I started this Blog after being diagnosed with Prostate Cancer in 2010. I thought I was going to die! It was a way of keeping family and friends informed but then became a campaigning tool, helping to make improvements in hospitals nationally. 11 years on, after successful surgery, my PSA is still undetectable. I'm not continuing to Blog about prostate cancer, I'm hoping to leave it in the past, but this blog contains a great archive of information.
My new e-book will be published later this year. First, I would like to put it out to my wider family (only) for comment, recommendation etc. If you would like access please let me know.... http://35finchingfieldway.blogspot.com/?zx=b204b65de107cb4
If your father or/and brother/s have had prostate cancer, and you're wondering what your risks are, and what you should do now to help yourself, then read on from this recent study in the USA...
Hereditary Prostate Cancer
In 1992, William Isaacs and other researchers at the Brady Urological Institute were the first to establish an undeniable link between a family history of prostate cancer and a man's risk of developing the disease, and to characterize the distinct phenomenon of Hereditary Prostate Cancer (HPC). We proved that prostate cancer, like other cancers, can be inherited - a fact once widely doubted.
Since that time we have assembled one of the largest collections of families with hereditary prostate cancer and have characterized a number of chromosomal sites where the genes responsible may be located. In 2012, in collaboration with investigators from the University of Michigan, we identified the first mutation responsible for hereditary prostate cancer in families – HOXB13. We are continuing to pursue other genes that may turn out to be informative and are anxious to enroll families with multiple affected members.
An estimated 250,000 American men may carry one of these defective genes; in these men, the odds of developing prostate cancer are extremely high. Having identified this mutation we have have a powerful tool to spot cancer early in men who have inherited this potentially lethal mutation. Also, discovering how this mutated gene triggers the cascade of prostate cancer may help us find new ways of preventing or treating the disease in all men. Although only about 10 percent of all cases of prostate cancer are thought to be purely hereditary, we believe that the defective gene or mechanisms involved in HPC are the same ones that somehow go askew in "sporadic" cancer (disease that just develops over the course of a lifetime - the kind most men get.) Here, as well, we have a one-of-a-kind resource - our pool of 2,500 families with HPC whose DNA may help us crack the genetic code of prostate cancer.
Hereditary Prostate Cancer Study
The Johns Hopkins Department of Urology is actively recruiting families with familial prostate cancer and benign prostate enlargement in an effort to identify genetic determinants of these diseases. Clinical information of interest to physicians and patients is also included below.
The importance of asking about a family history of prostate cancer The Department of Urology strongly encourages clinicians to take a family history of prostate cancer from each adult patient, as a positive family history markedly increases the risk of prostate cancer in first degree male relatives. For example, a patient with a father or brother with prostate cancer has two times the usual risk of developing prostate cancer. A man with both his father and brother affected with prostate cancer has almost a 50% chance of developing the disease. In addition, in such families prostate cancer occurs at an earlier age. At this time, our recommendation is that men with more than one first degree relative affected (father or brother) should be encouraged to undergo yearly digital rectal exam and yearly serum prostate specific antigen (PSA) beginning at age 40.
Thousands of men could be delayed or denied life-saving new
drugs under plans to cap spending by NHS England, prompting
"serious concern" and an online petition from leading health
and care charities.
Prostate Cancer UK has joined 10 other health and care charities* in calling for NHS England to urgently rethink plans for a new spending cap on treatments, which could see the next generation of life-saving prostate cancer drugs delayed indefinitely from reaching the men who need them.
We're urging everyone to ask NHS England and the National Institute for Health and Care Excellence (NICE) to reconsider their proposed 'budget impact threshold', which gives the option to postpone any new treatments that would cost more than £20 million in any of the first three years.
Proposals could devastate men with advanced prostate cancer
The restrictions would have meant the breakthrough drugs for advanced prostate cancer, enzalutamide and abriaterone, would have been delayed by negotiations with the manufacturers over costs for many years, arriving in NHS hospitals too late for the thousands of men whose lives they have extended.
"Abiraterone has without question given me several extra years," says Alan Oliver (pictured above with his wife and grandchild), who started taking the hormone therapy drug in 2014.
