-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Just a day later, a major study of ecDNA was published again in the leading academic journal, CellThis time, the scientists who led the study were from UCSD and Case Western Reserve UniversityThey found that there was also ring-like ecDNA in the malignant brain tumor of glioblastomaIt has not only the EGFR gene that promotes cancer development, but also many sequences that enhance itWhat's even more surprising is that some sequences are not originally around the EGFR geneThey are more like cancer cells being "drawn" from all parts of the genome, specifically designed to strengthen cancer-causing genes!how did this study work? It also starts with cancer-causing genesLong ago, scientists noticed that cancer-causing genes in cancer cells had a rise in the number of copiesSometimes, the number of unusually large increases is not only the sequence of coding, but also some non-coding DNAThe role of these non-coding DNA in cancer cells has been a mysteryin the study, the scientists decided to look at these uncoded DNA, which was a glioblastomaIn this extremely dangerous brain tumor, we can often observe overactivity of the EGFR geneWhen tumors have a large number of copies of EGFR genes, these cancer-causing genes tend to form ring-shaped ecDNA structuresAs the name suggests, this is a kind of DNA that is independent of chromosomes and looks like plasmid DNA from bacteriain the cells of glioblastoma, scientists observed the EGFR gene (red) outside the chromosome (photo source: Photo pharyy of Case Western Reserve)in this ring DNA, not only the EGFR gene existsInstead, in some tumor samples, they found that there were many booster sequences, or other regulatory elements, near the EGFR gene Some of these regulatory elements are very close to EGFR in their original position in the genome, which is also easy to understand But it's a mystery that other regulatory elements appear to have been grabbed from irrelevant parts of the genome! To understand the function of these regulatory elements, scientists used CRISPR gene editing to silence them one by one The results of the study are not encouraging - almost every regulatory element promotes tumor growth "It looks as if the cancer-causing gene will grab the 'switch' from all parts of the genome to maximize their expression." Professor Peter Scacheri, one of the authors of the study, said illustration of this study (Photo: Source: Supplied) subsequently, scientists found that such phenomena were not limited to the EGFR gene, but also to glioblastomas By consulting the public database of oncology genetics, similar phenomena exist in many cancer types The most common of these are the MYC gene in myeloma and the MYCN gene in neuroblastoma and, even if both types of tumors are driven by the same cancer-causing genes, the regulatory elements behind these cancer-causing genes are likely to be different To this end, the researchers point out, in the past, we have focused too much on the cancer-causing gene itself, while ignoring the enhanced human modifiers of the cancer-causing gene In the future, we should set a wider focus on cancer treatment While targeting cancer-causing genes, consideration is also needed to consider how to turn off the switch that activates these cancer-causing genes "It's not just what's observed in the lab, it's the message that really helps patients." Another correspondent, Professor Jeremy N Rich, said References: .
https:// https://doi.org/10.1016/j.cell.2019.10.039 Original title: yesterday just issued "nature", today also issued "cells"! The DNA associated with this cancer is completely on fire.