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Melanoma, a cancerous condition marked by extremely aggressive biological characteristics in people, spreads due to its resistance to current therapies. The melanoma cells devise ways to defend themselves from the person's immune system in those cells where they start to spread. Depending on the type of original tumor that metastasizes, the nature of the immunity may have a distinct impact on the growth of the malignancies. Therefore, the focus of this work is to emphasize a mechanistic account of how melanoma functions. The paper will briefly elaborate on the elements that encourage melanoma spread in order to accomplish this goal. According to Fridman, et al (2012), the process of interaction between the tumor cells with other extracellular matrix remains a critical component in melanoma metastases mechanism. Immediately when the melanoma cells settle in the metastatic sites, they develop mechanisms that protect them from any attack that may emanate from the immune system. Indeed, the abnormal growth of tissues begins when the tumor grows, starts progression, invades other body parts, and finally metastasis. In most cases, the melanoma cells have an intrinsic characteristic in that they have a cell-specific phenotype inherited from their cells of origin. According to a study conducted by Fridman, et al (2012), the primary location of melanoma often influences the metastases of melanoma which occurs mainly in the regional lymphatic vessels and nodes.
Different melanomas have different ligands or receptors, which affect their preferred mode of bonding of their cells either in the lymph nodes or tissues from distant sites. Some of these receptors include the chemokine receptors and adhesion molecules expressed on the T cells and the dendritic cells. Moreover, the difference in the kinds of integrin expressed by the melanomas determines the mechanism of progression. For example, those that express the alpha v beta three integrin tend to develop lung metastases, while the melanomas expressing alpha four beta 1 develop node metastases.
The formation of new blood vessels is of utmost importance in highlighting the mechanisms of melanoma metastases. Indeed, the melanoma cells require a solid structure of skeletal muscle as such new vessels can aid in their growth and progression to other body parts. Further, these cells change their mode of operation, which avert them from the attack by the immune cells. For example, the natural killer's cells (NK) that are one of the most effective means of protection from the cancer cells activate their receptors to fight any cancer cells (Fridman, et al 305). On the other hand, the melanoma ligands assist the melanoma cells from the effects of the NK cells. Nonetheless, the malignant cells propagation is inhibited by the cytokines in the body immune system.
Indeed, the melanoma cells mechanism takes place in distinct steps that involve the activation of the ligands to prevent the action of the immune system against the melanoma cells from metastases. However, as there exists a lot of evidence about the collaboration of the malignant cells with the endothelium, research should be conducted to expound the means of collaboration of the malignant cells with the lymphatic vessels. Evidently, the research should aim at highlighting how the melanoma cells survive in the lymph nodes and their mode of adhesion. Moreover, the migration of these cells should be addressed more closely as such this can assist in coming up with therapies that can hinder the progress of the melanoma cells to other body parts.
Fridman, Wolf Herman, et al. "The Immune Contexture in Human Tumours: Impact on Clinical Outcome." Nature Reviews Cancer 12.4 (2012): 298-306.
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