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CRITICAL PATHWAY IN CELL CYCLE MAY LEAD TO CANCER DEVELOPMENT AND CELLS MAKE COSTUME CHANGES FOR CARDIAC REGENERATION Lina Acevedo Forero Medicine Student

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CRIT ICAL PATHWAY IN CELL CYCLE MAY LEAD TO CANCER

DEVELOPMENT AND

CELLS MAKE COSTUME CHANGES FOR CARDIAC

REGENERATION

Lina Acevedo ForeroMedicine Student

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FOLDING

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FOLDING

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Now days the genetic engineering in human is not approved by ethical commite; most of the studies are in others animals but not in our spicie.

Thats why sometimes is difficult to use techniques that help the human health because they are only demostrate in other mammals.

The techniques that transfer genetic material have a vital importance for the study of certains pathologies. These techniques are helping the medicine world, finding cures for some diseases.

These news are giving us hopes about the future of patients with cancer or heart attack.

INTRODUCTION

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CRITICAL PATHWAY IN CELL CYCLE MAY LEAD TO CANCER DEVELOPMENT

The investigators already gave us a hard concepts about the process that explain the defense mechanism against uncontrolled growing of cells.

The main objective conduce to discover the mechanisms implicated in the failure of celular g1 step (p53) and telomeres, and develop strategies for avoid this modifications that is an importnt part of the cancer development.

FIRST NEW

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Karlseder identified an specific part of cell cycle called G1 phase which is altered when a person develop a tumor. It’s the causative phenomenon of the uncotrolled growing of cells and their subsequently lost – shortening of telomeres, an important defense entity that ends in cancer development.

FIRST NEW

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The investigators also discovered that one and important guilty of a tumors development is the natural caracteristic of aging. When the cells get older constantly lost the telomeres weight and the lost or reduction of this specific zone is directly involved with cancer.

FIRST NEW

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In conclusion, in this article we have the most important explanation of cancer development (others are enviroment factors and “luck”), and now there’s a necesity of continue studying and creating solutions to avoid the specific biological modications showed by karlseder.

FIRST NEW

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Actually, we are getting the results of futuristic investigator visions through molecular biology. The genome modifications are possible nowadays, and with this, all problems in genes have the risk of be repared.

This is the key of this article, what explain the route to a new generation of modifications in altered proteins, enzimes, or like this case, in the cell cycle.

FIRST NEW

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SECOND NEW

This study is showing us how after a heart attack, the heart is permanently damaged because of the long-term interrupted oxygen supply and it tissue dies.

The objective was try to stimulate the regeneration of damaged heart tissue and find a way that the results that they obteined can be also used in human cells.

Cells Make Costume Changes for Cardiac Regeneration

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After a heart attack the heart is damage because coronary arteries didn´t give it the blood necesary for the normal function.

In this study the scientist found that muscle cells from a zebrafish migrate from the undamaged atrium into the ventricle, trying to regenerate the died tissue.

SECOND NEW

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They didn´t only find the migration of the cells they also found a clear evidence of transdifferentiation of cells. The cells that migrates from the atria lost their characteristic properties and transformed into ventricular cells.

“With the progression of heart regeneration, these cells were permanently installed in the muscle tissue and made their contribution to the restoration of cardiac function”

SECOND NEW

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After a long study the scientist found that the zebrafish heart was in good conditions after a heart attack, thanks to the migration and transdifferentiation of atrium cells to ventricle cells.

SECOND NEW

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Im very impressed with the results of this article, because it can be the future of the cardiology process.

The findings of this studie will help to persons who had a heart attack to continue their lives with a normal heart activity.

This projects show us that everyday we can know sometime new about medicine; and that this science has still thousands of hidden things.

SECOND NEW

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Firstable, if researchers get a way for stop or repair mutations directly implicated in altered p53 function – telomere lenght, it would be analogued with the cancer cure because its an intervention in a specific cancer route.

MEDICAL UTILITYFIRST NEW

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Cancer is a compliated disease with treatment alternatives based in radiation, chemical drugs or ablation surgery, all this affects and destroys tumoral cells but also beat directly benign body cells too, becoming a heavy therapy for patients. The new medicaments based in article theory, would work before cancer development and would avoid the growing in big masses, more complicated for treat, and without the comorbilities caused for treatment used for destroyd tumors when are already formed.

MEDICAL UTILITYFIRST NEW

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This study is talking about problems with the heart , that in the present are becoming a pandemic.

If the migration of atrium cells is demostrate in human heart, the medicine will have a change in cardiology area.

This can be the solution for those who have diseases after a heart attack because of the unusual activity of the heart.

MEDICAL UTILITYSECOND NEW

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The findings obtained in this study give us hopes; if the atrium cells can can have the properties of ventricular cells in humans, those changes will help the damaged heart tissue after a herat attack to behave normal. And this can completely change the life of these kind of patients.

MEDICAL UTILITYSECOND NEW

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· MARTINEZ SANCHEZ, Lina Maria . Bilogia Molecular. 7. ed.Medellin: UPB. Fac. de Medicina, 2012.

· Critical Pathway in Cell Cycle May Lead to Cancer Development, Molecullar cell. July 11,2013.

http://www.sciencedaily.com/releases/2013/07/130711135223.htm

· Cells make costume changes for cardiac regeneration, Maxn-Planck-Gesellschaft. July 11, 2013.

http://www.sciencedaily.com/releases/2013/07/130711084508.htm

BIBLIOGRAPHY

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THANK´S