ELISA OROZCO GÓMEZ

Medicine student

DNA REPAIR

INTRODUCTION

Non-homologus end joining

Homologus recombinantion

p53 and statins

HEALTHY DNA

Technische Universität Darmstadt

February 2, 2017

Non-homologus joining and

homologus recombination are

mechanisms for reparing damaged

DNA.

Researchers recently found out

that enzymes act in the

damaged ends with the

purpose of replacing the lost

information with a copy before

the joining happens

Researchers thinks that knowing

about these enzymes it may be

useful for preventing hereditary

diseases such as cancer, by using

gene therapy.

This research is really important because

as many parts of the DNA can be

damaged by different factors and in the

future develop different diseases,

RESECTION IN THE LINGO might be the

solution that we have been waiting for our

DNA survival

University of Kansas, cancer center

January 24, 2017

p53 is known as a tumor

suppressor or the “guardian of the

genome” because this protein

avoids the mutation of our

genome by arresting the cell

cycle in the G1/S regulation point.

Research shows that statins such as

Lipitor, Crestor and Mevacor are the

key for preventing damage caused

by mutated p53.

DNAJA1 protects the mutated p53

with the purpose of avoiding its

destruction by enzymes, statins

prevents that DNAJA1 binds to the

mutated p53.

As the title of the research says, statins

might be the key for treating cancer, this

pills that so many people take for

lowering their cholesterol levels, have

more to offer to our organism, this would

avoid metastasis in cancer patients.

The reparation of the DNA by the

mechanisms and the different proteins that

were mentioned, can lead us to control

several diseases and develop prevention,

detection and treatment in our patients.

The research of statins

helped scientists to

understand how mutated

p53 is destroyed by statins,

and how it is protected

from destruction by

DNAJA1.

We are often exposed to

environmental and metabolic

changes that can damage our DNA,

the key to our survival are might be

just in front of our eyes: STATINS.

Statins that are so common in our

era, can avoid resistance to

chemotherapy and metastasis in

cancer patients, a disease that

affects any person of any social

group.

BIBLIOGRAPHY

1. Ronja Biehs, Monika Steinlage, Olivia Barton, Szilvia

Juhász, Julia Künzel, Julian Spies, Atsushi Shibata,

Penny A. Jeggo, Markus Löbrich. DNA Double-Strand

Break Resection Occurs during Non-homologous End

Joining in G1 but Is Distinct from Resection during

Homologous Recombination. Molecular Cell, 2017;

DOI: 10.1016/j.molcel.2016.12.016

2. Alejandro Parrales, Atul Ranjan, Swathi V. Iyer,

Subhash Padhye, Scott J. Weir, Anuradha Roy, Tomoo

Iwakuma. DNAJA1 controls the fate of misfolded mutant

p53 through the mevalonate pathway. Nature Cell

Biology, 2016; 18 (11): 1233 DOI: 10.1038/ncb3427

“What a wonderful thought it is that

some of the best days of our lives haven't

even happened yet.”