human Scalp: An Immunometabolic-Centered View. Int J Mol Sci. 2024 Nov 10;25(22) [PMC free article: PMC11593518] [PubMed: 39596133]

7.

D'Orazio J, Jarrett S, Amaro-Ortiz A, Scott T. UV radiation and the skin. Int J Mol Sci. 2013 Jun 07;14(6):12222-48. [PMC free article: PMC3709783] [PubMed: 23749111]

8.

Armstrong BK, Kricker A. How much melanoma is caused by sun exposure? Melanoma Res. 1993 Dec;3(6):395-401. [PubMed: 8161879]

9.

Matsuda K, Kurohama H, Kuwatsuka Y, Iwanaga A, Murota H, Nakashima M. Detection of genome instability by 53BP1 expression as a long-lasting health effect in human epidermis surrounding radiation-induced skin cancers. J Radiat Res. 2024 Dec 16;65(Supplement_1):i57-i66. [PMC free article: PMC11647933] [PubMed: 39679893]

10.

Dousset L, Mahfouf W, Younes H, Fatrouni H, Faucheux C, Muzotte E, Khalife F, Rossignol R, Moisan F, Cario M, Claverol S, Favot-Laforge L, Nieminen AI, Vainio S, Ali N, Rezvani HR. Energy metabolism rewiring following acute UVB irradiation is largely dependent on nuclear DNA damage. Free Radic Biol Med. 2025 Feb 01;227:459-471. [PubMed: 39667588]

11.

Li Y, Wang X, Liu X, Li X, Zhang J, Li Y. The dysregulation of PARP9 expression is linked to apoptosis and DNA damage in gastric cancer cells. PLoS One. 2024;19(12):e0316476. [PMC free article: PMC11687892] [PubMed: 39739965]

12.

Jasmine F, Argos M, Khamkevych Y, Islam T, Rakibuz-Zaman M, Shahriar M, Shea CR, Ahsan H, Kibriya MG. Molecular Profiling and the Interaction of Somatic Mutations with Transcriptomic Profiles in Non-Melanoma Skin Cancer (NMSC) in a Population Exposed to Arsenic. Cells. 2024 Jun 18;13(12) [PMC free article: PMC11201393] [PubMed: 38920684]

13.

Murgia G, Valtellini L, Denaro N, Nazzaro G, Bortoluzzi P, Benzecry V, Passoni E, Marzano AV. Gorlin Syndrome-Associated Basal Cell Carcinomas Treated with Vismodegib or Sonidegib: A Retrospective Study. Cancers (Basel). 2024 Jun 07;16(12) [PMC free article: PMC11201977] [PubMed: 38927872]

14.

López Riquelme I, Martínez García S, Serrano Ordónez A, Martínez Pilar L. Germline mutations predisposing to melanoma and associated malignancies and syndromes: a narrative review. Int J Dermatol. 2024 Dec 09; [PubMed: 39651613]

15.

Wu S, Han J, Laden F, Qureshi AA. Long-term ultraviolet flux, other potential risk factors, and skin cancer risk: a cohort study. Cancer Epidemiol Biomarkers Prev. 2014 Jun;23(6):1080-9. [PMC free article: PMC4151553] [PubMed: 24876226]

16.

Saladi RN, Persaud AN. The causes of skin cancer: a comprehensive review. Drugs Today (Barc). 2005 Jan;41(1):37-53. [PubMed: 15753968]

17.

Long Y, Pan Y, Yang H, Wang X, Jiang Z, Sun T. The Genetic Causal Effect of Autoimmune Diseases on pan-Cancers: Evidence from Mendelian Randomization. J Cancer. 2025;16(2):567-576. [PMC free article: PMC11685688] [PubMed: 39744497]

18.

Wheless L, Anand N, Hanlon A, Chren MM. Differences in Skin Cancer Rates by Transplanted Organ Type and Patient Age After Organ Transplant in White Patients. JAMA Dermatol. 2022 Nov 01;158(11):1287-1292. [PMC free article: PMC9520444] [PubMed: 36169974]

19.

Zhang Q, Man J, Zhao T, Sun D, Zhang Z. YTHDF2 promotes arsenic-induced malignant phenotypes by degrading PIDD1 mRNA in human keratinocytes. Chem Biol Interact. 2025 Jan 25;406:111352. [PubMed: 39675544]

20.