"It has allowed me to enjoy my four grandchildren, three of whom are now in school, and I just couldn't put a price on this.
"It scares me that if this so-called cost cap comes in then in the future drugs, like abiraterone, would not get through the threshold, and people like me could potentially have the chance of precious time with loved ones held just out of reach."
1-in-5 new treatments could be delayed by cap
These vital 'end-of-life' drugs used by men like Alan already face a stringent and lengthy licensing and approval process, which the government is currently looking to expedite through its Accelerated Access Review and reforms to the Cancer Drugs Fund.
The proposed spending cap would add yet another layer of unnecessary bureaucracy and could stall up to 1-in-5 new treatments currently under review.
"Although we recognise the significant financial challenges facing the NHS, this arbitrary limit is not the solution and we're seriously concerned for the treatments of the future," says Angela Culhane, CEO of Prostate Cancer UK.
"NHS England and NICE need to hear this is unacceptable for patients and come up with a proposal that makes sure patients get the drugs and treatments they need, when they need them."
Bloody marvelous! I was 17, my relationship with my parents had always been very 'different' to that of my friends, their mums and dads seeming fairly normal; like you'd see on Coronation Street! This was my chance of a fresh start, I'd have a mother who'd hug me, a father who'd call me Daniel, not 'bastard' or 'imbecile'; maybe even some brothers and sisters I liked!
I'd been trying to trace my family tree on the Belgian side for years, but had found most had died during the war. That was apart from one distant Aunt, Lucienne who lived in Brussels, aged over 90 at the time, but we exchanged a few letters. She wrote in French and I replied in English, so I guess as much a struggle for her as it was for me. One day, I opened her latest letter, and there it was... "This is a photo of your mother and father's wedding"! The photo showed a young man in a sailor uniform, obviously my father, and a smartly dressed and beautiful woman, but hey, hang on, that wasn't even vaguely like my mother! Instant conclusion...I had to be adopted! Hallelujah! I could escape! It fulfilled a dream, why question it! For about a month I made all sorts of plans as to what I'd say to my new, real mother when I met her. How I'd forgive her and tell her all about my horrible life since she gave me away. How she'd hug me, crying, and say how sorry she was (must have seen that on TV). Did I have half brothers and sisters? They couldn't be worse than the ones I had, surely! The name of the woman (bride) was mentioned in the letter, Molly Cohen, now I could start my search.
First the London telephone directories at my local post office, and in book form there were dozens (no digital search then)! Cohen was a fairly common name, so starting at the beginning, I phoned every one; about a weeks wages. But, half way through... Bingo! I found her! But all was not to end well. She told me that she had know my father once, but would be grateful if I'd never contact her again, putting the phone down on me. I was shattered, my own mother didn't want to know me. There was little I could do at the time, and it took years for it all to slowly work further back in my mind.
It wasn't until later in life that I was contacted by a woman of similar age to me, Cynthia Rose Kovar, who explained that she was the daughter of Molly and Norbert (my dad) Sencier. We shared the same father, who was now sadly dead, and Cynthia had never met him since she was a baby. She had so many questions. She was under the impression that our father had moved to South Africa, yet all her life he had been no more than an hours drive away. I tried to reassure her, that even though he was a hard working and decent man, she hadn't missed out on the, 'ideal father' relationship that she'd probably imagined. He'd been severely damaged by the war years, was very reclusive and had spent very little time with us as children. He was also agoraphobic, staying in his room reading books, only going out to work when darkness fell. We used to think he might even be a vampire! (TV again)
She had taken the name of Dr. Ilya Kovar, who she'd married, but had then changed back to become Cynthia Rose Sencier, my little half sister. So the photo in the wedding picture was my father's first wife, Molly Cohen, a jewish girl who he'd married several years before meeting my mother, Ellen Patricia Laffan. Cynthia and I met several times in the years after that, most memorably for the first time in York Minster, after she had travelled north from London, and I south from Edinburgh. We spent the day talking about our lives, our parents and our families. I met her lovely children and she met some of mine. She was less than 5 foot tall but 2 years older than me, and as I was over 6 foot tall, she used the age factor to call me her, 'little brother'. 6 years ago, I told her I had cancer, and she disappeared in the same breath! I've never been able to make contact since, and often wonder what happened in her mind to destroy a relationship that seemed to be going so well. Since then, her mother has died and so has mine! Wherever you are Cynthia Rose Sencier, know that I still love you, 'big Sis'. I'm in Bangkok now, doing well, still in remission, hoping that you are doing well too.
