Prostate cancer used to be treated almost automatically, but now doctors have to make much more complicated decisions, weighing the biology of the tumour, the patient’s life expectancy, and their quality of life against a growing number of high-tech tools.
A common type of cancer that doesn’t always act the same way
In many Western countries, prostate cancer is the most common type of cancer in men, but it often hides in plain sight. Most of the time, cases grow slowly and don’t cause problems. A smaller but important part of it becomes aggressive, spreads beyond the prostate, and becomes life-threatening.
This split personality makes it very hard to make decisions about testing and treatment. The prostate, a small gland under the bladder, can hold small tumours for years without causing clear urinary problems. When warning signs do show up, like needing to pee a lot at night, bone pain, or unexplained tiredness, the disease is sometimes already advanced.
For a long time, the standard tests were a digital rectal exam and a blood test for prostate-specific antigen (PSA). Both are still used a lot, but neither is very precise. Infection or benign enlargement can raise PSA levels, and some dangerous cancers don’t make much PSA at all.
Doctors are moving toward smarter, risk-based strategies because mass screening of all men with PSA has not cut deaths enough to make the risk of overdiagnosis and overtreatment worth it.
That change is at the heart of what many cancer doctors now call a “quiet revolution” in how prostate cancer is treated.
Screening that is specific instead of general
The time of “one-size-fits-all” screening is coming to an end. In 2025, experts will increasingly say that who gets tested and when is just as important as the test itself.
In many centers, PSA is now used as a first filter, but not as the last word. Doctors now routinely order a multiparametric MRI before reaching for biopsy needles when PSA levels rise or the physical exam seems suspicious.
MRI first means fewer unnecessary biopsies, better mapping of areas that look suspicious, and a clearer idea of which tumours are really dangerous.
Who is most likely to get something good out of screening?
Guidelines are slowly coming together on a more selective method:
Men between the ages of 50 and 74 who are expected to live more than 10 years
Men aged 45 and older with a significant familial history of prostate or breast cancer.
Men with genetic mutations that put them at high risk, like BRCA1 or BRCA2
There is a reason for the focus on life expectancy. Finding a small, slow-growing tumour in a man in his late 70s who already has other serious health problems could put him at risk for side effects with little chance of survival benefit.
At the same time, new blood tests like the Prostate Health Index (PHI) and 4Kscore are being used to make risk estimates more accurate. Researchers are also testing “liquid biopsies,” which look for bits of tumour DNA that are floating around in the blood.
A well-organised, risk-adjusted screening program was linked to about a 13% drop in prostate cancer deaths over 23 years in a long-term study that came out in 2025. The gain is small but real, and it is making health systems think about structured, data-driven screening instead of doing nothing or testing everyone.
Treatment is becoming less automatic and more planned.
When cancer was confirmed, the usual thing to do was to either take out the prostate or hit it hard with radiation in almost every case. That way of thinking is changing quickly.
Surgery, radiation therapy, and hormone therapy are still the main ways to treat the disease. What is new is that doctors are becoming more sure of themselves and are less likely to act when the risk is low.
Active surveillance instead of treatment right away
Many centers now recommend active surveillance for men with low-risk, localised disease, which means small tumours, low PSA levels, and biopsies that show no signs of cancer. That means keeping a close eye on things with repeated PSA tests, scans, and biopsies, and only switching to curative treatment if the tumour clearly shows signs of progression.
Active surveillance seeks to prevent incontinence and sexual dysfunction in men while keeping the option of curative treatment available should the cancer recur.
The playbook is different for local disease that is intermediate or high risk. Radiotherapy combined with hormone therapy is still the main treatment, but newer hormone-blocking drugs like enzalutamide are being used in very specific cases.
So far, trials have shown that adding enzalutamide to radio-hormone therapy for all high-risk cases may not always work. The balance shifts in its favour for patients whose PSA levels rise quickly after treatment, even if scans don’t show any metastases yet. In the US, regulators have already approved this use in some high-risk relapse situations.
Throughout, doctors are more openly weighing the possible benefits of survival against the side effects. Some people may not want to trade in an extra drug that adds years on paper but makes them tired, stops them from having sex, and makes them have hot flashes or mood swings.
Imaging that can see cancer move, almost in real time
One of the most amazing things that has happened in the last few years is not a drug at all, but a new way of seeing.
A new generation of nuclear imaging, such as whole-body SPECT scans, is starting to find micro-metastases in bone and other tissues that older scans miss. The method makes 3D pictures of tumour activity and can be done again to see how those tiny deposits react to treatment.
