Prostate cancer is a common cancer affecting men globally, often developing slowly over many years. Among its various forms, “castration-sensitive prostate cancer” (CSPC) represents a stage where the cancer’s growth remains responsive to treatments that reduce male hormone levels. This responsiveness to hormone-based therapies is central to its management.
What Castration-Sensitive Prostate Cancer Means
Castration-sensitive prostate cancer (CSPC) refers to prostate cancer that still relies on androgens, male hormones like testosterone, for its growth. Androgens stimulate prostate cancer cells, promoting their proliferation and survival. These hormones are primarily produced in the testes, though the adrenal glands also contribute smaller amounts.
Treatments for CSPC aim to lower androgen levels, effectively “starving” the cancer cells of the fuel they need to thrive. This approach is known as androgen deprivation therapy (ADT). The term “castration” in this context refers to the reduction of androgen levels to levels typically seen after surgical removal of the testes. CSPC is distinct from castration-resistant prostate cancer (CRPC), where the cancer has evolved to grow even when androgen levels are very low.
Identifying the Disease
Identifying prostate cancer, especially determining if it is castration-sensitive and its extent, involves several diagnostic procedures. A Prostate-Specific Antigen (PSA) blood test is often an initial step, measuring a protein produced by prostate cells; elevated PSA levels can suggest prostate cancer. A digital rectal exam (DRE), where a doctor manually checks the prostate for abnormalities, may also be performed.
If these initial tests suggest cancer, a prostate biopsy is performed to confirm the diagnosis. During a biopsy, small tissue samples are taken from the prostate and examined under a microscope to identify cancer cells and determine their aggressiveness. Once cancer is confirmed, imaging scans are used to assess if the cancer has spread beyond the prostate, a process known as metastasis. Common imaging techniques include bone scans to check for spread to bones, and CT or MRI scans to examine soft tissues and lymph nodes. PET scans, often using PSMA-targeted tracers, can also be employed to detect metastatic disease with high sensitivity.
Primary Treatment Strategies
Androgen Deprivation Therapy (ADT) is the primary treatment for castration-sensitive prostate cancer. ADT works by reducing testosterone levels, the primary male hormone, which fuels the growth of prostate cancer cells. This can be achieved through medical or surgical methods. Medical castration typically involves luteinizing hormone-releasing hormone (LHRH) agonists or antagonists. These injections prevent the testes from producing testosterone. LHRH agonists, such as leuprolide or goserelin, initially cause a temporary testosterone surge before suppression, while LHRH antagonists, like degarelix, reduce testosterone levels more quickly without an initial surge.
Surgical castration, known as orchiectomy, involves the permanent removal of the testes, an effective and immediate way to eliminate the primary source of testosterone and achieve androgen deprivation. While ADT is the main treatment, other therapies may be used in combination for patients with more aggressive or high-volume metastatic CSPC. Chemotherapy, often with docetaxel, can be added to ADT to improve outcomes in some cases. Newer generation hormone therapies, such as abiraterone acetate or enzalutamide, which target androgen production or signaling pathways more broadly, may also be combined with ADT. Radiation therapy can also be considered for specific areas of disease, particularly in the prostate itself or for symptomatic metastatic sites.
Managing the Disease and What to Expect
Managing castration-sensitive prostate cancer involves ongoing monitoring to track the effectiveness of treatment and detect any changes in the disease. Regular Prostate-Specific Antigen (PSA) blood tests are a primary method for this, as declining PSA levels indicate a positive response to androgen deprivation therapy (ADT). The frequency of these tests is determined by the patient’s specific treatment plan and response.
While ADT is initially effective in controlling CSPC, the cancer may eventually evolve to grow independently of low androgen levels, leading to castration-resistant prostate cancer (CRPC). This progression typically occurs after several months to a few years of ADT. Managing potential ADT side effects, such as hot flashes, fatigue, decreased bone density, and sexual dysfunction, is also an important aspect of care. Despite potential progression, CSPC is treatable, and many individuals can effectively manage the disease for an extended period with appropriate therapy and monitoring.