DNA THERAPEUTICS - FAQs

DNA THERAPEUTICS - FAQs 1) What is the DNA bait concept / technology? The DNA bait concept is a pathway-targeted/mechanism-oriented approach, using substrate mimics of DNA double strand breaks (DSBs). DNA bait Technology is an alternative approach to all existing molecular therapies. It targets a class of DNA lesions’ sensing, signaling and repair pathway, hence disabling key cancers’ defenses towards existing treatments.2) What is new in the DNA bait concept / technology? The DNA bait concept represents a paradigm shift, from single-gene/protein targeting to multi-gene/protein and pathway targeting, enhancing the efficiency of emerging molecular therapies. Thus it is the most recent breakthrough in molecular therapy, based on a unique pathway-targeted/mechanism-oriented approach. As such, DNA bait technology exploits a new field of molecular therapy beyond gene/protein-targeted approaches, and beyond siRNAs.3) What are siDNA molecules? siDNA® (short inhibiting DNA) are proprietary modified DNA molecules that mimick double strand breaks (DSBs) in genomic DNA caused by genotoxic agents, such as chemotherapeutic agents and ionizing irradiation used in cancer treatment.4) How do siDNA molecules / DNA bait approach enhance efficacy of radio - and chemotherapy? siDNA molecules impair the DSB repair system which allows cancer cells to escape from radio - and chemotherapy, by neutralizing transiently the targeted DSB repair capacity in the treated cancer cell. DNA bait is a first-in-class therapeutic approach, to overcome radio - and chemo-resistance of tumors. Therefore, it considerably adds value to the existing therapies, not only radio - and chemotherapies, but also other emerging molecular therapies, instead of running into a head-to-head competition with other players.5) Why is the treatment of siDNA selective to cancer cells? Cancer cells are more sensitive to the inhibition of DNA repair than normal cells for a number of reasons:they divide rapidly and have less time to carry out DNA repair;they usually replicate under conditions of stress, increasing levels of endogenous DNA damage;their greater instability than normal cells and their reliance on fewer DNA repair pathways ensures that disrupting a specific DNA repair pathway has a greater effect on such cells. Our data on siDNA and others available in the literature on low mass inhibitors of DNA repair enzymes suggest that short term DNA repair inhibition is not lethal to normal cells.


Карта сайта


Информационный сайт Webavtocat.ru