MacRae JD, Abbott MD, Fufaa GD. Cancer incidence associations with drinking water arsenic levels and disinfection methods in Maine, USA. J Water Health. 2024 Nov;22(11):2246-2256. [PubMed: 39611682]

21.

Anh Luong TL, Hoang TL, Tran DP, Le TM, Tran H, Ho PT, Hoang HN, Giang H, Vu DL, Dinh NH, Nguyen MT, Nguyen HS. Identification of novel variants of XPA and POLH/XPV genes in xeroderma pigmentosum patients in Vietnam. Per Med. 2024;21(6):341-351. [PubMed: 39655645]

22.

Moodley M, Ortman C. Neurofibromatosis type 2-related schwannomatosis - An update. Semin Pediatr Neurol. 2024 Dec;52:101171. [PubMed: 39622611]

23.

Constantinou SM, Bennett DC. Cell Senescence and the Genetics of Melanoma Development. Genes Chromosomes Cancer. 2024 Oct;63(10):e23273. [PubMed: 39422311]

24.

Gamissans M, Muntaner-Virgili C, Penín RM, Marcoval J. Characteristics of Spontaneous Regression in Merkel Cell Carcinoma: A Retrospective Analysis of Patient and Tumor Features. Clin Exp Dermatol. 2024 Dec 14; [PubMed: 39673745]

25.

Gordon R. Skin cancer: an overview of epidemiology and risk factors. Semin Oncol Nurs. 2013 Aug;29(3):160-9. [PubMed: 23958214]

26.

Guy GP, Thomas CC, Thompson T, Watson M, Massetti GM, Richardson LC., Centers for Disease Control and Prevention (CDC). Vital signs: melanoma incidence and mortality trends and projections - United States, 1982-2030. MMWR Morb Mortal Wkly Rep. 2015 Jun 05;64(21):591-6. [PMC free article: PMC4584771] [PubMed: 26042651]

27.

Guy GP, Zhang Y, Ekwueme DU, Rim SH, Watson M. The potential impact of reducing indoor tanning on melanoma prevention and treatment costs in the United States: An economic analysis. J Am Acad Dermatol. 2017 Feb;76(2):226-233. [PMC free article: PMC5737631] [PubMed: 27939556]

28.

Kao SZ, Ekwueme DU, Holman DM, Rim SH, Thomas CC, Saraiya M. Economic burden of skin cancer treatment in the USA: an analysis of the Medical Expenditure Panel Survey Data, 2012-2018. Cancer Causes Control. 2023 Mar;34(3):205-212. [PMC free article: PMC11001479] [PubMed: 36449145]

29.

Guy GP, Machlin SR, Ekwueme DU, Yabroff KR. Prevalence and costs of skin cancer treatment in the U.S., 2002-2006 and 2007-2011. Am J Prev Med. 2015 Feb;48(2):183-187. [PMC free article: PMC4603424] [PubMed: 25442229]

30.

Bradford PT. Skin cancer in skin of color. Dermatol Nurs. 2009 Jul-Aug;21(4):170-7, 206; quiz 178. [PMC free article: PMC2757062] [PubMed: 19691228]

31.

Thamm JR, Schuh S, Welzel J. Epidemiology and Risk Factors of Actinic Keratosis. What is New for The Management for Sun-Damaged Skin. Dermatol Pract Concept. 2024 Sep 01;14(3 S1) [PMC free article: PMC11566825] [PubMed: 39133637]

32.

Aristizabal MA, Zieman D, Berman HS, Williams KA, Markham DJ, Heckman MG, Hochwald A, Barbosa NS, Degesys C. Disparities in Basal Cell Carcinoma: A Comparative Analysis of Hispanic and Non-Hispanic White Individuals. J Clin Aesthet Dermatol. 2024 Oct;17(10):24-27. [PMC free article: PMC11495162] [PubMed: 39445326]

33.

Duan R, Jiang L, Wang T, Li Z, Yu X, Gao Y, Jia R, Fan X, Su W. Aging-induced immune microenvironment remodeling fosters melanoma in male mice via γδ17-Neutrophil-CD8 axis. Nat Commun. 2024 Dec 30;15(1):10860. [PMC free article: PMC11685811] [PubMed: 39738047]

34.

Holdam ASK, Koudahl V, Frostberg E, Rønlund K, Rahr HB. Prevalence, incidence and trends of keratinocyte carcinoma in Denmark 2007-2021: A population-based register study. Cancer Epidemiol. 2025 Feb;94:102732. [PubMed: 39708578]

35.