Whole-body SPECT changes a still picture into a time-lapse movie of how metastatic disease acts.
For men with advanced or metastatic prostate cancer, this level of detail can push doctors to start more focused radiation therapy or change systemic treatment sooner than they would have otherwise. It also helps scientists do more accurate research by letting them see how different drug combinations affect different groups of metastases.
New biological targets that could change how we care for people in the future
Researchers are working hard in the background to figure out why some prostate cancers don’t respond to hormone therapy and keep growing even after aggressive treatment.
The TRβ pathway: hormones other than testosterone
One area of research is centred on the thyroid hormone receptor called TRβ. In preclinical models, this receptor functions as a tumour suppressor by inhibiting cell division and enhancing the sensitivity of cancer cells to both anti-androgen therapies and radiation.
Researchers are testing experimental drugs that turn on TRβ, usually with other drugs like enzalutamide. The goal is to make resistant tumours sensitive again or stop resistance from happening in the first place.
The cutting edge of gene editing and CRISPR
At least in the lab, CRISPR-Cas9 gene editing is starting to have an effect. Researchers have found proteins that act as important “helpers” for the androgen receptor, which is what most prostate cancers are based on, using CRISPR screening.
One of these helpers, PTGES3, looks like it is very important for turning on the androgen receptor. It seems that knocking it out in cell models makes cancer cells much more likely to respond to hormone therapy. Early research shows that changing these pathways might also make radiotherapy work better.
It’s not likely that CRISPR will be injected directly into patients anytime soon, but it’s already finding new weak spots in prostate tumours that drugs could use.
Parallel strategies are aimed at fixing DNA repair problems, especially in men whose tumours have BRCA or ATM mutations. Combining standard treatments with targeted drugs that stop tumour DNA repair is becoming a major area of research.
Precision medicine is going from a catchphrase to a common practice.
More and more, oncologists are using the plural form of “prostate cancer.” The same label can hide very different genetic backgrounds.
Many teams now send tumour samples, and sometimes blood, for genomic sequencing when the disease is advanced or resistant. They look for changes in genes like BRCA1, BRCA2, and other repair pathways that are called HRR or HRD.
| Profile | Typical finding | Potential treatment angle |
|---|---|---|
| DNA repair‑deficient tumour | BRCA1/2 or related mutation | PARP inhibitors plus hormone therapy |
| Hormone‑resistant tumour | Altered androgen receptor pathway | Next‑generation anti‑androgens, TRβ research drugs |
| Heavily pre‑treated metastatic disease | Complex mutation pattern | Clinical trials combining targeted agents and radiotherapy |
PARP inhibitors like olaparib, talazoparib, and niraparib, which are already used to treat breast and ovarian cancers, are now being used in this area. Some studies show that they can help some men with advanced prostate cancer, especially those with DNA repair mutations, after standard hormone therapy has failed.
However, access is not equal. Genomic testing that is very accurate, coordination between urologists, oncologists, and radiologists, and specialised centers are all needed for these drugs. A lot of health systems are still behind.
Things that patients and their families should remember
The fast pace of change can be too much to handle, especially for men who have just been diagnosed with prostate cancer. There are a few useful things to keep in mind when talking to doctors.
Some prostate cancers don’t need to be treated right away; others are better off being watched closely.
It can be helpful to ask if an MRI has been done before a biopsy.
If you have advanced disease, asking about genetic testing may lead to trials or drugs that work for you.
Quality of life, including urinary function, sexual health, and fatigue, should be part of every treatment discussion.
For a lot of men, this is what a realistic scenario looks like: a high PSA leads to an MRI and targeted biopsies. The cancer turns out to be low risk, and the team suggests active surveillance. Years may go by with regular checks and no action. There is still a chance of curative treatment if the disease gets worse.
Some people may have a more aggressive type that needs a mix of surgery, radiation, and hormone therapy. In that case, new imaging, new hormone agents, and more and more molecular profiling offer more ways to customise than were available ten years ago.
We should clarify a few terms. “Biochemical recurrence” means that the PSA level goes up after treatment, even if scans show no signs of cancer. This means that cancer is still active at a very small level. “Metastatic” means that the disease has spread from the prostate to other parts of the body, like bones or organs. “Surveillance” is not “doing nothing.” It is planned, structured monitoring with clear reasons to act.
As research goes on, combinations will be more important than single breakthroughs. Drugs that change hormone pathways, agents that damage DNA repair, precision radiotherapy guided by whole-body scans, and maybe vaccines or metabolic treatments may work best together. The goal is not only to extend life, but also to keep men active, independent, and informed while living with a disease that is slowly being understood from the inside out.
