Moles and Skin Cancer
'Why don’t all moles progress to melanoma?' is the questioned posed and answered by this study referred to by the linked news release.
The news release cites the fact that moles are found on everyone but are generally only a cosmetic nuisance. Sometimes though, abnormal cell division leads to cancer. According to the article one in 65 Americans contracts skin cancer during their lifetime. But what triggers skin cancer also known as melanoma?
Mutations, that are cancer causing, exist in nine out of ten moles according to the article and three out of ten melanomas start in a mole. Yet it has been apparent that something inhibits the development of cancer in moles. The inhibiting mechanism is associated with a cellular organelle known as the endoplasmic reticulum of which there are two types: the rough endoplasmic reticulum and the smooth endoplasmic reticulum.
Like all mechanisms cellular mechanisms can malfunction. Amino acid chains in an endoplasmic reticulum, which are folded to specific functional shapes by other proteins known as chaperones, can at times accumulate too quickly and overload the system. This in turn can be lethal to the cell containing the ER.
The article reveals that in response the ER is able to send out signals initiating what is known as the UPR or unfolded protein response. If this works protein production can be adjusted so that the backlog is eliminated. If this fails the ER can initiate a process known as apoptosis which results in cellular suicide.
Researchers have found that the ER can sense oncogene activity and respond with a strategy that prevents malignant cell transformation. The strategy involves stopping the cell cycle thus preventing cell division. The cells live but do not proliferate.
Together with apoptosis this cellular defense mechanism helps ensure that moles do not become melanomas. In most cases the strategy is successful.
The news release cites the fact that moles are found on everyone but are generally only a cosmetic nuisance. Sometimes though, abnormal cell division leads to cancer. According to the article one in 65 Americans contracts skin cancer during their lifetime. But what triggers skin cancer also known as melanoma?
Mutations, that are cancer causing, exist in nine out of ten moles according to the article and three out of ten melanomas start in a mole. Yet it has been apparent that something inhibits the development of cancer in moles. The inhibiting mechanism is associated with a cellular organelle known as the endoplasmic reticulum of which there are two types: the rough endoplasmic reticulum and the smooth endoplasmic reticulum.
Like all mechanisms cellular mechanisms can malfunction. Amino acid chains in an endoplasmic reticulum, which are folded to specific functional shapes by other proteins known as chaperones, can at times accumulate too quickly and overload the system. This in turn can be lethal to the cell containing the ER.
The article reveals that in response the ER is able to send out signals initiating what is known as the UPR or unfolded protein response. If this works protein production can be adjusted so that the backlog is eliminated. If this fails the ER can initiate a process known as apoptosis which results in cellular suicide.
Researchers have found that the ER can sense oncogene activity and respond with a strategy that prevents malignant cell transformation. The strategy involves stopping the cell cycle thus preventing cell division. The cells live but do not proliferate.
Together with apoptosis this cellular defense mechanism helps ensure that moles do not become melanomas. In most cases the strategy is successful.
posted by Paul at 10:33 PM
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