Development of a novel patient-reported outcome measure for disseminated coccidioidomycosis (valley fever).

Background: Coccidioidomycosis (Valley Fever) is a dimorphic fungal infection endemic to the southwest United States, Mexico, Central and South America, which can lead to chronic debilitating illness and death.

Objectives: This qualitative study was conducted to develop a bespoke patient-reported outcome measure for patients with chronic disseminated coccidioidomycosis to assess health-related quality of life (HRQoL) impacts.

Patients And Methods: Online, first-person narratives of patient experiences of disseminated coccidioidomycosis were used to create a patient-centred conceptual model of symptoms and impacts of the condition.

CDK4/6 inhibitors promote PARP1 degradation and synergize with PARP inhibitors in non-small cell lung cancer.

Despite widespread deregulation of CDK4/6 activity in non-small cell lung cancer (NSCLC), clinical trials with CDK4/6 inhibitor (CDK4/6i) as a monotherapy have shown poor antitumor activity. Preclinical studies indicate that CDK4/6i may collaborate by influencing DNA damage repair pathways during radiotherapy. Since PARP1 expression was also significantly upregulated in NSCLC, we analyzed the efficacy of combining PARP1 and CDK4/6 inhibition in NSCLC models.

CDK4/6 inhibitors promote PARP1 degradation and act synergistically with PARP inhibitors in non-small cell lung cancer.

Despite the widespread deregulation of CDK4/6 activity in non-small cell lung cancer (NSCLC), the clinical trials with CDK4/6 inhibitors (CDK4/6is) as a monotherapy have shown poor antitumor activity. However, our preclinical studies have revealed a significant potential for CDK4/6is to collaborate by influencing DNA damage repair pathways during radiotherapy. Given the considerable upregulation of PARP1 expression in NSCLC, we analyzed the efficacy of combined PARP and CDK4/6 inhibition in NSCLC models.

Glutamine antagonists may KEAP lung cancer in check.

The glutamine antagonist DRP-104 blocks purine synthesis and combines with checkpoint inhibitors to promote antitumor immunity in KEAP1/NRF2-mutant lung cancers.