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This article was originally written by Translational Medicine.
Please indicate the source.
Author: Ashley Introduction: Although therapy targeting specific genes provides a personalized approach to cancer treatment, most patients with advanced disease quickly develop drug resistance
.
Recent studies have shown that these therapies rely on repair of DNA double-strand breaks with ataxia telangiectasia mutations (ATM), representing a potential mechanism to overcome this resistance
.
Several ATM kinase inhibitors are already in clinical development, which represents an opportunity to overcome resistance in multiple cancer types in combination with targeted therapy
.
Cancer therapies that target specific genes or disease pathways can prolong life, but they can also lead to high drug resistance in tumors when small reservoirs of cancer cells survive treatment, growth and spread
.
In their search for ways to prolong the survival benefits of targeted therapies, a team led by researchers at Duke Cancer Institute has identified a potential new strategy for disrupting the repair mechanisms that cancer cells use after treatment, blunting their regeneration ability
.
This approach may suggest new therapeutic strategies
.
The research team's findings "Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells" were recently reported in the journal Science Translational Medicine
.
"We urgently need to find ways to make targeted therapies more effective," said senior author Kris Wood, Ph.
Well, longer lasting
.
This study offers a potential strategy to do this with drugs currently under investigation
.
"Wood and colleagues found that targeted therapy induces DNA strand breaks in cancer cells that survive treatment
.
Efficient repair of these DNA breaks is critical for tumor cell survival and relies on a process known as ataxia capillaries.
A molecule that expands mutant (ATM) enzymes
.
"We were surprised to find that the ATM pathway was frequently activated by these surviving cancer cells," Wood said
.
This discovery leads to the next question: Can we disrupt the repair process? "The researchers used ATM inhibitors that are currently under study, and the answer was yes
.
Testing in mouse models and in laboratory-grown non-small cell lung cancers, they found that an ATM kinase inhibitor, combined with targeted therapy, could Eradication of residual cancer cells, resulting in more durable cancer remission
.
Further confirmation in real-world cases is evident
.
Certain lung cancer patients with ATM mutations and reduced function receive targeted therapy compared to patients lacking the ATM mutation Progression-free survival was longer
.
"Taken together, these findings provide a rationale for the mechanism-based integration of ATM inhibitors with existing targeted therapies," Wood said
.
"Reference: https://medicalxpress.
com/news/2022-03-cancer-mechanism-potential-drug.
html Note: This article is intended to introduce the progress of medical research and cannot be used as a reference for treatment plans
.
For health guidance, please Go to a regular hospital for treatment
.
Recommendation·Event Click the text to view the details.
March 30th 19:00-21:00 Online Seminar on Frontier Progress of Proteomics and Prospects of Innovative Technologies March 31st 19:00-21:00 Sharing Global Technology Online| Oncology Precision Diagnosis Innovation and Development Webinar April 13th 19:00-21:00 Online Innovative Drug R&D and Research and Development Salon (coming soon) April 14th 15:00-16:20 Online based on real-time living cells Imaging-based targeted tumor therapy (to be announced soon) April 20, 09:00-18:00 How to improve the efficiency of new macromolecular drug research and development from basic experiments (to be announced soon)
Please indicate the source.
Author: Ashley Introduction: Although therapy targeting specific genes provides a personalized approach to cancer treatment, most patients with advanced disease quickly develop drug resistance
.
Recent studies have shown that these therapies rely on repair of DNA double-strand breaks with ataxia telangiectasia mutations (ATM), representing a potential mechanism to overcome this resistance
.
Several ATM kinase inhibitors are already in clinical development, which represents an opportunity to overcome resistance in multiple cancer types in combination with targeted therapy
.
Cancer therapies that target specific genes or disease pathways can prolong life, but they can also lead to high drug resistance in tumors when small reservoirs of cancer cells survive treatment, growth and spread
.
In their search for ways to prolong the survival benefits of targeted therapies, a team led by researchers at Duke Cancer Institute has identified a potential new strategy for disrupting the repair mechanisms that cancer cells use after treatment, blunting their regeneration ability
.
This approach may suggest new therapeutic strategies
.
The research team's findings "Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells" were recently reported in the journal Science Translational Medicine
.
"We urgently need to find ways to make targeted therapies more effective," said senior author Kris Wood, Ph.
Well, longer lasting
.
This study offers a potential strategy to do this with drugs currently under investigation
.
"Wood and colleagues found that targeted therapy induces DNA strand breaks in cancer cells that survive treatment
.
Efficient repair of these DNA breaks is critical for tumor cell survival and relies on a process known as ataxia capillaries.
A molecule that expands mutant (ATM) enzymes
.
"We were surprised to find that the ATM pathway was frequently activated by these surviving cancer cells," Wood said
.
This discovery leads to the next question: Can we disrupt the repair process? "The researchers used ATM inhibitors that are currently under study, and the answer was yes
.
Testing in mouse models and in laboratory-grown non-small cell lung cancers, they found that an ATM kinase inhibitor, combined with targeted therapy, could Eradication of residual cancer cells, resulting in more durable cancer remission
.
Further confirmation in real-world cases is evident
.
Certain lung cancer patients with ATM mutations and reduced function receive targeted therapy compared to patients lacking the ATM mutation Progression-free survival was longer
.
"Taken together, these findings provide a rationale for the mechanism-based integration of ATM inhibitors with existing targeted therapies," Wood said
.
"Reference: https://medicalxpress.
com/news/2022-03-cancer-mechanism-potential-drug.
html Note: This article is intended to introduce the progress of medical research and cannot be used as a reference for treatment plans
.
For health guidance, please Go to a regular hospital for treatment
.
Recommendation·Event Click the text to view the details.
March 30th 19:00-21:00 Online Seminar on Frontier Progress of Proteomics and Prospects of Innovative Technologies March 31st 19:00-21:00 Sharing Global Technology Online| Oncology Precision Diagnosis Innovation and Development Webinar April 13th 19:00-21:00 Online Innovative Drug R&D and Research and Development Salon (coming soon) April 14th 15:00-16:20 Online based on real-time living cells Imaging-based targeted tumor therapy (to be announced soon) April 20, 09:00-18:00 How to improve the efficiency of new macromolecular drug research and development from basic experiments (to be announced soon)
