Does the presence of an ATM mutation in advanced stage ovarian cancer influence the decision to use Bev vs PARP inhibitor for maintenance?

I would not use the presence of an ATM mutation alone to inform decisions between bevacizumab vs PARPi maintenance. There are several options for maintenance in the 1L setting, and these include single agent PARPi, PARPi + bevacizumab, or bevacizumab monotherapy. Using data from the PAOLA-1 trial, it was shown that HRRm alone are not predictive of response to PAPRi + bevacizumab and we understand that the relevance of individual HRRm (aside from BRCAm) has yet to be completely defined, and can vary across solid tumors. In this setting, I would be more interested in the HRD status. If the tumor was HRD+, I would be inclined to use PARPi + Bevacizumab. Conversely, if HRP (irrespective of the presence of an ATM mutation), I would counsel my patient regarding PAPRi maintenance or Bevacizumab maintenance (and some may choose observation). 

ATM plays a central role in the repair of DNA double-strand breaks, which can be induced by ionizing radiation, chemotherapy drugs, or oxidative stress, or occur during normal physiologic events like meiotic recombination. Somatic ATM mutations or deletions are commonly found in lymphomas and a variety of solid tumors and may result in chemotherapy resistance and adverse prognosis. This can be exploited by existing or emerging targeted therapies that produce synthetic lethal states. The use of PARPi therapy is being studied in cancers with ATM mutations.

The ATR-checkpoint kinase 1 pathway is another potential target for therapy in ATM-deficient cancers, as it is a primary mediator of SSB DNA repair. Combination PARPi and ATR inhibition is also being studied in early phase trials. 

An ATM mutation alone would not determine upfront maintenance therapy in ovarian cancer, but HRD status would be helpful in that decision regarding use of PARPI therapy +/- Bevacizumab.