"PSA testing is not worth it because it only saves 1 in 1000 men!"
Well I'm one of those 1 in a 1,000! I'm happy the other 999 escaped, but let me tell you, it feels pretty good to be alive.
A very good article from Healthline, who I have every respect for, BUT even they miss out this crucial fact, and one that saved my life.........
It's not how high your PSA is that gives the biggest clue as to you possibly having Prostate Cancer. It's the change of growth over time. Example: If you go to the doctor and have a PSA test resulting in a 1.9, that's within normal limits. If you have a test a year later which is 4.5, so is that.
BUT ALARM BELLS SHOULD RING! Your PSA has doubled in just a year! As mine had! You need to see a specialist and fast!
Now if your PSA had been 12.5 and the following year 12.7, both outside the limits, your probably OK.
So read this, BUT remember the above.
They look like glowing jade necklaces of such unearthly brilliance they could be a Ming emperor’s. But if Dr. Gerardo Fernandez is right, the green fluorescent images of prostate cells could be even more valuable, at least to the thousands of men every year who unnecessarily undergo aggressive treatment for prostate cancer.
That’s because the glimmering images promise to show which prostate cancers are destined to remain harmless for the rest of a man’s life, and thus might spare many patients treatment that can cause impotence and incontinence.
There’s now no reliable way to tell a lethal prostate cancer from one that’s so slow-growing it can safely be left alone: the prostate specific antigen (PSA) test can’t, and neither can looking at the cancer cells under a microscope. Butresearchers are developing genetic tests, imaging tests, and algorithms like those in face-recognition software in an effort to reduce the 1 million US men a year who have prostate biopsies and, even more important, reduce the thousands who get treatment they don’t need.
“The field is on fire,” said Dr. Laurence Klotz, of Sunnybrook Health Sciences Center in Toronto, whose research has shown that many men diagnosed with prostate cancer can safely choose active surveillance — monitoring to make sure their cancer isn’t spreading —rather than treatment. “There are a whole slew of blood and urine tests already available or on the way that can take a guy whose PSA is mildly elevated and tell him he doesn’t need a biopsy. How much could we drive down overdiagnosis? A lot.”
But both sides agree on two things. First, too many men with an elevated PSA have a biopsy that turns up no cancer. That’s a biopsy — usually done by inserting a thin, 12-gauge needle through the rectum, which can cause infection and other harmful consequences — that could have been avoided. Second, too many men are needlessly treated for a cancer.
“This has been a long and chronic problem, in that we have very imperfect tools for cancer detection,” said Dr. Clare Tempany, a prostate cancer specialist at Brigham and Women’s Hospital in Boston. “Ever since PSA came into disrepute, everyone woke up and said, we have to be smarter about this.”
Already a number of beyond-PSA tools let more and more men opt out of biopsy after an elevated PSA reading, which many physicians consider 4 or higher. One-quarter to one-third of men with a PSA of 4 to 10 who have a biopsy will turn out to have cancer, and most of those are harmless.
For instance, a blood test called the Prostate Health Index measures several forms of PSA, not the one kind measured by the standard PSA test; it reduces unnecessary biopsies by about 36 percent, but it misses 2.5 percent of dangerous prostate cancers. The 4K Score, also based on a blood test, “is better than PSA at picking up aggressive cancers,” said urological surgeon Dr. David Penson of Vanderbilt-Ingram Cancer Center. It can reduce unnecessary biopsies by as much as 60 percent, but misses nearly 5 percent of serious cancers.
That has spurred researchers around the world to try to do better, with many labs developing advanced imaging as a way to reduce unnecessary prostate biopsies following an elevated PSA. One, called multiparametric MRI, can reveal the size and density of a prostate cancer, and how well-connected it is to the blood supply. Multiparametric MRI reduced unnecessary biopsies by 70 percent, Dutch researchers reported at a European urology meeting in March, but was as good as biopsy at not missing aggressive cancers.
