Last reviewed by Dr. Dharmender Malik on 13 May 2026 · this article reflects the published evidence and current clinical practice at FMRI Gurugram.
Introduction
Prostate cancer is the most commonly diagnosed cancer in men globally and a leading cause of cancer mortality in men. In India, the incidence is rising as life expectancy increases and as PSA testing becomes more accessible, but the disease is often diagnosed at a later stage than in countries with established screening programmes. Across all stages, outcomes for prostate cancer are heavily influenced by how early the disease is detected, how accurately it is staged, and how appropriately it is matched to the right treatment pathway.
This guide is a clinically grounded, patient-focused look at prostate cancer — covering the disease's biology, risk factors, screening, staging, treatment by stage, the management of advanced and metastatic disease, and the increasingly important role of nuclear medicine theranostics. It is written for patients and their families who want a clear picture, and for referring physicians who want a current overview.
Anatomy, function, and the disease
The prostate is a walnut-sized gland that sits below the bladder, surrounding the upper part of the urethra. It produces fluid that contributes to semen and is regulated by androgen hormones — primarily testosterone, which is converted within the prostate to the more potent dihydrotestosterone. Prostate cancer arises when cells within the gland (most commonly in the peripheral zone) acquire genetic changes that drive uncontrolled growth.
The vast majority of prostate cancers are adenocarcinomas. They typically grow slowly, particularly in their early stages, which is why many men are diagnosed with localised disease that has not yet spread. A smaller proportion of cases are aggressive at presentation and behave very differently — these tend to be high-grade adenocarcinomas or, rarely, neuroendocrine differentiation of prostate cancer, which has a much more aggressive clinical course.
Risk factors and prevention
The strongest non-modifiable risk factors for prostate cancer are age (incidence rises steeply after 50), family history (particularly a first-degree relative diagnosed before 65), and inherited genetic variants (BRCA1, BRCA2, HOXB13, and Lynch syndrome genes). Men of African descent have higher incidence and tend to present with more aggressive disease; the pattern in South Asian populations is intermediate but increasing.
Modifiable risk factors are less clearly established than they are for some other cancers, but a Mediterranean-style diet, regular physical activity, maintaining a healthy weight, and not smoking are all associated with lower prostate cancer mortality. There is no single supplement or dietary intervention with proven prevention benefit. For men with a strong family history or known genetic predisposition, earlier screening (from age 40 or 45) is recommended, often with PSA monitoring and, where appropriate, genetic counselling.
Screening: PSA and the digital rectal examination
Screening for prostate cancer uses two main tools: the prostate-specific antigen (PSA) blood test and the digital rectal examination (DRE). PSA is a protein produced by the prostate; elevated levels can indicate cancer but can also reflect benign prostatic enlargement, prostatitis, or recent activity (cycling, ejaculation, urological procedures). PSA is therefore not a perfectly specific test — it is a starting point for further investigation, not a definitive cancer diagnosis on its own.
Current screening recommendations vary internationally. In broad terms: men at average risk are typically offered baseline PSA testing from age 50, with the frequency and interpretation tailored to their baseline value and clinical context. Men at higher risk (family history, genetic predisposition, African descent) are offered earlier screening, often from age 40 to 45. An abnormal PSA or DRE triggers further evaluation — typically a multiparametric MRI of the prostate, with targeted biopsy if a suspicious lesion is identified.
Staging: how the disease is mapped
Once prostate cancer is diagnosed by biopsy, staging determines how much disease is present and where. Standard staging includes: a Gleason score (now reported as ISUP grade groups 1 to 5, reflecting the aggressiveness of the cancer cells); a tumour, node, and metastasis (TNM) assessment based on imaging; and a calculation of overall risk category (low, intermediate, high, very high risk; or, for metastatic disease, hormone-sensitive vs castration-resistant).
Imaging is increasingly anchored by Ga-68 PSMA PET-CT. Compared with conventional bone scan and CT, PSMA PET-CT detects metastases earlier and more accurately, and has substantially changed initial staging decisions for many intermediate- and high-risk patients. MRI of the prostate remains the standard for assessing local disease extension. The combination of PSMA PET-CT plus MRI now constitutes contemporary best-practice imaging for prostate cancer staging.
Treatment by stage: a brief map
Low-risk localised disease often qualifies for active surveillance — regular PSA, imaging, and biopsy without immediate treatment. Many men can avoid treatment for years or indefinitely. Intermediate-risk localised disease is typically treated with radical prostatectomy or with radiotherapy (external beam, brachytherapy, or both). High-risk localised disease is treated with combined-modality therapy: surgery or radiation, often with androgen deprivation therapy (ADT).
Metastatic hormone-sensitive prostate cancer is treated with ADT combined with either chemotherapy (docetaxel), a novel hormonal agent (abiraterone, enzalutamide, apalutamide, or darolutamide), or both, depending on disease burden and clinical context. When the disease progresses despite castrate testosterone levels — castration-resistant prostate cancer (CRPC) — the next-line options include further novel hormonal agents, chemotherapy, Lu-177 PSMA therapy, Ra-223 (for bone-predominant disease), and PARP inhibitors for patients with specific genetic mutations.
Advanced disease: where theranostics fits
For metastatic castration-resistant prostate cancer (mCRPC) that has progressed on prior treatment, Lu-177 PSMA radioligand therapy is now an established option backed by the VISION randomised phase III trial. Patient selection depends on a Ga-68 PSMA PET-CT confirming adequate PSMA expression — the same scan that often identified the metastases in the first place. For patients whose disease progresses on Lu-177, Ac-225 PSMA (an alpha-emitter version of the same therapy) is available as a salvage option under the Helsinki Declaration framework with written informed consent.
