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Overview
Malignant melanoma is often cited as one of the most common types of cancer of the skin affecting populations of Caucasian origin (Haydu et al., 2010), with available statistics demonstrating that it is the 5th most commonly diagnosed cancer in the United States (Zhihong et al., 2011). Melanoma can be described as cancer that begins in the melanocytes (colored cells which lie in the epidermis) and can occur anywhere on the skin, though extant literature demonstrates it is more likely to start in specific locations such as the trunk (chest and back), legs, neck or face (American Cancer Society, n.d.).
Official figures released in 2008 by the American Academy of Dermatology cited in Vickers (2009) demonstrate that “…melanoma is the most common form of cancer for young adults 25 to 29 years old and the second most common form of cancer for young adults 15 to 29 years of age” (p. 15). It is reported in the literature that the risk of malignant melanoma is high in light-skinned individuals of European origin with both phenotypic vulnerability and sustained history of sun exposure (Bastuji-Garin & Diepgen, 2002).
Pathophysiology
It is important to underscore the fact that as with other forms of cancer, a sequence of genetic shifts takes place in melanoma cells that leads to mounting aptitude for growth of the affected cells as they become increasingly malignant. As acknowledged by Ralph (2007), “…a key issue emerging more recently in understanding the progression of malignant melanoma is the role played by the tumor microenvironment and the impact of the relationship between the immune system and inflammatory processes in promoting tumor cell development” (p. 125). At the cellular level, the ultra-violent (UV) mediated damage to skin keratinocytes and melanocytes is known to trigger DNA mutational shifts in the expression of growth regulatory genes in already predisposed individuals, resulting in uninhibited cell proliferation. The surrounding tissue damage and drying cells alert the individual’s immune system to the destruction being occasioned (Barnhill et al., 2007), with available literature demonstrating that this alert stimulates transient immune cell infiltrates, which in turn trigger the release of inflammatory signals into the surrounding microenvironment (Ralph, 2007).
But when the above process is taking place, the pro-inflammatory signals engaged in skin healing and repair produce the twin effect of not only arousing the cells of the immune system but also enhancing “…the growth and emergence of selected clones of tumor cells responsive to the very same signals used by the immune surveillance system, thereby helping the tumor cells to establish, escape, and evade immune detection” (Ralph, 2007, p. 125). Thus, during this materialization stage, immune cytokine signaling aspects such as interferon (IFN)-y or granulocyte-macrophage colony-stimulating aspect can and do advance tumor cell growth, survival, and even metastasis when present in small quantities, while at big quantities these aspects would stimulate immune responses to repress tumor progression (Ralph, 2007). This author further suggests that local immune cell activation may also be repressed by the operations “…of the a-melanocyte stimulating hormone, a factor released by dermal fibroblasts that promote the production of pigmented melanocytes to help protect the skin from further damage by continued UV exposure” (p. 125). At this juncture, melanocyte clones appear that prolong to advance in response to the continuing immune cytokine signals, ultimately occasioning the individual to develop nevi that may or may not become dysplastic.
Diagnosis
Krausz et al (2002) note that “…melanoma can present in a variety of histological forms and frequently appears camouflaged as a morphologically similar but a biologically completely different pathologic condition” (p. 120). Although the histologic mimics of malignant melanoma differ according to the anatomic site, pathologic level, tumor phenotype, and presence or absence of the colored cells in the epidermis (Krausz et al., 2002), histopathologic diagnosis typically entails several criteria which include “…asymmetry, diameter <5-6 mm, organizational aberrations including pagetoid melanocytosis, prominent confluence and high cellular density of melanocytes, diminished or absent maturation, effacement or ulceration of epidermis, significant cytologic atypia, and mitoses in the dermal component” (Barnhill et al., 2007, p. 140). Overall, it is important to note that early discovery and diagnosis of the disease are the most essential factors for survival rates (Vickers, 2009).
Treatment/Management
The 2009 evidence-based American Joint Commission on Cancer/International Union against Cancer (AJCC/UICC) melanoma staging and classification system should be used to treat and manage the disease according to the stage of progression. Although surgical excision is the principal treatment for malignant melanoma because recent guidelines demonstrate that a wide local excision should be done with margins correlating to Breslow thickness (Giudici & McPhee, 2011), other treatment methodologies such as isolated limb infusion, intralesional injections with Interleukin-2, and radiation are also used (Hallock et al., 2011).
According to Giudici & McPhee (2011), the sentinel lymph node biopsy (SNLB) should be performed using two tracer substances, blue dye, and radioactively labeled sulfur colloid, to determine the treatment protocol to be adopted. Complete resection, high doses of IFNa-2b treatment, and adjuvant chemotherapy with or without radiation are often used to treat stage I-III malignant melanoma, whereas patients presenting with stage IV are often exposed to systematic treatment using chemotherapy and/or targeted therapy (Zhihong et al., 2011).
Localized treatments such as surgery or radiotherapy are capable of achieving tumor control in stages I-III of the disease, thereby prolonging the survival of patients. Individualized treatments with Interleukin-2, IFNa-2b and other adjuvant chemotherapies not only kill the cancerous cells, but also stimulate the production of the needed immune system cells, assist to improve the effectiveness of the immune system cells, and ultimately cause the cells to produce more cytokines to boost the body’s immune system (Barnhill et al., 2007; Hallock et al., 2011).
Reference List
American Cancer Society. (n.d.). Melanoma skin cancer. Web.
Barnhill, R.L., Mihm, M.C., & Elgart, G. (2007). Malignant melanoma. In K. Nouri (Eds.), Skin cancer (pp. 140-167). New York City, NY: McGraw-Hill.
Bastuji-Garin, S., & Diepgen, T.L. (2002). Cutaneous malignant melanoma, sun exposure, and sunscreen use. British Journal of Dermatology, 146(61), 24-30.
Giudici, N., & McPhee, M. (2011). Diagnosis and treatment of malignant melanoma in pregnancy. Journal of Gynecologic Surgery, 27(3), 171-174.
Hallock, A., Vujovic, O., & Yu, E. (2011). Is radiotherapy an effective option for malignant melanoma? A case report of short course, long-fraction radiation and a literature review. Canadian Journal of Plastic Surgery, 19(4), 153-155.
Haydu, L.E., Holt, P.E., Karim, R.Z., Madronio, C.M., Thompson, J.F., Armstrong, B.K., & Scolyer, R.A. (2010). Quality of histopathological reporting on melanoma and influence of use of a synoptic template. Histopathology, 56(6), 768-774.
Krausz, T., McKee, P.H., Milim, M.C., Spatz, A., Mooi, W.J., Pepper, D.S…Muijen, G.N.P. (2002). Symposium 8: Pathology and pathophysiology of melanocystic disorder. Histopathology, 41(2), 120-146.
Ralph, S.J. (2007). An update on malignant melanoma vaccine research. American Journal of Clinical Dermatology, 8(3), 123-141.
Vickers, A. (2009). Evidence-based practice guidelines for skin cancer screening. Dermatology Nursing, 21(1), 15-18.
Zhihong, C., Siming, L., Xinan, S., Lu, S., Chuanliang, C., Mei, N., & Jun, G. (2011). Clinical presentation, histology, and prognoses of malignant melanoma in ethnic Chinese: A study of 552 consecutive cases. BMC Cancer, 11(1), 85-94.
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