Terrell M, Dongarwar D, Rashid R, Hamisu S, Orengo I. Inpatient prevalence and factors associated with Merkel Cell Carcinoma inpatient hospitalization in the United States. Arch Dermatol Res. 2024 Jul 27;316(8):489. [PubMed: 39066821]

36.

Ruffieux Y, Mwansa-Kambafwile J, Metekoua C, Tombe-Nyahuma T, Bohlius J, Muchengeti M, Egger M, Rohner E. HIV-1 Viremia and Cancer Risk in 2.8 Million People: the South African HIV Cancer Match Study. Clin Infect Dis. 2024 Dec 30; [PubMed: 39736138]

37.

Sharma K, Dixon KM, Münch G, Chang D, Zhou X. Ultraviolet and infrared radiation in Australia: assessing the benefits, risks, and optimal exposure guidelines. Front Public Health. 2024;12:1505904. [PMC free article: PMC11688272] [PubMed: 39744344]

38.

Indini A, Didoné F, Massi D, Puig S, Casadevall JR, Bennett D, Katalinic A, Sanvisens A, Ferrari A, Lasalvia P, Demuru E, Ragusa R, Mayer-da-Silva A, Blum M, Mousavi M, Kuehni C, Mihor A, Mandalà M, Trama A., EUROCARE-6 Working Group. Incidence and prognosis of cutaneous melanoma in European adolescents and young adults (AYAs): EUROCARE-6 retrospective cohort results. Eur J Cancer. 2024 Dec;213:115079. [PubMed: 39546860]

39.

Didona D, Paolino G, Bottoni U, Cantisani C. Non Melanoma Skin Cancer Pathogenesis Overview. Biomedicines. 2018 Jan 02;6(1) [PMC free article: PMC5874663] [PubMed: 29301290]

40.

Vile GF, Tanew-Ilitschew A, Tyrrell RM. Activation of NF-kappa B in human skin fibroblasts by the oxidative stress generated by UVA radiation. Photochem Photobiol. 1995 Sep;62(3):463-8. [PubMed: 8570706]

41.

Beltrán FJ, Chávez AM, Jiménez-López MA, Álvarez PM. Kinetic modelling of UV_C and UV_C/H₂O₂ oxidation of an aqueous mixture of antibiotics in a completely mixed batch photoreactor. Environ Sci Pollut Res Int. 2024 Sep;31(43):55222-55238. [PMC free article: PMC11415419] [PubMed: 39225925]

42.

Mohania D, Chandel S, Kumar P, Verma V, Digvijay K, Tripathi D, Choudhury K, Mitten SK, Shah D. Ultraviolet Radiations: Skin Defense-Damage Mechanism. Adv Exp Med Biol. 2017;996:71-87. [PubMed: 29124692]

43.

Mori M, Kobayashi H, Sugiyama C, Katsumura Y, Furihata C. Effect of aging on unscheduled DNA synthesis induction by UV-B irradiation in hairless mouse epidermis. J Toxicol Sci. 2000 Aug;25(3):181-8. [PubMed: 10987125]

44.

Schmidt-Rose T, Pollet D, Will K, Bergemann J, Wittern KP. Analysis of UV-B-induced DNA damage and its repair in heat-shocked skin cells. J Photochem Photobiol B. 1999 Nov-Dec;53(1-3):144-52. [PubMed: 10672538]

45.

Fotopoulou A, Angelopoulou MT, Pratsinis H, Mavrogonatou E, Kletsas D. A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence. Aging Cell. 2025 Mar;24(3):e14422. [PMC free article: PMC11896172] [PubMed: 39698891]

46.

Yan L, Cao X, Wang L, Chen J, Sancar A, Zhong D. Dynamics and mechanism of DNA repair by a bifunctional cryptochrome. Proc Natl Acad Sci U S A. 2024 Dec 10;121(50):e2417633121. [PMC free article: PMC11648919] [PubMed: 39621923]

47.

Ghosh S, Orman MA. UV-Induced DNA Repair Mechanisms and Their Effects on Mutagenesis and Culturability in Escherichia coli. bioRxiv. 2024 Nov 14; [PubMed: 39605428]

48.

Black AP, Ogg GS. The role of p53 in the immunobiology of cutaneous squamous cell carcinoma. Clin Exp Immunol. 2003 Jun;132(3):379-84. [PMC free article: PMC1808735] [PubMed: 12780682]

49.

