Breakthrough: Three scientists jointly develop a new "detoxification version" erythromycin, side effects greatly reduced!

Introduction to bamboo: Although the anti-cancer effect of adriamycin is great, its toxic and side effects should not be underestimated.other drugs are "San Fen Du", in which they have to become "Qi Fen Du".the most typical damage is myocardial function.if its side effects can be greatly reduced, patients with different types of cancer will benefit from it.this idea has been circulating in the literature for many years, but it has not been proved by experiments.scientists in the Netherlands, the United Kingdom and the United States have modified it, and achieved a great breakthrough in mouse experiments.a new study reports that the drug can be adjusted to reduce its toxic and side effects, especially heart damage, without weakening its ability to inhibit tumor.this study overturns the conventional thinking about doxorubicin and related drugs, showing that they can kill cancer cells without directly destroying DNA.the study was published in the proceedings of the National Academy of Sciences.why is it called "red devil"? Adriamycin is one of the most effective anticancer drugs in the treatment of cancer, but it has great side effects, such as alopecia, bone marrow suppression and cardiotoxicity, especially cardiotoxicity, which limits its clinical application.it is called "red devil" because of its unique color and terrible toxicity.the development of doxorubicin (doxorubicin), belonging to anthracycline, was originally extracted from Streptomyces.they have antibiotic properties, but have also proven to be one of the most effective chemotherapies ever discovered.anthracyclines are used every year to treat 1 million cancer patients, especially those with leukemia and breast cancer.doxorubicin has two activities: DNA damage and chromatin damage.because anthracyclines can cause heart damage, doctors generally do not recommend the use of anthracyclines in the treatment of elderly patients.many childhood cancers can be treated with high-dose drugs, but in later life, patients are prone to heart disease, accompanied by new tumors, which doctors attribute to DNA damage caused by drugs. liposome doxorubicin is a kind of common doxorubicin which is encapsulated in liposome. After liposome drug loading, the drug is redistributed in the body, and the drug concentration in heart, kidney and gastrointestinal tract tissue is significantly reduced. Therefore, it can reduce the toxic effect on these organs, especially on the heart, but the effect is limited. Jacques, a chemist at Leiden University in the Netherlands Neefjes led the team to try a different approach, based on a surprising discovery about how drugs fight cancer, and they and another US team reported in 2013 that drugs kill rapidly dividing cells, such as those in tumors, by blocking enzymes that need to unravel and repair DNA as they replicate. but the researchers found that doxorubicin can also kill cancer cells by scavenging histone, a spherical protein with a structure called chromatin formed by winding DNA around a spool. this chromatin disruption obviously interferes with gene transcription into proteins and other cellular processes. safer doxorubicin Sherif El khamisy, deputy director of the Institute for healthy lifespan at the University of Sheffield in the UK, and his team plan to test two potentially safer doxorubicin drugs in humans. in this new work, Leiden's team tested two anthracycline drug variants that remove histones without damaging DNA: an approved anticancer drug, aclarubicin, and a modified doxorubicin (called dime DOXO). adriamycin was used in Europe for leukemia, but it was withdrawn from the market in the 1990s due to manufacturing problems. the concept of dime DOXO was proposed by scientists from the National Cancer Institute in the 1980s, but it has not been further developed. these compounds are as effective, if not better, than the original drug in killing cultured cancer cells, and almost as effective in slowing tumor growth in mice. however, tumor prone mice did not show any signs of heart damage, suggesting that people treated with the drug may not be affected by these effects. the Leighton team reported in the June 17 online issue of the proceedings of the National Academy of Sciences that these mice were also significantly less likely to develop cancer later. the future of the new doxorubicin, Professor Katerina gurova, is from the first cancer center in the United States, the Roswell Park Comprehensive Cancer Center in Buffalo, New York. he is developing a cancer drug that works by destroying chromatin and is learning more about how to reduce the toxicity of these widely used drugs. neefjes said that neither drug is now patented, which means the company is not interested. as a result, his team has raised funds from both public and private sources to produce dime DOXO and acrabicin to the quality standards that patients need, so they can conduct clinical trials as academic work. the results show that both drugs are worth studying - adriamycin seems to be the most effective for blood cancer, while dime DOXO seems to be more effective for solid tumors. the team has received a large amount of funding from the Dutch cancer society and will start clinical trials of arubicin in patients with recurrent leukemia from next year. Ref. [1] [2] Jacques neefjes El Al. Uncoupling DNA damage from chromatin damage to toxic doxorubicin. Proceedings of the National Academy of Sciences Jun 2020, 117 (26) 15182-15192; Doi: 10.1073/pnas.1922072117 recommended reading: fight against the epidemic situation, translational medicine network content team series reports: [new discovery] compounds produced by intestinal microorganisms can damage arteries, thus increasing the risk of heart disease [agenda] gene - π digital PCR training camp - quality control system of digital PCR quantitative medicine advanced treatment (Chengdu Station) [Nature journal] University of Southern California combined with 10x Genomics develops new single cell technology to reveal genetic diversity of cancer! Click to read the original