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Understanding the Spread of Cancer: Role of Death Receptor 6 and Apoptosis, Essays (university) of Cancer Cytogenetics

Recent research on the spread of cancer in the body, focusing on the role of death receptor 6 (dr6) and the protein p53 in apoptosis. Researchers are investigating the potential of disabling dr6 to slow down cancer spread, while others suggest alternative mechanisms such as angiotropism and loss of apoptosis gatekeeper p53. The findings have significant implications for future cancer research.

Typology: Essays (university)

2019/2020

Uploaded on 05/05/2020

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In a article published in 2016 it shows how we may slow down the spread of
cancer through are body. In the article it talks how most people that die from
cancer don’t die by the original tumor but from the spreading cancer. Also it talks
about how cancer moves around the body. They found out that metastases targets a
molecule called Death Receptor 6 (DR6). What this does is set off a self destruct
process in the blood vessels allowing the cancer to spread. The universities
studying this were trying to explain if they disable (DR6) it may slow down or
block the spread of cancerous cells through the body. The only the researchers
need to know is what are the possible side effects that we as human posses if we
disable (DR6). Although saying that cancer spreads because of the failure in (DR6)
other researchers say that there other ways to. UCLA has an idea and say that
tumor cells could spread through the body outside blood vessels and the
bloodstream. Also the researchers behind this also stated that some melanoma
cancers could use a mechanism called angiotropism. What this does is that the
melanoma could cling outside a blood vessel and move rather than penetrate. That
why many think that disabling (DR6) could be a choice but if the study concludes
that melanoma uses angiotropim disabling (DR6) wont do to much. The other
article talks about how cells are avoiding apoptosis. One of the ways that cells
avoid apoptosis is by loss of the apoptosis gatekeeper, protein P53. Most types of
human cancer have missing or mutated gene for P53. The problem with P53 being
mutated is that this protein is responsible for cell division and cell death along with
Retinoblastoma. When this occurs the result is repeated uncontrolled cell division.
Most of the stronger types of cancer have both Retinoblastoma and P53 mutations.
The result of this is how rapidly tumors grow because they have extremely low
levels of apoptosis meaning that cancerous cells don’t die and high levels of cell
division meaning that the tumor has a rapid growth. What’s interesting about both
articles is that all types of cancer have different types of behavior and different
forms of spreading. This findings have a great impact on how future researchers
could investigate how cancer spreads. The other thing that I mostly found
interesting is how cancer modifies certain proteins to take advantage and keep
growing.
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In a article published in 2016 it shows how we may slow down the spread of cancer through are body. In the article it talks how most people that die from cancer don’t die by the original tumor but from the spreading cancer. Also it talks about how cancer moves around the body. They found out that metastases targets a molecule called Death Receptor 6 (DR6). What this does is set off a self destruct process in the blood vessels allowing the cancer to spread. The universities studying this were trying to explain if they disable (DR6) it may slow down or block the spread of cancerous cells through the body. The only the researchers need to know is what are the possible side effects that we as human posses if we disable (DR6). Although saying that cancer spreads because of the failure in (DR6) other researchers say that there other ways to. UCLA has an idea and say that tumor cells could spread through the body outside blood vessels and the bloodstream. Also the researchers behind this also stated that some melanoma cancers could use a mechanism called angiotropism. What this does is that the melanoma could cling outside a blood vessel and move rather than penetrate. That why many think that disabling (DR6) could be a choice but if the study concludes that melanoma uses angiotropim disabling (DR6) wont do to much. The other article talks about how cells are avoiding apoptosis. One of the ways that cells avoid apoptosis is by loss of the apoptosis gatekeeper, protein P53. Most types of human cancer have missing or mutated gene for P53. The problem with P53 being mutated is that this protein is responsible for cell division and cell death along with Retinoblastoma. When this occurs the result is repeated uncontrolled cell division. Most of the stronger types of cancer have both Retinoblastoma and P53 mutations. The result of this is how rapidly tumors grow because they have extremely low levels of apoptosis meaning that cancerous cells don’t die and high levels of cell division meaning that the tumor has a rapid growth. What’s interesting about both articles is that all types of cancer have different types of behavior and different forms of spreading. This findings have a great impact on how future researchers could investigate how cancer spreads. The other thing that I mostly found interesting is how cancer modifies certain proteins to take advantage and keep growing.