The role of theranostics in earlier disease stages is a major focus of ongoing research. Trials are evaluating Lu-PSMA in earlier-line mCRPC, in hormone-sensitive metastatic disease, and even in high-risk localised disease in combination with other modalities. The principle that the scan and the therapy use the same biology is increasingly central to how advanced prostate cancer is managed.
Where to seek care
Prostate cancer care benefits from a multidisciplinary team approach — urology, medical oncology, radiation oncology, and nuclear medicine working together. For early-stage disease, the care is anchored by the urologist and radiation oncologist. For advanced and metastatic disease, the medical oncologist and nuclear medicine physician become central. At FMRI Gurugram, the nuclear medicine team contributes to staging (PSMA PET-CT), advanced therapy (Lu-PSMA, Ac-225 PSMA), and treatment monitoring (response assessment scans).
If you have been newly diagnosed with prostate cancer, the most useful steps are: obtain a copy of your biopsy report (Gleason score / ISUP grade group), arrange a PSMA PET-CT for accurate staging if you have intermediate-or-higher-risk disease, and ensure your case is reviewed by a multidisciplinary tumour board. Decisions made with this complete picture are very different from decisions made with PSA alone.
For patients & referring clinicians
Frequently asked questions
Q01
What are the early signs of prostate cancer?
Most early-stage prostate cancer has no symptoms — which is why screening matters. When symptoms do occur, they may include urinary frequency or urgency, weak stream, getting up at night to urinate, blood in urine or semen, erectile difficulty, or pelvic discomfort. These symptoms are not specific to cancer — they overlap with benign prostatic enlargement and prostatitis — so any persistent urinary change warrants evaluation, but is not in itself a cancer diagnosis.
Q02
What is the PSMA PET-CT and why is it important?
A PSMA PET-CT is a nuclear medicine scan that uses a small radioactive tracer (typically Ga-68 or F-18 labelled to a PSMA-binding molecule) to map prostate-specific membrane antigen expression across the body. Because PSMA is expressed at very high levels on prostate cancer cells, the scan can identify cancer deposits with sensitivity and specificity that far exceed the older bone scan + CT approach. It is now the standard staging tool for intermediate- and high-risk prostate cancer and is required for eligibility for Lu-PSMA therapy.
Q03
What is the difference between hormone-sensitive and castration-resistant prostate cancer?
Hormone-sensitive prostate cancer responds to therapies that reduce testosterone (androgen deprivation therapy). Castration-resistant prostate cancer is disease that has progressed despite testosterone being suppressed to castrate levels. The two stages are biologically and clinically distinct, and the treatment options differ — including Lu-PSMA radioligand therapy, which is approved for metastatic castration-resistant disease after prior taxane chemotherapy.
Q04
Is prostate cancer curable?
Localised prostate cancer is often curable with surgery, radiotherapy, or in some low-risk cases simply with active surveillance and no treatment. Locally advanced disease is curable in many cases with combined-modality therapy. Metastatic prostate cancer is generally not curable in the conventional sense but is often controllable for many years with a sequence of therapies. The realistic conversation about cure versus long-term control depends on the stage at diagnosis and the cancer's biology.
Q05
Who should be screened for prostate cancer?
Men at average risk are typically offered baseline PSA from age 50, with frequency tailored to the baseline value and clinical context. Men at higher risk — family history of prostate cancer (especially first-degree relatives diagnosed before 65), known BRCA1/BRCA2 mutations, Lynch syndrome, or African descent — are typically offered earlier screening, from age 40 to 45. Screening is a conversation with informed consent, not an unconditional recommendation, because PSA testing has both benefits and limitations.
Q06
What is Lu-PSMA therapy and who is it for?
Lu-PSMA therapy is a radioligand treatment in which Lutetium-177 is attached to a small molecule that binds to prostate-specific membrane antigen. The therapy is delivered as an infusion (typically four to six cycles) and is currently approved for metastatic castration-resistant prostate cancer that has progressed on prior taxane chemotherapy. Eligibility requires a recent PSMA PET-CT showing adequate uptake on the cancer deposits.
Q07
How is care for advanced prostate cancer organised?
Advanced prostate cancer care is best managed by a multidisciplinary team that includes a medical oncologist, a radiation oncologist, a urologist, and a nuclear medicine physician. Decisions about the sequence of therapies — novel hormonal agents, chemotherapy, Lu-PSMA, Ra-223, PARP inhibitors — are made in tumour-board review and tailored to the individual's disease pattern, prior treatments, and overall fitness. At FMRI Gurugram, this multidisciplinary review is the standard of care for advanced prostate cancer.
Citations & references
Mottet N, Cornford P, van den Bergh RCN, et al. EAU-EANM-ESTRO-ESUR-SIOG Guidelines on Prostate Cancer.
European Urology. Continuously updated.
ReferenceSartor O, de Bono J, Chi KN, et al. Lutetium-177–PSMA-617 for Metastatic Castration-Resistant Prostate Cancer.
N Engl J Med. 2021;385(12):1091-1103.
Reference
About the Author
Dr. Ishita B. Sen
MBBS · MD (Nuclear Medicine) · DNB · Post-doctoral Fellowship, Memorial Sloan Kettering Cancer Center, New York
Director and Chief of Nuclear Medicine at Fortis Memorial Research Institute. Co-founder of Theranostic Physicians Private Limited (TPPL). Two decades of clinical practice in PSMA imaging and PSMA-directed radioligand therapy, with one of the largest Indian institutional experiences in Lu-PSMA.