Next week’s annual meeting of the American Urological Association will feature dozens of studies on advanced MRI. Although many confirm the results of the Dutch study, others are less encouraging. One, for instance, finds that advanced MRI missed the main cancer in 63 percent of cases. But other studies have found fewer misses and either larger or smaller reductions in unnecessary biopsies, leaving many physicians unsure whether to trust it.
“To do an MRI [rather than a biopsy] on the first pass” after an elevated PSA “is an area of active investigation,” Dr. Anthony D’Amico of Brigham and Women’s said diplomatically.
Physicians are therefore eagerly awaiting results from a large clinical trial of MRI called PRECISE. Led by Klotz and launched last year, it aims to test whether MRI is good enough at detecting dangerous cancers, and distinguishing them from harmless ones, to reduce the need for biopsies. From early data, Klotz estimates that it could “allow 250,000 men per year in the US and Canada to avoid unnecessary biopsies and the associated complications including hospitalization, without compromising our ability to identify clinically significant cancers.”
Besides being far from perfect, however, multiparametric MRI costs $1,000 to $2,000. That has made researchers investigate other kinds of imaging that, they hope, will be more precise and possibly cheaper. “There are promising indications that PET and other imaging might do better,” said D’Amico.
PET scans that detect prostate-specific membrane antigen (PSMA), a protein that is prevalent on prostate cancer cells but rare in healthy ones, has shown promise in predicting whether the cancer will spread; a prostate cancer that stays in that gland is almost never dangerous, let alone fatal. Studies are underway to identify which radioactive “markers” will best let PET scans detect PMSA.
“The issue is how precise the scans can be, but the hope is that aggressive cancer cells will take up the markers more than indolent cancer cells,” said Dr. Jeffrey Karnes, a prostate cancer specialist at the Mayo Clinic.
No genetic tests on the market have been shown to identify which men with a high PSA can skip biopsy, but one that Dr. Brian Helfand of NorthShore University HealthSystem and his colleagues are developing — based on more than 100 DNA variants — is showing promise. It seems to pick out the one-third of patients who are most likely to have aggressive prostate cancer, meaning other men can opt out of biopsy.
One 64-year-old patient had a PSA of 4.6, considered the low end of elevated and one that leads many physicians to recommend biopsy, but a genetic risk score 40 percent below the average, Helfand said: “Other urologists he saw were advocating a repeat biopsy, but I recommended we hold off,” which the man did.
At the AUA meeting, European researchers will describe a combination of six biomarkers — proteins in the blood — that reduced unneeded prostate biopsies in men with PSAs of 2 to 10. Of 474 men in the study, 141 of 236 negative biopsies could have been avoided, the researchers will report, which is “significantly more accurate than [PSA] alone in determining the absence of prostate cancer.” The biomarker approach could halve the number of unnecessary prostate biopsies, they estimate.
The second problem both sides in the PSA wars want to solve is that too many men, after a biopsy suggests a dangerous prostate cancer, undergo treatment that they actually didn’t need (because the cancer was in fact harmless). Today’s system of analyzing biopsies can’t reliably tell threatening cancers from harmless ones.
Gleason scores, developed in the 1960s, classify prostate cells by their appearance.
Called the Gleason score, it is a 2-to-10 grading system developed in the 1960s based on a pathologist’s eyeballing the stained, biopsied cells. Those that are regularly shaped and not too packed are unlikely to be a significant cancer, and are graded 3 or lower. Those that are irregularly shaped, angular, elongated, and tightly packed are more likely to be a significant cancer. “A 3 has zero ability to metastasize and is not life-threatening, ever,” Klotz said. “But a 4 is aggressive.”
The challenge comes when a man has mostly 3 but some 4, which produces a score called 3 + 4. These are the men most likely to undergo surgery or radiation or both for a cancer that would never have harmed them.
One hope is that genetic tests can tell dangerous prostate cancers from harmless ones. At least three already in use test for the presence — in ground-up slurries of biopsied cells — of genes linked to aggressive, metastatic cancer.
