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How do PARP inhibitors work to reduce the side effects of breast and ovarian cancer treatment?

How do PARP inhibitors work to reduce the side effects of breast and ovarian cancer treatment?

Researchers Unveil Strategies to Minimize Breast and Ovarian Cancer Treatment Side Effects

Cancer treatments have long been a double-edged sword, effectively combating the disease but often at a high cost to the patient’s healthy cells. However, a groundbreaking study from the University of Geneva, in collaboration with FoRx Therapeutics, offers new hope in reducing such side effects, especially for those battling breast and ovarian cancer. This new approach centers around an innovative use of PARP inhibitors, promising a brighter future for cancer care.

Understanding the Basics: What Are PARP Inhibitors?

PARP inhibitors target a very specific part of the cancer-fighting process. Designed for individuals with breast or ovarian cancer who carry the BRCA gene mutation, these inhibitors work by hindering PARP proteins. PARP proteins are essential in signaling the repair process for DNA damage. By blocking these signals, PARP inhibitors prevent cancer cells from repairing themselves, leading to their death. This form of treatment has been a beacon of hope for about 15 years, yet its effect on healthy cells has limited its potential.

The Downside of Current Treatments

Every day, our DNA sustains thousands of lesions but is remarkably adept at repairing itself, thanks in part to repair proteins coded by genes such as BRCA1 and BRCA2. Mutations in these genes, however, can greatly increase one’s risk of developing breast, ovarian, or even prostate cancer. PARP inhibitors exploit this weakness in cancer cells but, unfortunately, also compromise the health of rapidly dividing healthy cells like hematopoietic cells, which are crucial for blood cell production. Thus, the challenge has been to maximize the drugs’ cancer-fighting properties while minimizing harm to healthy cells.

A New Direction in Cancer Treatment

Researchers at UNIGE and FoRx Therapeutics have made a significant breakthrough in understanding how PARP inhibitors work. Their study, published in the journal Nature, reveals that not all PARP inhibitors act the same way. While they all block the PARP protein’s ability to signal for DNA repair, some forms of these inhibitors also trap the PARP protein on the DNA. This trapping action is harmful not just to cancer cells but to healthy cells as well.

Their findings show that PARP inhibitors can be designed to block the enzyme’s activity without trapping it on the DNA. This selective inhibition successfully kills cancer cells by preventing them from repairing their DNA, without the collateral damage to fast-growing healthy cells. This research could pave the way for the development of safer, more effective PARP inhibitors.

Hope on the Horizon

“We discovered that inhibiting the enzyme activity is sufficient to kill cancer cells, whereas the trapping effectively kills normal cells as well,” explains Michalis Petropoulos, a leading researcher on the study. By distinguishing between these two effects, scientists can now focus on creating treatments that target cancer cells while sparing healthy ones.

This discovery opens up exciting possibilities for cancer treatment. With PARP inhibitors that only inhibit enzyme activity without trapping on DNA, patients may experience fewer side effects, improving their quality of life during and after treatment.

For many, this research represents a significant leap forward in cancer care, highlighting the promise of personalized, precise treatment options that go beyond the traditional one-size-fits-all approach. As the scientific community continues to explore and refine these findings, the hope is that more cancer patients will benefit from treatments that are as effective as they are gentle.

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