Kim MY, Park HJ, Baek SC, Byun DG, Houh D. Mutations of the p53 and PTCH gene in basal cell carcinomas: UV mutation signature and strand bias. J Dermatol Sci. 2002 May;29(1):1-9. [PubMed: 12007715]

50.

Ascierto PA, Kirkwood JM, Grob JJ, Simeone E, Grimaldi AM, Maio M, Palmieri G, Testori A, Marincola FM, Mozzillo N. The role of BRAF V600 mutation in melanoma. J Transl Med. 2012 Jul 09;10:85. [PMC free article: PMC3391993] [PubMed: 22554099]

51.

Helgadottir H, Olsson H, Tucker MA, Yang XR, Höiom V, Goldstein AM. Phenocopies in melanoma-prone families with germ-line CDKN2A mutations. Genet Med. 2018 Sep;20(9):1087-1090. [PMC free article: PMC6916246] [PubMed: 29215650]

52.

Gabriel JA, Weerasinghe N, Balachandran P, Salih R, Orchard GE. A Narrative Review of Molecular, Immunohistochemical and In-Situ Techniques in Dermatopathology. Br J Biomed Sci. 2024;81:13437. [PMC free article: PMC11687224] [PubMed: 39741925]

53.

Makwana K, Velazquez EJ, Marzese DM, Smith B, Bhowmick NA, Faries MB, Hamid O, Boiko AD. NRF-1 transcription factor regulates expression of an innate immunity checkpoint, CD47, during melanomagenesis. Front Immunol. 2024;15:1495032. [PMC free article: PMC11685207] [PubMed: 39742254]

54.

Lagacé F, Mahmood F, Conte S, Mija LA, Moustaqim-Barrette A, LeBeau J, McKenna A, Maazi M, Hanna J, Kelly ASV, Lazarowitz R, Rahme E, Hrubeniuk TJ, Sweeney E, Litvinov IV. Investigating Skin Cancer Risk and Sun Safety Practices Among LGBTQ+ Communities in Canada. Curr Oncol. 2024 Dec 19;31(12):8039-8053. [PMC free article: PMC11674060] [PubMed: 39727716]

55.

Lam J, Ellis SR, Sivamani RK. Inflamed actinic keratoses associated with pemetrexed and carboplatin therapy. Dermatol Online J. 2017 Oct 15;23(10) [PubMed: 29469794]

56.

Stafford HD, Dokic Y, Huttenbach Y, Wasko C, Ranario JS. Report of Basal Cell Carcinoma Occurring With a Desmoplastic Trichilemmoma Successfully Treated With Mohs Micrographic Surgery. Cureus. 2024 Jun;16(6):e61910. [PMC free article: PMC11227905] [PubMed: 38975532]

57.

Teoh J, Gan A, Ramalingam J, Elsheikh S, Jerrom R. Papular lesion occurring within a longstanding warty plaque, in skin of colour Fitzpatrick type 4-5. Skin Health Dis. 2024 Apr;4(2):e328. [PMC free article: PMC10988697] [PubMed: 38577042]

58.

Daniel Jensen J, Elewski BE. The ABCDEF Rule: Combining the "ABCDE Rule" and the "Ugly Duckling Sign" in an Effort to Improve Patient Self-Screening Examinations. J Clin Aesthet Dermatol. 2015 Feb;8(2):15. [PMC free article: PMC4345927] [PubMed: 25741397]

59.

Matthews NH, Li WQ, Qureshi AA, Weinstock MA, Cho E. Epidemiology of Melanoma. In: Ward WH, Farma JM, editors. Cutaneous Melanoma: Etiology and Therapy [Internet]. Codon Publications; Brisbane (AU): Dec 21, 2017. [PubMed: 29461782]

60.

Green A, MacLennan R, Youl P, Martin N. Site distribution of cutaneous melanoma in Queensland. Int J Cancer. 1993 Jan 21;53(2):232-6. [PubMed: 8425760]

61.

Peris K, Fargnoli MC. Conventional treatment of actinic keratosis: an overview. Curr Probl Dermatol. 2015;46:108-14. [PubMed: 25561214]

62.

Chung AT, Taguibao JN, Siripunvarapon AH, Frez MLF. Cutaneous Squamous Cell Carcinoma and Multiple Basal Cell Carcinomas in Xeroderma Pigmentosum-Variant Type Treated with Imiquimod 5% Cream and Radiotherapy: A Case Report. Acta Med Philipp. 2024;58(17):100-105. [PMC free article: PMC11484572] [PubMed: 39431256]

63.

