The evolutionary perspective of cancer

The evolutionary perspective of cancer aids in explaining why a cure for melanoma remains elusive, while also pointing the way toward new types of treatment. Indeed, the metastatic process of melanoma makes it difficult to treat, resulting in complications and deaths (Lee, et al.). Nonetheless, the precise link between tumors and the metastatic process is unknown. As a result, developing ways for regulating metastasis at the molecular level can aid in the development of improved and innovative cancer treatment approaches.

The complexity of melanoma and its adaptive nature. The phylogenic analyses of melanoma reveal complex configurations of metastasis. The role of this essay is to research on the melanoma disease provide an evolutionary explanation for its adaptation, and the components needed for this disease to happen in humans and non-humans. Indeed, the analysis will assist in understanding the complexity that makes melanoma an illness that is hard to cure.

Genetic variation and its impact on melanoma

According to studies conducted by Goode, Cornelia, and John (2002), the presence of genetic variation in DNA repair genes can affect the ability to repair the already damaged DNA and consequently predispose the individual to cancer. The studies elucidated the association that exists between polymorphism in a gene and the impact it had on the disease (Goode, Cornelia, and John). Indeed the kind of mutations in the melanoma varies because of such factors as the frequency of the mutations, and the tissues of origin of the tumor. Apart from the tissues of origin, the age of diagnosis of cancer, and the exposure to sunlight, they influence the level of mutation that occurs at the tissue level of the melanoma cells. Nonetheless, the melanoma cells comprise of biologically distinct types. Clearly, the BRAF mutations are present in those individuals with sun-damaged skins and the younger patients (Brose, et al.).

Different routes of melanoma evolution

In retrospective, the melanomas with NRAS mutations show their occurrence in the sun-damaged skin of the older patients. Indeed, research indicates that the BRAF melanomas always arise from the benign nevi while those with NRAS mutations were associated with the melanomas in situ (Brose, et al.). Nonetheless, the in situ melanomas had already amassed themselves on other body parts. It is clearly evident that different melanomas subtypes show an evolution based upon different routes.

Targeting RAS mutations for treatment

For the majority of the RAS mutations, they occur in deadly malignant diseases such as melanoma, colon cancer, lung cancer, and pancreatic cancer. It is largely the reason why therapists in most cases target RAS as a critical priority in suppressing any forms of cancer. However, any approved treatment continues to remain elusive leading to research aimed at developing genetically targeted treatments to treat any NRAS melanomas (Brose, et al.). As stated before, the NRAS mutations occur at a relatively consistent rate, which includes the sun-exposed and non-exposed skins. Moreover, the NRAS mutations depict thicker tumors, with increased rate of mitosis and small instances of ulceration. Importantly, the patients affected by the NRAS mutations are linked to a poorer rate of survival (Brose, et al.).

Risk factors and genetic history

Every person remains at risk of melanoma, but the risk largely depends on factors such as the exposure to sunlight, the presence of nevus, the skin type of the individual, and the genetic history of the person. In most cases, the hereditary factors play a significant role as the majority of the patients with melanoma have a family member with its history. However, the genetic risk factors such as BRAF play a part in causing many melanomas. The research that led to the discovery of BRAF resulted in the production of drug that could inhibit BRAF and thus regulate the level of melanoma progression (Brose, et al.). The studies of p53 genes have indicated that its association with certain kinds of melanoma as such a breakthrough can lead to the analysis of patients with melanoma and highlight the defective genes (Davies, et al). For non-humans, research has shown that certain species develop a particular kind of melanoma. The non-human mammalian species include marine mammals to other household pets.

The challenges of treatment and potential solutions

The adaptation of the tumors of patients with BRAF mutant melanoma and their resistance to the RAF kinase inhibitors makes the tumors to regress completely (Davies, et al). Indeed, this makes the therapeutic effects of the RAF kinase inhibitors to be temporary with several theories coming up trying to explain the reason for the resistance, but none gives a plausible reason (Davies, et al). Research to identify an effective treatment option for the mutant RAS continues. However, this gene drives the majority of the most aggressive malignant cells of the melanoma. Indeed, researchers are looking towards options of an immune-based treatment to become the cornerstone of the treatment of the malignant tumors. However, the immune therapies are prevalently used majorly for those patients with BRAF melanoma mutation (Brose, et al.).

Conclusion

Evidently, the above research provides a succinct description of the adaptation of the different melanoma subtypes in both human and non-human species. The BRAF and RAS melanoma subtypes portray different characteristics that make them affect different individuals. Indeed, the NRAS subtype is the most prevalent of the melanomas but causes high mortality rates because of its poor prognosis. Indeed, the nature of the NRAS subtype has made the treatment remain elusive, but new targeted therapies continue that will provide effective treatments.

Works Cited

Brose, Marcia S., et al. “BRAF and RAS mutations in human lung cancer and melanoma.” Cancer research 62.23 (2002): 6997-7000.

Davies, Helen, et al. ”Mutations of the BRAF gene in human cancer.” Nature 417.6892 (2002): 949-954.

Goode, Ellen L., Cornelia M. Ulrich, and John D. Potter. ”Polymorphisms in DNA repair genes and associations with cancer risk.” Cancer Epidemiology and Prevention Biomarkers 11.12 (2002): 1513-1530.

Lee, Jeong-Hyung, et al. ”KiSS-1, a novel human malignant melanoma metastasis-suppressor gene.” Journal of the National Cancer Institute 88.23 (1996): 1731-1737.