Tuesday, August 16, 2022

Spanish researchers discover ‘weak point’ in tumors resistant to multiple drugs

Researchers from the National Center for Cancer Research (CNIO) have discovered cell lines one of the reasons multi-drug resistance And a strategy potential for face it,

one of the following Major challenges in cancer to understand why there is patients what they don’t answer To remedy, in some cases, tumor current known as multi-resistance, Which intelligently limits the therapeutic options for patients.

“Our result explains why in some tumors? Many Common Treatments Don’t Workand recognizes at the same time weak point of these cancers resistant, now we know that vulnerability This Blow employment drugs what already exists”, details Oscar Fernandez-Capatilo, head of the CNIO Genomic Instability Group and lead author of this research, which is published in the scientific journal ‘EMBO Molecular Medicine’.

As the study shows, mutation which inactivates the function of a specific gene, FBXW7, “reduces” sensitivity for the vast majority of therapies available”, and “at the same time they return” To be embroiled in a blow or accident cells of Tumor For a specific type of drug of action: those that activate the “integrated stress response” (ISR). FBXW7 is one of the ten genes most frequently mutated in human cancer and is associated with bad existence in all of them.

A very common mutation in human cancer

study started with mutation search which generate resistance to antitumor agents such as cisplatin, rigosertib or ultraviolet light, using CRISPR technology in mouse stem cells. mutation emerged rapidly in the FBXW7 gene, suggesting that such a mutation may confer multi-resistance,

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Bioinformatic analysis of databases such as the Cancer Cell Line Encyclopedia (CCLE), information about answer more than a thousand lines human cancer cells for thousands of compounds, confirmed that mutant cells FBXW7 son resistant for most of the drugs available in this data set.

regardless of the mutationAdditional analyzes in the Cancer Therapeutic Response Portal (CTRP) revealed that low level The expression of FBXW7 is also a . was associated with worse response to chemotherapy, The authors suggest, in fact, to be able to use FBXW7 levels as a biomarker Forecast patient feedback for medicines.

Without FBXW7, mitochondria become stressed

established Relationship Between FBXW7 deficiency and multi-resistance, researchers sought their cause, they found him in mitochondriaParts of the cell involved in metabolism and cellular respiration.

Showed cells deficient in FBXW7 high protein intake related to mitochondriasomething that has been seen before related for drug resistance. Detailed analysis of these organelles further revealed that the mitochondria of these multi-resistant cells appeared under a lot of stress,

This is the last data that will appear cleve to be able to recognize Strategies that they overcome drug resistance of cells with mutations in FBXW7. mitochondria are the remains of ancient bacteria, which merged billions of years ago into primitive eukaryotic cells; and if Antibiotics attack bacteriaResearchers have thought that if a Antibiotics kill a cancer cell very rich in mitochondria,

They have been identified in the past antitumor properties Definitely Antibiotic medicinesbut it was almost isolated cases and therefore potentially responsible individual mutation -unknown – of patients.

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Fernandez-Capatilo and his group demonstrated that, in fact, Antibiotic medicines tigecycline es toxic For cells deficient in FBXW7, which are a . opens new avenues of research To deal with multi-resistance.

But perhaps even more relevant is the discovery of why Antibiotic medicines have properties antitumorless, The authors of the now published work show that tigecycline kills cells Through over-excitement Integrated stress response (ISR), and also shows that other drugs capable of activating the ISR are also toxic cells with mutations A FBXW7.

Many of these are ISR activating drugs. oncology treatment in common clinical use today, and which until now was believed to work other systems, However, this work shows that part of its antitumor efficacy because of its effect on Active ISR.

“Our study, along with other recent studies, indicate that activating the ISR may be a way overcome resistance to chemotherapy. Even then, there is a lot to do, What are the drugs that best and most activate ISR? Which patients will benefit the most from this strategy? “We intend to devote ourselves in the immediate future to trying to answer these questions,” says Fernández-Capatilo.

The work has received funding from the Ministry of Science and Innovation, the Spanish Association Against Cancer (AECC) and the “La Caixa” Foundation, among others.

Nation World News Desk
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