Joo V, Abdelhamid K, Noto A, Latifyan S, Martina F, Daoudlarian D, De Micheli R, Pruijm M, Peters S, Hullin R, Gaide O, Pantaleo G, Obeid M. Primary prophylaxis with mTOR inhibitor enhances T cell effector function and prevents heart transplant rejection during talimogene laherparepvec therapy of squamous cell carcinoma. Nat Commun. 2024 Apr 30;15(1):3664. [PMC free article: PMC11063183] [PubMed: 38693123]

64.

Sleiwah A, Wright TC, Chapman T, Dangoor A, Maggiani F, Clancy R. Dermatofibrosarcoma Protuberans in Children. Curr Treat Options Oncol. 2022 Jun;23(6):843-854. [PubMed: 35394606]

65.

Gil-Lianes J, Marti-Marti I, Morgado-Carrasco D. Secondary Intention Healing After Mohs Micrographic Surgery: An Updated Review of Classic and Novel Applications, Benefits and Complications. Actas Dermosifiliogr. 2025 Jan 02; [PubMed: 39755147]

66.

Żółkiewicz J, Banciu L, Sławińska M, Frumosu M, Tebeică T, Sobjanek M, Leventer M. The Application of Mohs Micrographic Surgery in the Treatment of Acral Basal Cell Carcinoma: A Report of Two Cases. J Clin Med. 2024 Nov 05;13(22) [PMC free article: PMC11594616] [PubMed: 39597787]

67.

Frampton JE, Basset-Séguin N. Vismodegib: A Review in Advanced Basal Cell Carcinoma. Drugs. 2018 Jul;78(11):1145-1156. [PubMed: 30030732]

68.

Mbous YPV, Mohamed R, Sambamoorthi U, Bharmal M, Kamal KM, LeMasters T, Kolodney J, Kelley GA. Effectiveness and Safety of Treatments for Early-Stage Merkel Cell Carcinoma: A Systematic Review and Meta-Analysis of Randomized and Non-Randomized Studies. Cancer Med. 2025 Jan;14(1):e70553. [PMC free article: PMC11696246] [PubMed: 39749718]

69.

Gamret AC, Roberts JE, Srivastava D, Nijhawan RI. Mohs Micrographic Surgery: A Brief Overview. Semin Plast Surg. 2024 Nov;38(4):264-267. [PMC free article: PMC11651823] [PubMed: 39697403]

70.

Yacoub I, Rayn K, Choi JI, Bakst R, Chhabra A, Qian JY, Johnstone P, Simone CB. The Role of Radiation, Immunotherapy, and Chemotherapy in the Management of Locally Advanced or Metastatic Cutaneous Malignancies. Cancers (Basel). 2024 Nov 22;16(23) [PMC free article: PMC11640331] [PubMed: 39682109]

71.

Nassief G, Anaeme A, Moussa K, Chen D, Ansstas G. Where Are We Now with Oncolytic Viruses in Melanoma and Nonmelanoma Skin Malignancies? Pharmaceuticals (Basel). 2024 Jul 09;17(7) [PMC free article: PMC11279659] [PubMed: 39065766]

72.

Lugowska I, Teterycz P, Rutkowski P. Immunotherapy of melanoma. Contemp Oncol (Pozn). 2018 Mar;22(1A):61-67. [PMC free article: PMC5885078] [PubMed: 29628796]

73.

Pelosi E, Castelli G, Testa U. Braf-Mutant Melanomas: Biology and Therapy. Curr Oncol. 2024 Dec 03;31(12):7711-7737. [PMC free article: PMC11674697] [PubMed: 39727691]

74.

Aran BM, Duran J, Gru AA. A Case of Leukemia Cutis (Acute Myeloid Leukemia) With Epidermotropism. Am J Dermatopathol. 2025 Feb 01;47(2):141-144. [PubMed: 39751635]

75.

Pawar PM, Mandli SJ, Solanki K, Sutaria AH. Pityriasis Lichenoides Chronica-Like Mycosis Fungoides: A Diagnostic Dilemma. Skinmed. 2024;22(6):482-484. [PubMed: 39748587]

76.

