potential cancer cells and therapy to treat melanoma
TRANSCRIPT
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POTENCIAL CANCER CELLS AND THERAPY TO TREAT MELANOMA
Luisa Fernanda Montoya Vargas.Molecular biology.
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FACTSFACTS
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INTRODUCTION
• During the cell cycle process it is necessary to have checkpoints due to a successfully regulation.
• Cancer cells contain damage DNA, mutations in multiple genes causing higher rate of division than normal cells.
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Gene keeps potential cancer cells in check
Biotech research and innovation center. University of Copenhagen.
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Gene keeps potential cancer
cells in check.
Gene P53 makes a control in G2 checkpoint in the cell cycle, however gene P53 is not the only gene that coordinates cellular division if there is a mutation in the DNA. Gene Cyclin-F has an important role suppressing Oncogene B-Myb, a gene that stimulates cell division.
Researchers discovered that Cyclin-F was also in charge of supervising the regulation process because they exposed human cells to radiation, so DNA could be damaged. Once they did this procedure they observe which of the 559 genes they examined was involved in cellular division.
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Gene keeps potential cancer
cells in check.
In cancer there is a higher activity of stimulating genes, such as Oncogene B-Myb.
Future investigations allows the possibility to understand genes mechanisms completely.
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Gene keeps potential cancer cells in
check
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OBSERVATION
I think it is important tounderstand genesmechanisms in order toproduce an effectivetreatment for people withcancer, besides that knowingmore paths and genes thatare involved in cellulardivision gives scientists morepossibilities to work with andmore probabilities to attackdifferent targets.
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STUDY TRACTS COMBINATION THERAPY TO TREAT MELANOMA
Research news, Vanderbilt University.
JANUARY 8, 2015
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STUDY TRACTS COMBINATION THERAPY TO TREAT MELANOMA.
Patients with melanomahave been resistant toBRAF inhibitor therapy.
Blocking AURKA andMDM2 proteins, tumor cellsstops multiplying and die.
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STUDY TRACTS COMBINATION THERAPY TO TREAT MELANOMA
In melanoma gene TP53 ismutated so is easily for MDM2 toattack P53, therefore cells divideuncontrollably.
Higher expression of AURKA inmelanoma so cell division occurs ata higher rate too.
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STUDY TRACTS COMBINATION THERAPY TO TREAT MELANOMA
In this investigation they use mouse models and they observe that both MDM2 antagonist and AURKA inhibitor function was helping inmune cells to attack the tumor.
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OBSERVATION
I think further investigations aboutmelanoma should be focused inmaking healing treatments thatguarantee a more lasting effectand using different routes toattack tumor cells.
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MEDICAL UTILITY
Extensive bases for further investigations that would help to the next coming generations to understand cancer mechanisms.
New possibilities to block tumor cells proliferation in order to create an efficient treatment.
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MEDICAL UTILITY
A higher expectancy to treat cancer.
Higher probability to produce a combined effective therapy.
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MEDICAL UTILITY
New medicines that could have a long lasting effect avoiding drug resistance.
Increasing investigative spirit.
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BIBLIOGRAPHY
Cyclin F suppresses B-Myb activity to promote cell cyclecheckpoint control', Nature Communications, 2015. [Internet] 2015 Jan [Fecha de acceso 22 enero de 2015]. Disponible en:www.bric.ku.dk/newslist/news/2015/gene_keeps_cancer_in_check/
Study tracts to treat melanoma, Vanderbilt University, 2015. [Internet] 2015 Jan [Fecha de acceso 23 enero de 2015].Disponible en: http://news.vanderbilt.edu/2015/01/study-tracks-combination-therapy-to-treat-melanoma/
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