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Skin Cancer by Mind Map: Skin Cancer

1. Pathophysiologic etiology

1.1. UV radiation is separated into 3 wavelengths:

1.1.1. UVA: Most of earth's received radiation Weaker than UVB Penetrates deeper into the skin More constant throughout the year despite changes of weather (McCance, 2019).

1.1.2. UVB: Some of earth’s received radiation Affects the outer layer of the skin (McCance, 2019).

1.1.3. UVC: Does not increase health risks as much when compared to UVB (McCance, 2019).

1.2. Ultraviolet Radiation (UV Radiation)

1.2.1. Comes from sunlight and specialized lights (e.g. tanning lamps, black lights, mercury vapor lamps) (McCance, 2019).

1.2.2. Can be beneficial to health as it produces vitamin D that helps calcium and phosphorus absorption; important for bone development (McCance, 2019).

1.2.3. Can result in acute and chronic changes on the skin, eye, and immune system as a result of prolonged UV radiation exposure (McCance, 2019).

1.3. Leads to loss of keratinocyte repair functions and apoptosis resistance of DNA-damaged cells (McCann & Huether, 2019). Beta cells of dark skinned individuals contain the pigment melanin, which is a protective factor against sun exposure; thus, lowering the chances of this population to develop malignant skin tumors (McCann & Huether, 2019).

1.4. Consequently, continued exposure to the sun and artificial light sources will increase skin cancer risk (McCance, 2019). Genetic mutations in oncogenes and tumor-suppressor genes are associated with skin cancers (McCann & Huether, 2019).

1.4.1. Melanoma; cancer that forms in melanocytes (pigment cells) derived from the neural crest (McCance, 2019). Most lethal form of skin cancer; occurs on any skin surface and may arise from mucosal surfaces or uveal (intraocular) tract (McCance, 2019). Pathogenesis is complex; there is an accumulation of genetic mutations that activate oncogenes, inactivate tumor-suppressor genes, and impair DNA repair genes (McCann & Huether, 2019). Most familial melanomas correlate with cyclin-dependent kinase 4 genes (CDK4) and cyclin-dependent kinase inhibitor 2A genes (p16/CDKN2A) located on chromosome 9p21 (McCann & Huether, 2019). Both CDKN2A and CDK4 result in melanomas (McCann & Huether, 2019). Proto-oncogenes, BRAF point mutations and NRAS, are involved in mitogen-activated protein kinase (MAPK) regulation and other signaling pathways (McCann & Huether, 2019). As a result of stimulation by UVR, melanomas have a high mutation rate; thus, making gene sequencing difficult (McCann & Huether, 2019).

1.4.2. Basal cell carcinoma (BCC); cancer in the lower part of the epidermis or outer layer of skin (McCance, 2019). Most common skin cancer (McCann & Huether, 2019). A surface epithelial tumor of the skin origination from basal or stem cells; arises from mutation in the TP53 tumor-suppressor gene that leads to loss of keratinocyte repair functions and apoptosis resistance of DNA-damaged cells (McCann & Huether, 2019). Other oncogenic pathways include inhibition of the PTCH gene with overexpression in the Sonic Hedgehog signaling pathway (McCann & Huether, 2019). Has numerous subtypes: Superficial, nodular, pigmented, morpheaform (sclerosing), and combinations of each; resulting in different clinical presentations (McCann & Huether, 2019).

1.4.3. Squamous cell carcinoma (SCC); cancer in the flat cells that form on the skin’s surface (McCance, 2019). Composed of uncontrolled growth of keratinizing cells (McCann & Huether, 2019). Second most common (McCann & Huether, 2019). Mutation of TP53 gene and other oncogenic signals (McCann & Huether, 2019). Two subtypes: Invasive In situ (Bowen disease)

2. Causative factors

2.1. Evidence shows exposure to sun and UV radiation are associated with an increased risk of basal cell carcinoma (BCC) and squamous cell carcinoma (McCance, 2019).

2.2. Intermittent acute sun exposure leading to sunburn is associated with melanoma (McCance, 2019).

2.3. Recipients of organ transplants taking immunosuppressive medications are at increased risk of skin cancer; particulary squamous cell carcinoma (SCC) (McCance, 2019; McCann & Huether, 2019).

2.4. Arsenic exposure increases risk for cutaneous SCC (McCance, 2019; McCann & Huether, 2019).

2.5. Chronic UV light exposure, radiation exposure, severe actinic exposure, radiation therapy (McCance, 2019; McCann & Huether, 2019).

3. Risk factors

3.1. Risk factors vary, however, include:

3.1.1. light natural skin tone color

3.1.2. family history of skin cancer

3.1.3. genetic predisposition

3.1.4. personal history of skin cancer

3.1.5. exposure to the sun

3.1.6. history of sunburns (especially early on in life)

3.1.7. history of artificial tanning use

3.1.8. people who tan poorly, get freckles on the skin easily, and/or burn easily after sun exposure

3.1.9. skin that reddens easily or becomes painful in the sun

3.1.10. individuals who have blue or green eyes

3.1.11. individuals who have blonde or red hair

3.1.12. individuals who have certain types of moes or a large number of moles

3.1.13. Geographic location

3.1.14. Pesticide exposure

3.1.15. (McCance, 2019; McCann & Huether, 2019).

4. Diagnostic tests

4.1. Early identification of specific skin lesions of concern with subsequent accurate clinical assessment to determine whether a lesion is clinically different from other non-cancerous skin lesions (Gershenwald & Nelson, 2017).