Bazzacco G, Zalaudek I, Errichetti E. Dermoscopy to differentiate clinically similar inflammatory and neoplastic skin lesions. Ital J Dermatol Venerol. 2024 Apr;159(2):135-145. [PubMed: 38650495]

77.

Choudhary S, Srivastava A, Sahni M, Joshi D. Atypical Morphology of a Typical Mycobacterial Infection. Skinmed. 2023;21(6):439-440. [PubMed: 38051246]

78.

Luppi JB, Pereira de Souza R, Florezi GP, Nico MMS, Lourenço SV. The Role of Reflectance Confocal Microscopy in the Evaluation of Pigmented Oral Lesions and Their Relationship With Histopathological Aspects. Am J Dermatopathol. 2022 Sep 01;44(9):658-663. [PubMed: 35503878]

79.

Smolle J, Wolf P. Is favorable prognosis of squamous cell carcinoma of the skin due to efficient immune surveillance? Arch Dermatol. 1997 May;133(5):645-6. [PubMed: 9158419]

80.

Pei M, Wiefels M, Harris D, Velez Torres JM, Gomez-Fernandez C, Tang JC, Hernandez Aya L, Samuels SE, Sargi Z, Weed D, Dinh C, Kaye ER. Perineural Invasion in Head and Neck Cutaneous Squamous Cell Carcinoma. Cancers (Basel). 2024 Nov 01;16(21) [PMC free article: PMC11545267] [PubMed: 39518134]

81.

Catalano M, Nozzoli F, De Logu F, Nassini R, Roviello G. Management Approaches for High-Risk Cutaneous Squamous Cell Carcinoma with Perineural Invasion: An Updated Review. Curr Treat Options Oncol. 2024 Sep;25(9):1184-1192. [PMC free article: PMC11416415] [PubMed: 39102167]

82.

D'Angelo SP, Bhatia S, Brohl AS, Hamid O, Mehnert JM, Terheyden P, Shih KC, Brownell I, Lebbé C, Lewis KD, Linette GP, Milella M, Georges S, Shah P, Ellers-Lenz B, Bajars M, Güzel G, Nghiem PT. Avelumab in patients with previously treated metastatic Merkel cell carcinoma: long-term data and biomarker analyses from the single-arm phase 2 JAVELIN Merkel 200 trial. J Immunother Cancer. 2020 May;8(1) [PMC free article: PMC7239697] [PubMed: 32414862]

83.

Schadendorf D, Lebbé C, Zur Hausen A, Avril MF, Hariharan S, Bharmal M, Becker JC. Merkel cell carcinoma: Epidemiology, prognosis, therapy and unmet medical needs. Eur J Cancer. 2017 Jan;71:53-69. [PubMed: 27984768]

84.

Lebbe C, Becker JC, Grob JJ, Malvehy J, Del Marmol V, Pehamberger H, Peris K, Saiag P, Middleton MR, Bastholt L, Testori A, Stratigos A, Garbe C., European Dermatology Forum (EDF), the European Association of Dermato-Oncology (EADO) and the European Organization for Research and Treatment of Cancer (EORTC). Diagnosis and treatment of Merkel Cell Carcinoma. European consensus-based interdisciplinary guideline. Eur J Cancer. 2015 Nov;51(16):2396-403. [PubMed: 26257075]

85.

Hali F, Bousmara R, Mellouki A, Kerouach A, Marnissi F, Diouri M, Chiheb S. Comparative study of cutaneous malignant melanoma according to anatomical site: plantar versus non-plantar melanoma. Arch Dermatol Res. 2024 Nov 20;317(1):35. [PubMed: 39565418]

86.

Hauschild A, Garbe C, Ascierto PA, Demidov L, Dreno B, Dummer R, Eggermont A, Forsea AM, Gebhardt C, Gershenwald JE, Hamid O, Hoeller C, Kandolf L, Kaufmann R, Kirkwood JM, Lebbé C, Long GV, Malvehy J, Martin-Algarra S, McArthur G, Neyns B, Richtig E, Robert C, Schadendorf D, Scolyer R, Sondak VK, Wainstein A, Weichenthal M, Nuti P., Melanoma World Society Study Group. Neoadjuvant or perioperative therapy for melanoma metastasis in clinical practice: an international survey. Lancet Oncol. 2025 Jan;26(1):12-14. [PubMed: 39756440]

87.

