SCIENCETECH

DNA Repair and Cancer Cell Death : DNA Repair's Role in Cancer Cell Death Post-Radiotherapy

DNA Repair's Role in Cancer Cell Death Post-Radiotherapy
Australian researchers have discovered that DNA repair may influence how cancer cells die following radiotherapy, a finding that could improve cancer treatment and cure rates.

Synopsis

Australian researchers reveal that DNA repair influences how cancer cells die after radiotherapy, potentially enhancing treatment strategies and survival rates.

Key Takeaways

  • DNA repair mechanisms can determine cancer cell death.
  • Homologous recombination leads to unnoticed cell death.
  • Alternative repair methods can activate immune response.
  • Blocking homologous recombination may enhance treatment.
  • Research published in Nature Cell Biology.

Sydney, Jan 14 (NationPress) Researchers from Australia have discovered that DNA repair processes may influence how cancer cells perish after undergoing radiotherapy, according to a groundbreaking study that could enhance treatment efficacy and survival rates.

To investigate the mechanisms behind the death of cancerous tumor cells post-radiotherapy, scientists from the Sydney's Children's Medical Research Institute (CMRI) observed irradiated cells over a week following radiation therapy, utilizing advanced live cell microscopy technology, as reported by CMRI and Xinhua News agency.

“Our unexpected finding reveals that DNA repair, which typically safeguards healthy cells, actually dictates the death of cancer cells following radiotherapy,” stated Tony Cesare, leader of the CMRI Genome Integrity Unit.

He elaborated that the research revealed the capability of DNA repair mechanisms to identify significant damage inflicted by radiotherapy and guide cancer cells towards death.

When DNA damage caused by radiation was rectified through a process known as homologous recombination, it was observed that cancer cells succumbed during cell division, a phase termed mitosis.

Cesare noted that this form of death during cell division remains unnoticed by the immune system and hence does not trigger the desired immune response.

Conversely, cancer cells that managed radiation-induced DNA damage through alternative repair mechanisms survived cell division but emitted byproducts that mimic a viral or bacterial infection.

“For the cell, these repair byproducts appear to signify an infection, prompting the cancer cell to die in a way that activates the immune system, which is our goal,” Cesare remarked.

The researchers demonstrated that inhibiting homologous recombination altered the death process of cancer cells to provoke a robust immune response.

This discovery paves the way for the potential use of drugs that inhibit homologous recombination to compel radiotherapy-treated cancer cells to die in a manner that signals the immune system to target the malignancy.

The findings, published in the journal Nature Cell Biology, may pave the way for novel strategies to optimize cancer treatments and enhance cure rates, as per the announcement.

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