• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
4 presentacion
 

4 presentacion

on

  • 129 views

 

Statistics

Views

Total Views
129
Views on SlideShare
129
Embed Views
0

Actions

Likes
0
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    4 presentacion 4 presentacion Presentation Transcript

    • BRCA1-DEFICIENT CANCER CELLS TAKE ADVANTAGE OF DNA.SILIBININ KILLS SKIN CELLS MUTATED BY UVA RADIATION. REPAIR MECHANISM. Tatiana Gil Franco Medicine Student 3° semestre U.P.B
    • Introduction The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination. Silibinin, kills skin cells mutated by UVA radiation and protects against damage by UVB radiation.
    • BRCA1-deficient cancer cells takeadvantage of DNA repair mechanism. The Journal of Cell Biology. (Jan 22, 2013)
    • BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISMBRCA1 It’s a human caretaker gene that produces a protein called breast cancer type 1 susceptibility protein, responsible for repairing DNA. The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination.
    • BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISM53BPA1 Cathepsin L It’s a protein that helps  It’s a protease that orchestrate a different destroys 53BP1 by DNA repair entering the nucleus. mechanism, nonhomol ogous end joining  vitamin D is a (NHEJ) cathepsin L inhibitor Cells lacking BRCA1 compensate by cutting back on 53BP1.
    • BRCA1-DEFICIENT CANCER CELLS TAKEADVANTAGE OF DNA REPAIR MECHANISM When they cultured breast cancer cells that were missing BRCA1, the cells stopped growing. After two weeks of lethargy, however, BOGA cells (BRCA1-deficient cells that overcome growth arrest), began to divide again. These cells showed increased levels of cathepsin L and reduced amounts of 53BP1. Eliminating cathepsin L from BOGA cells or dosing them with vitamin D, a cathepsin L inhibitor, prevented the decline in 53BP1 abundance.
    • PERSONAL OPINION This article explains how cancer cells by cathepsin, 53BP1 attack, inhibiting DNA repair mechanism. I think this is very important because the authors are proposing a treatment for breast cancer.
    • Silibinin kills skin cells mutated byUVA radiation and protects against cancer. Photochemistry and photobiology. (Jan. 31, 2013 )
    • SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER  Silibinin, also known as silybin, is the major active constituent of silymarin, a standardized extract of the milk thistle seeds containing mixture of flavonolignans.  Silibinin has also demonstrated in vitro anti-cancer effects, estrogen dependent and independent human breast carcinoma cells.
    • SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER The first study, published in the journal Photochemistry and Photobiology worked with human skin cells subjected to UVA radiation. The Agarwal Lab treated these UVA-affected cells with silibinin. With silibinin, the rate at which these damaged cells died increased dramatically.
    • SILIBININ KILLS SKIN CELLS MUTATED BY UVARADIATION AND PROTECTS AGAINST CÁNCER  The second study shows that instead of beneficially killing cells damaged by UVA radiation, treatment with silibinin protects human skill cells from damage by UVB radiation.  The UVB radiation makes up about 5 percent of the suns radiation reaching Earth.
    • PERSONAL OPINION I think that it’s a very important new because this tell us about the great damage that UV light causes us and show us how with the help of the silibinin and a DNA repair mechanism can prevent this damage.
    • MEDICAL UTILITY Knowing about the mechanisms of DNA repair is very important in the field of medicine as these mechanisms are closely linked to health problems such as cancer.
    • MEDICAL UTILITY In the first news tell us about breast cancer and the BRCA1 protein function in this pathology.
    • MEDICAL UTILITY The second new describe us the operation of silibinin killing cells damaged by UV rays.
    • REFERENCES News medical “Silibinin kills skin cells mutated by UVA radiation and protects against cáncer”Jan 31, 2013. Photochemistry and photobiology.< http://www.news-medical.net/news/20130131/Silibinin-kills-skin-cells-mutated-by-UVA-radiation-and-protects-against-cancer.aspx> News medical “BRCA1-deficient cancer cells take advantage of DNA repair mechanism”Jan 22, 2013. The Journal of Cell Biology.<http://www.news-medical.net/news/20130122/BRCA1-deficient-cancer-cells-take-advantage-of-DNA-repair-mechanism.aspx> MARTINEZ SÁNCHEZ, Lina María. Biología molecular. 2. ed. Medellín: UPB. Fac. de Medicina, 2006. 208 p.