Folding

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Precise Gene Editing In Monkeys Paves The Way For Valuable Human Disease Models AND New Study Shows Promise For Preventing Therapy Resistance In Tumor Cells Vanessa Pérez Carrillo Medicine student III semester Molecular biology

Transcript of Folding

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Precise Gene Editing In Monkeys Paves The Way For Valuable Human

Disease ModelsAND

New Study Shows Promise For Preventing Therapy Resistance In

Tumor Cells

Vanessa Pérez CarrilloMedicine student

III semesterMolecular biology

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INTRODUCTIONMolecular biology techniques have become a really important tool,

because scientists can explore the

humans´s DNA and can modify some

charateristcs.

This important investigation open the panorama of

what is cancer and how physians can access for a better

possible cure.

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SCIENCEDAILY, JANUARY 30, 2014

Thanks to the implement of CRISPR/Cas9 system, the investigators have had the posibility to modificate monkey’s genes , the reason is because targeted genetic modification in monkeys is invaluable for the generation of human disease models.

the CRISPR/Cas9 system enables simultaneous disruption of two target genes in one step without producing off-target mutations.

Precise Gene Editing In Monkeys Paves The Way For Valuable Human Disease Models

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SCIENCEDAILY, JANUARY 30, 2014

The CRISPR/Cas9 system is a gene editing tool capable of targeting specific DNA sequences in the genome.

Cas9 proteins, which are directed by molecules called single-guide RNAs to specific sites in the genome, generate mutations by introducing double-stranded DNA breaks

Precise Gene Editing In Monkeys Paves The Way For Valuable Human Disease Models

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The scientist injected messenger RNA molecules encoding Cas9, in addition to single-guide RNAs designed to target three specific genes, into one-cell-stage embryos of cynomolgus monkeys.

After sequencing genomic DNA from 15 embryos, they found that eight of these embryos showed evidence of simultaneous mutations in two of the target genes.

Precise Gene Editing In Monkeys Paves The Way For Valuable Human Disease Models

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Precise Gene Editing In Monkeys Paves The Way For Valuable Human Disease Models

The researchers transferred genetically modified embryos into surrogate females, one of which gave birth to a set of twins. By sequencing the twins' genomic DNA, they found mutations in two of the target genes.

the CRISPR/Cas9 system did not produce mutations at genomic sites that were not targeted, suggesting that the tool will not cause undesirable effects when applied to monkeys

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I found this news really great because it shows me how the medicine keeps improving everyday, how to search about new alternatives for the study about our

DNA, also let us know the importance of some animals that have similitudes to humans for evaluate disease models, compare the DNA and try to create

and discover new alternatives to make a correct prevention, diagnosis and treatment of a lot of

pathologies.

OBSERVATION

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researchers suggests that activating the tumor suppressor p53 in normal cells causes them to secrete Par-4.

Par-4 is another potent

tumor suppressor protein that induces cell death in cancer cells.

New Study Shows Promise For Preventing Therapy

Resistance In Tumor Cells JA

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Loss of the tumor suppressor p53 often contributes to therapy resistance in tumors.

The investigators activated wild type p53 in normal cells to trigger cell death in the p53-deficient cancer cells.

p53 is intact and functional in normal cells, the researchers harnessed its potential to inhibit the growth of p53-deficient cancer cells.

New Study Shows Promise For Preventing Therapy Resistance In Tumor

Cells

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The tumor suppressor Par-4 specifically kills cancer cells.

Par-4 is really special because

it is not mutated as frequently as other known suppressors.

The secretion from normal cells can be induced by activating p53 so that Par-4 enters circulation, thereby potentially targeting tumor cells at distant sites.

New Study Shows Promise For Preventing Therapy Resistance In

Tumor Cells

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Scientists gets to empower the normal cells to trigger cell death in p53-deficient cancer cells

All of this findings have potential for targeting local, as well as metastatic tumors, and future studies will use FDA-approved drugs to induce Par-4 secretion.

New Study Shows Promise For Preventing Therapy

Resistance In Tumor Cells

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I really like this news because I learned about the effects of tumor suppressor Par-4, it shows us the

way to implement a new technique that let us know more about the tumor cell activity and control the cell

born and death. Its really usefull for investigate the way of making studies to find solutions for cancer.

Also it invite me to be more interested in what can I do for the humanity.

OBSERVATION

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MEDICAL UTILITY 1

The knowledge about primate´s genes is an

excellent opportunity for science to research and evaluate similitudes with humans genes, and then, with this nformation we can work for a healthier

life.

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MEDICAL UTILITY 1

The implement of this important, safer and

specific system CRISPR/Cas9 will

significantly advance the development of

therapeutic strategies in biomedical research

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MEDICAL UTILITY 2

It give us a major source of discovery and

development of more effective approaches to

cancer prevention, diagnosis and treatment

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MEDICAL UTILITY 2

It is really important to know about the effects of the Par-4 protein because it is a special way to find

the possible cure of cancer thanks to all the

qualities.

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Martínez S. Lina María. Biología molecular, 5 ed. Medellín, UPB, facultad de medicina.

Ravshan Burikhanov, Tripiti Shrestha, Nikhil Hebbar, Gerard P. Zambetti, Vivek M. RangnekaR. Paracrine apoptotic effect of p53 mediated by tumor supresor Par 4. Cell Report, January 9, 2014. (online magazine) http://www.sciencedaily.com/releases/2014/01/140109175519.htm

Yuju Niu, Bin Shen, Yiqiang Cui, Yongchang Chen, Jianying Wang, Lei Wang, Yu Kang, Xiaoyang Zhao, Wei Si, Wei Li et al. Generation of Gene-Modified Cynomolgus Monkey via Cas9/RNA- Mediated Gene Targeting in One- Cell. Embryos. Cell 30 January 2014. (online magazine) http://www.sciencedaily.com/releases/2014/01/140130121607.htm

Bibliography

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