4.1.1. Can be assessed utilizing the mnemonic ABCDE; any of these findings should be concern for melanoma and non-melanomas (e.g. BCC and SCC) (Gershenwald & Nelson, 2017). A: asymmetry B: border irregularity and (perhaps most importantly) evolution (recent change) of the lesion. C: variegated colours D: diameter >6mm E: evolution (recent change) of the lesion (Gershenwald & Nelson, 2017).

4.2. Dermatologists may also perform dermoscopy with a dermatoscope to better visualize skin lesions; has a 10× magnifying lens coupled with either polarized light or a liquid interface to minimize epidermal light refraction (Gershenwald & Nelson, 2017).

4.3. Diagnostic algorithms can also assist by generating an estimate of the probability that a lesion is malignant (Gershenwald & Nelson, 2017).

4.3.1. Parameters of algorithms can be adjusted to balance sensitivity (‘true positive’, or confidence that a positive result truly reflects melanoma) and specificity (‘true negative’, or confidence that a negative result truly excludes melanoma) (Gershenwald & Nelson, 2017).

4.3.2. To maximize sensitivity, lesions are ‘flagged’ as concerning, but are confirmed to be benign upon pathological tissue analysis following diagnostic biopsy (Gershenwald & Nelson, 2017).

4.4. Diagnostic biopsy (Gershenwald & Nelson, 2017).

5. Facts

5.1. In the United States, skin cancer is the most commonly diagnosed malignancy with 76,380 cases of individuals diagnosed with melanoma in 2016, with 10,100 dying from this disease as a result (McCance, 2019).

5.2. Death rates vary by race and ethnicity; white men and women have a higher incidence of death from melanoma when compared to any other group (McCance, 2019).

5.3. Nonmelanoma skin cancer (e.g. 95% of cases being BCC and SCC) is the most common malignancy in humans; 3,300,000 annual cases are reported in the United States alone (Marka, Carter, Toto & Hassanpour, 2019).

5.4. Increased intake of coffee correlated with a decreased risk of melanoma in a U.S. cohort study (McCance, 2019).

6. Common findings

6.1. Melanoma is often found on men; on the head, neck, between the shoulders, and on the hips, and on women; on the skin of the lower legs, between the shoulders, and on the hips (McCance, 2019).

6.2. Melanoma is rare on dark skinned individuals, but can be found under the fingernails and toenails, on the palms of the hands and/or on the soles of the feet (McCance, 2019).

6.3. Basal cell carcinoma is commonly found on the head and neck (McCance, 2019).

6.4. Squamous cell carcinoma is found commonly on men who work outdoors, but can occur in anyone and usually occurs on the nose, ears, lower lip, and dorsa of the hand; lower lip is the most common site (McCance, 2019; McCann & Huether, 2019).

7. Treatments

7.1. Cutaneous Melanoma

7.1.1. Radiation therapy

7.1.2. Chemotherapy

7.1.3. Immunotherapy used to inhibit the MAPK pathway and BRAF mutations

7.1.4. MEK inhibition

7.1.5. (McCann & Huether, 2019).

7.2. Beta cell carcinoma

7.2.1. Complete surgical excision

7.2.2. Radiotherapy

7.2.3. Curettage

7.2.4. Cryotherapy

7.2.5. Photodynamic therapy

7.2.6. Topical applications of imiquimod or 5-fluorouracil

7.2.7. (McCann & Huether, 2019).

7.3. Squamous cell carcinoma

7.3.1. Cryotherapy

7.3.2. 5-FU

7.3.3. Photodynamic therapy

7.3.4. Complete microsurgical excision

7.3.5. Radiotherapy with adjunct chemotherapy

7.3.6. (McCann & Huether, 2019).

8. Prevention

8.1. The most preventable causative factor is exposure to UV light from either the sun or artificial sources (McCance, 2019).

8.2. Early Detection is key; however, major harm can occur as a result of overdiagnosis and overtreatment (Gershenwald & Nelson, 2017; McCance, 2019).

8.2.1. Multiple benign lesions can mimic melanoma and nonmelanoma cancers, which causes unnecessary morbidity through invasive biopsies and treatments (Marka, Carter, Toto & Hassanpour, 2019).

8.3. Protection from the sun and avoidance of artificial light sources, particularly in early life, reduces the risk of skin cancer later in life (McCann & Huether, 2019).

8.4. Discovering melanoma at an early stage can increase survival rate by 5 years (McCann & Huether, 2019).

9. References

9.1. Gershenwald, J. E., & Nelson, K. C. (2017). Skin cancer: Have melanoma and skin cancer finally met their match? Nature Reviews. Clinical Oncology, 14(5), 267-268. doi:

9.2. Marka, A., Carter, J. B., Toto, E., & Hassanpour, S. (2019). Automated detection of nonmelanoma skin cancer using digital images: A systematic review. BMC Medical Imaging, 19. doi:

9.3. McCance, K. L. (2019). Cancer epidemiology. In K. L., McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (8th ed., pp. 410-411). St. Louis, MO: Mosby Elsevier.

9.4. McCann, S. A., & Huether, S. E. (2019). Structure, function, and disorders of the integument. In K. L., McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (8th ed., pp. 1519-1522). St. Louis, MO: Mosby Elsevier.

10. Inflammation

10.1. Reactive oxygen species (ROS) can induce transcription factors and can increase the levels of regulating genes that induce inflammation; inflammation is a key component for tumor progression (McCance, 2019)

11. Immunity

11.1. Prolonged exposure to solar UV radiation results in acute and chronic health effects on the skin, eye, and immune system (McCance, 2019).