Two strategy to combat the resistant melanoma :
a)target the ras activity
b)MEK inhibitor
Let go first with ras target what are the pros and cons of targetting ras
So if we go for ras then they target the raf gene, via ras, altogether. Although this may nullify melanoma's resistance to the drug, it will initiate an onslaught of problems, since the activation of the ras protein, and consequently the raf gene, is tightly regulated and has overlaps with other essentially functions. For instance, in humans, those that have a faulty raf gene, whether by point mutation, or amino acid substitution, may have Noonan syndrome, where affected individuals are abnormally short in stature (limbs, especially) and have congenital heart defects. Also, humans with an inactive/mutated raf gene may experience LEOPARD syndrome, an acronym for Lentigo, Electrocardiographic abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retarded growth, Deafness), and a slew of other complications.
a)target the ras activity
b)MEK inhibitor
Let go first with ras target what are the pros and cons of targetting ras
So if we go for ras then they target the raf gene, via ras, altogether. Although this may nullify melanoma's resistance to the drug, it will initiate an onslaught of problems, since the activation of the ras protein, and consequently the raf gene, is tightly regulated and has overlaps with other essentially functions. For instance, in humans, those that have a faulty raf gene, whether by point mutation, or amino acid substitution, may have Noonan syndrome, where affected individuals are abnormally short in stature (limbs, especially) and have congenital heart defects. Also, humans with an inactive/mutated raf gene may experience LEOPARD syndrome, an acronym for Lentigo, Electrocardiographic abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retarded growth, Deafness), and a slew of other complications.
On the other hand, MEK (mitogen-activated protein kinase/extracellular signal regulated kinase) inhibitor would be a good, and likely choice for a stock investment because they do not target the entire gene, itself, but rather serves as a "roadblock" in the signal pathways that have caused the mutation in the raf protein--the cause for the resistant properties that the cancer possesses. Essentially, and fortunately for the infected individual, the resistance to the cancer drugs does not happen immediately and must go through a long and complex list of cellular events/cascades called kinases. What the MEK does is block these pathways, where the enzyme that would catalyze the initiation of the next kinase (that would eventually activate the mutation in the raf gene, i.e. the resistance to the drug) no longer recognizes the active site of the normal substrate it would bind to, and thus the cascade is halted--hence the idea of a road block. With this road block in the MAPK (MEK)/ERK pathways (these are the major "players," the melanoma cannot become resistant since it never receives the message from the long domino-effect like cascade of kinases to become
So if we want to make a drug against resistant melanoma the we should go for MEK inhibitor
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