Minimal residual disease in prostate cancer patients after primary treatment: theoretical considerations, evidence and possible use in clinical management

Abstract

Minimal residual disease is that not detected by conventional imaging studies and clinically the patient remains disease free. However, with time these dormant cells will awaken and disease progression occurs, resulting in clinically and radiological detectable metastatic disease. This review addresses the concept of tumor cell dissemination from the primary tumor, the micrometastatic niche and tumor cell survival and finally the clinical utility of detecting and characterizing these tumor cells in order to guide management decisions in treating patients with prostate cancer.

Impact of prostate focused alignment on planned pelvic lymph node dose

“…This study discusses the planning consequences of operating under with the assumption that the lymph nodes move in concert with the prostate. Murray 9 reviews the intrinsic threat of low coverage for prostate cancer patients: micro disease. The presences of lymph node micro disease impacts prudent treatment methods and negatively impacts outcomes 10 .…”

Metastatic Spread in Prostate Cancer Patients Influencing Radiotherapy Response

“…The authors found that CTC positivity correlates with early relapse while DTC positivity is associated with late failure. Therefore, they propose the existence of two forms of MRD representing different clinical characteristics ( 264 , 265 ). This leads to the hypothesis that the dynamics of MRD determines therapy response and patient outcome.…”

Leveraging sequences missing from the human genome to diagnose cancer

“…We next tested whether neomers could be used to diagnose cancer in cfDNA. We focused on prostate cancer, due to the following reasons: 1) It is the fifth leading cause of death worldwide, the second most frequent cancer in males and is responsible for 3.8% of all cancer deaths (39); 2) the availability of both WGS datasets and cfDNA samples; 3) the current primary screen for this cancer, measuring levels of the prostate-specific antigen in the blood, has high false negative and false positive rates (40); 4) the need for more accurate screening for minimal residual disease after treatment or surgical interventions (41,42); 5) the number of neomers per this subtype (N=5,270, median per patient=29.5) is on the low end of all 21 tissues that we analyzed (Table S1), allowing us to asses our ability to diagnose cancer with a relatively small number of neomers; 6) localized prostate cancer has a low abundance of ctDNA making it difficult to detect by ultra low pass WGS or targeted cfDNA sequencing (43) or via methylation (44) compared to metastatic (45), providing a challenging test for our neomer approach.…”