Prostate-Specific Antigen Screening: How a Simple Blood Test Saved Marvin’s Life
When Marvin Sanders first received the diagnosis of prostate cancer, he laughed to keep himself from crying.
“I was scared and I was shocked,” Marvin said. “And I wanted to make sure my wife, Melanie, had support, because I knew she would be crying.”
Before his diagnosis, Marvin was consistent with his annual physicals — a gold star patient for men in their 60s. One day, he received a call from his doctor, Michael Dennis, M.D., at the University of Florida because his prostate-specific antigen, or PSA, level was high. They wanted to run the test again to confirm the results. The second test confirmed the worrisome PSA.
When Marvin and Melanie went back to the doctor’s office to plan what to do next, they were reassured by a UF Health Urology team that moved quickly and efficiently.
“There were no gaps,” Melanie said. “They got hold of us quickly and everything moved expeditiously. It was a scary process, but it was comforting to know that the care team was constantly with us.”
A biopsy confirmed Marvin’s cancer. Not too long after, he was scheduled for surgery with Wayne Brisbane, M.D., an assistant professor in the UF Department of Urology.
“When I first met Dr. Brisbane, he sat down with me for a few minutes,” Marvin said. “Before we started talking about a treatment plan, he made sure I was comfortable.”
When it was time to discuss treatment options, Brisbane answered their questions thoroughly and gave them the information they needed to make a decision that would be best for Marvin’s health.
Ultimately, Marvin and his care team decided a prostatectomy would be the best treatment option. Although he was worried about the possible side effects of the procedure, including urinary incontinence and erectile dysfunction, Marvin was confident in Brisbane’s expertise.
New Clinical Trials Open for Enrollment
A Phase 2, open-label, non-randomized study evaluating the safety of administering high dose cytarabine (HiDAC) consolidation therapy on days 1-3 of each cycle, as compared to standard administration on days 1, 3, & 5 of each cycle, in patients 61 years or older with acute myeloid leukemia (AML).
Principal Investigator: Jack Hsu, M.D. | Cell: 352-672-0704
A Phase 2, randomized study that investigates the use of the Signaterra ctDNA assay versus the standard scan-based approach to guide treatment in patients with metastatic colorectal cancer. The aim of this study will be to measure and compare the overall survival, progression-free survival, and best overall response while on study of patients whose treatment has been guided by these two approaches.
Principal Investigator: Sherise Rogers, M.D. | Cell: 718-614-5727
A Dose Finding Phase 1 of Sarilumab plus Capecitabine in HER2/neu-Negative Metastatic Breast Cancer and a Single-arm, Historically-controlled Phase 2 Study of Sarilumab plus Capecitabine in Stage I-III Triple Negative Breast Cancer with High-Risk Residual Disease
Patients with locally advanced TNBC are at high risk of developing lethal metastatic disease within 2 years of diagnosis, especially for those without a pathologic complete response (pCR) after neoadjuvant chemotherapy. This study will advance a novel and potent strategy to eliminate minimal residual disease (MRD) in triple negative breast cancer (TNBC) present even after multimodal treatment, thereby improving survival and increasing cure rate in this aggressive cancer.
Principal Investigator: Karen Daily, D.O. | Cell: 352-222-1423
This disease-agnostic, Phase 2 trial tests the PARP inhibitor Talazoparib (a highly selective and potent inhibitor that also provides significant PARP trapping activity) in advanced stage cancers with mutations to DNA damage response genes. Blocking the PARP protein abrogates a major DNA repair pathway, resulting in ineffective DNA repair mechanisms and encouraging apoptosis in tumor cells. Patients with advanced solid tumors may be eligible with any of the following germline or somatic dDDR mutations: BRCA1/2 (including those previously treated with a different PARPi), ARID1A, ATM, ATR, BACH1 (BRIP1), BAP1, BARD1, CDK12, CHK1, CHK2, IDH1, IDH2, MRE11A, NBN, PALB2, RAD50, RAD51, RAD51B, RAD51C, RAD51D, and RAD54L, as well as loss of function in any of the Fanconi anemia genes (FANCA, FANCB, FANCC, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM, FANCN).
Principal Investigator: Thomas George, M.D. | Cell: 352-339-6672