LAST WEEK TODAY!

A summary of what was published on ProstateWarriors.com during the past week

Hello fellow warriors! We never stop scouting for new weapons to fight this battle. Stay strong and fight on!

As usual, we also have a podcast if you prefer to listen to the newsletter, you can find it HERE.

Clinical Research

• Phase 3 Trial: Saruparib Maintenance in mHSPC (EvoPAR‑Prostate05)​
  The EvoPAR‑Prostate05 trial is evaluating the PARP1-selective inhibitor saruparib (AZD5305) as a maintenance therapy for men with metastatic hormone-sensitive prostate cancer (mHSPC). To be eligible, patients must have completed an upfront intensive regimen of docetaxel or 177Lu radioligand therapy and currently have a PSA level of 0.2 ng/mL or higher, indicating residual disease. The study is double-blind and placebo-controlled, randomizing approximately 1,330 participants to receive either saruparib or a placebo in addition to a standard androgen receptor pathway inhibitor (ARPI). The primary goal is to determine if this next-generation PARP inhibitor can prolong radiographic progression-free survival over a follow-up period of four to five years.​
• Phase 1/2 Trial: SL-28 for Advanced Solid Tumors​
  A Phase 1/2 clinical trial has begun recruiting up to 60 patients to test SL-28, an allogeneic donor leukocyte therapy, in individuals with advanced solid tumors. This “off-the-shelf” cell therapy is derived from healthy donors and modulated to enhance its cancer-killing and immunomodulatory properties without requiring HLA matching or genetic engineering. The treatment is of particular interest in the prostate cancer community due to a case report of a man with metastatic hormone-sensitive disease who achieved a complete response with SL-28 monotherapy, even without ongoing androgen deprivation therapy. Clinical signals of efficacy have also been documented in case reports for pancreatic and non-small cell lung cancer (another complete response for the latter).​
• Phase 1 Trial: VIR-5500 Expansion into mHSPC​
  In April 2026, the clinical development of VIR-5500 reached a milestone with the first patient dosed in Phase 1 dose-expansion cohorts specifically for metastatic hormone-sensitive prostate cancer (mHSPC). While the therapy is also being studied as a monotherapy for late-line metastatic castration-resistant prostate cancer (mCRPC), this expansion focuses on its use in combination with androgen receptor pathway inhibitors. The move into earlier disease stages was supported by earlier dose-escalation data that showed a favorable safety profile and promising signs of antitumor activity in heavily pretreated patients. (Sorry people, I missed that update in April!)​
• Biallelic Loss in DDR Genes and Its Clinical Impact​
  Research involving a 3,005-patient cohort has demonstrated that germline DNA damage repair (DDR) variants are significant in metastatic prostate cancer, though their clinical impact depends heavily on the specific gene involved. BRCA2 stands out as the most aggressive marker; when a tumor experiences biallelic loss (the loss of both gene copies), patients typically face worse pathology at diagnosis and faster progression to castration resistance. While ATM variants also frequently result in biallelic inactivation, they appear more heterogeneous and do not carry the same uniformly severe survival signal as BRCA2. These findings highlight the importance of broad germline testing to capture structural variants and ensure accurate patient risk classification.​

Preclinical Research & Reviews

• How DNA “Switches” May Open New Treatment Paths​
  Preclinical researchers at USC have discovered that prostate cancer cells rely on a complex 3D network of DNA “switches” called enhancers to maintain the activity of cancer-promoting genes. By analyzing over 200 datasets, the team identified 3,216 enhancers that form an interconnected network specific to cancer cells but absent in healthy tissue. Crucially, certain enhancers act as central hubs for this network; when these hubs were deleted using CRISPR, the entire network was disrupted, leading to the deactivation of cancer genes and slowed cell growth. This suggests a future therapeutic strategy focused on targeting these regulatory control points rather than attempting to target every individual “bad” gene.

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And…that’s all folks! For today at least!
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Have a great weekend!

Max