McKenzie NC, Hickey MD, De la Sancha C, Coates SJ, Leslie KS. Ulcerative erythematous papules and plaques on the face and lower legs of a man living with HIV: a clinicopathological challenge. Int J Dermatol. 2024 Nov;63(11):1522-1524. [PubMed: 38965065]

88.

Ung CY, Warwick A, Onoufriadis A, Barker JN, Parsons M, McGrath JA, Shaw TJ, Dand N. Comorbidities of Keloid and Hypertrophic Scars Among Participants in UK Biobank. JAMA Dermatol. 2023 Feb 01;159(2):172-181. [PMC free article: PMC9857738] [PubMed: 36598763]

89.

Chen A, Dusza S, Bromberg J, Goldfarb S, Sanford R, Markova A. Quality of Life in Patients with Malignant Wounds Treated at a Wound Care Clinic. Res Sq. 2024 Sep 02; [PubMed: 39281876]

90.

Niculescu AG, Georgescu M, Marinas IC, Ustundag CB, Bertesteanu G, Pinteală M, Maier SS, Al-Matarneh CM, Angheloiu M, Chifiriuc MC. Therapeutic Management of Malignant Wounds: An Update. Curr Treat Options Oncol. 2024 Jan;25(1):97-126. [PubMed: 38224423]

91.

Landov H, Baum S, Mansour R, Liberman B, Barzilai A, Alcalay J. Comparison of Surgical Treatment Using Mohs Micrographic Surgery versus Wide Local Excision for the Treatment of Dermatofibrosarcoma Protuberans. Isr Med Assoc J. 2024 Dec;26(11):682-687. [PubMed: 39692386]

92.

Müller A, Dolbeault S, Piperno-Neumann S, Clerc M, Jarry P, Cassoux N, Lumbroso-Le Rouic L, Matet A, Rodrigues M, Holzner B, Malaise D, Brédart A. Anxiety, depression and fear of cancer recurrence in uveal melanoma survivors and ophthalmologist/oncologist communication during survivorship in France - protocol of a prospective observational mixed-method study. BMC Psychiatry. 2024 Nov 15;24(1):812. [PMC free article: PMC11566303] [PubMed: 39548476]

93.

Thompson JR, Gomes L, Kouvelis G, Smith AL, Lo SN, Kasparian NA, Saw RPM, Dieng M, Seaman L, Martin LK, Guitera P, Milne D, Schmid H, Cust AE, Bartula I. Short-Term Effectiveness of a Stepped-Care Model to Address Fear of Cancer Recurrence in Patients With Early-Stage Melanoma. Psychooncology. 2024 Dec;33(12):e70041. [PubMed: 39681994]

94.

Liu R, Chen Y, Wu SN, Ma W, Qiu Z, Wang J, Xu X, Chen C, Wang W. Adverse drug events associated with capecitabine: a real-world pharmacovigilance study based on the FAERS database. Ther Adv Drug Saf. 2024;15:20420986241303428. [PMC free article: PMC11660075] [PubMed: 39713991]

95.

Stasiak K, Stevens AD, Bolte AC, Curley CT, Perusina Lanfranca M, Lindsay RS, Eyo UB, Lukens JR, Price RJ, Bullock TNJ, Engelhard VH. Differential T cell accumulation within intracranial and subcutaneous melanomas is associated with differences in intratumoral myeloid cells. Cancer Immunol Immunother. 2024 Nov 02;74(1):10. [PMC free article: PMC11531463] [PubMed: 39487854]

96.

Clements S, Jeha GM, Tripuraneni P, Kelley B, Greenway H. Recurrence Rates of Mohs Micrographic Surgery vs Radiation Therapy for Basal Cell Carcinoma of the Ear. Cutis. 2024 May;113(5):216-217. [PubMed: 39042118]

97.

Adefusika JA, Pimentel JD, Chavan RN, Brewer JD. Primary mucinous carcinoma of the skin: the Mayo Clinic experience over the past 2 decades. Dermatol Surg. 2015 Feb;41(2):201-8. [PubMed: 25627628]

98.

Li W, Hao N, Liu W, An D, Yan B, Li J, Liu L, Luo R, Zhang H, Lei D, Zhou D. The experience of the multidisciplinary team in epilepsy management from a resource-limited country. Epilepsia Open. 2019 Mar;4(1):85-91. [PMC free article: PMC6398094] [PubMed: 30868118]

Disclosure: Nishad Sathe declares no relevant financial relationships with ineligible companies.

Disclosure: Patrick Zito declares no relevant financial relationships with ineligible companies.