They “can show if a patient in this gray zone [a score of 3 + 4] has a biologically less aggressive cancer than other men with that,” said urologist Dr. Stacy Loeb of NYU Langone Medical Center. “What to do with 3 + 4 is the most controversial call, so a genomic test can be a tiebreaker.” In a study she will present at the urology meeting, one of the tests, called Decipher, could change minds — assuring a man who was leaning toward treatment that he would be fine with active surveillance, and vice versa — about one-fifth of the time.
But the genetic tests are pricey, around $3,000 or $4,000, and not necessarily covered by insurance. More problematic, they do not give a yes/no answer to whether cancer cells are harmless. Instead, they indicate whether a man has a very low, low, intermediate, or high risk of harboring an aggressive, metastatic cancer.
“The problem is, genetic tests don’t necessarily shift the risk much,” said Mayo’s Karnes. “A man might have a 30 percent risk of an aggressive cancer, before a genetic test, and the test might shift that to 35 percent. What you want is a test that tells you the risk is more like 0 percent or 100 percent.”
Even short of perfection, however, genetic tests are offering men reassurance that they can choose active surveillance rather than treatment. Duane Foulkes, 70, recently sold the manufacturing business he founded near Madison, Wis., when, in late 2015, his PSA test came back over 5. It rose to above 9 three months later, and he had a biopsy at Mayo. His Gleason score of 6 “concerned me at first,” Foulkes said.
But a genetic test indicated that he had at most “a slow-growing, non-aggressive type of cancer,” Foulkes said, giving him confidence to choose active surveillance.
Fernandez’s jade necklaces might do even better. They are prostate cells whose telltale molecules have been tagged with a fluorescent marker that shows up in images of prostate cells taken under a robotic microscope. In the diagnostic system called Precise MD, Fernandez and his colleagues at Mount Sinai Hospital in New York have identified five molecules, including proteins produced by malignant cells but not healthy ones, that promise to tell harmful prostate cancer cells from benign ones.
The researchers started with about 10,000 features, Fernandez said, and then “used artificial intelligence [AI] to whittle that down to the 30 best.” To those 30 they added a couple dozen features that show up on imaging and 5 to 10 variables such as a man’s PSA level and age. “Then the AI goes through thousands of permutations and combinations to put together those that best predict the outcome,” he said, and the resulting algorithm calculates the likelihood of a harmful cancer.
Although Precise MD is still being tested, early results suggest it is significantly better at predicting aggressive cancer than Gleason scores. If more extensive testing confirms that, “we’ll be able to tell men, you’re a good candidate for active surveillance or not,” Fernandez said. “This can really alter the course of treatment.”
Does consuming milk increase the risk getting prostate cancer?
A great article from Healthline...
Research has shown that men who consume a lot of milk are more
likely to develop prostate cancer than men who don’t eat calcium-heavy
diets. An older study published in 1998 found evidence that men who
drank more than two glasses of milk a day were at higher risk of advanced
prostate cancer than men who did not consume that much milk. Whole milk
seems to cause the highest increase in risk, although studies have also found
a greater risk associated with low-fat milk.
Researchers have suggested the strong associations between milk
intake and prostate cancer could be due to milk’s fat, calcium, and
hormone levels. Other theories suggest the link could be caused by:
the negative impact high-calcium foods have on vitamin D balance
the increase in serum insulin-like growth factor I (IGF-I) concentrations caused by dairy
the effect of dairy on testosterone levels
Scientists have also looked at the impact of dairy on prostate cancer progression. According to a 2012 study, men with prostate cancer who drank whole milk had a greater risk of lethal prostate cancer. The researchers, though, did not find this association to be true of other dairy or milk products.
A newer study from 2016 looked at the impact of milk and dairy products on health and determined that the evidence of a correlation between prostate cancer and milk is inconclusive. More research is needed to confirm this relationship, but if you’re already at risk for prostate cancer, talk to your doctor about whether you may benefit from skipping milk.
Other dairy products
Studies on high calcium intake and prostate cancer seems to focus mostly on milk, but other dairy products have also been seen to increase risk. Those foods include ice cream and hard cheese, like American and cheddar cheeses. Research is scarce on how yogurt, cream, butter, and other dairy-based products affect prostate cancer risk.
What are other risk factors for prostate cancer?
There are five common risks factors for prostate cancer:
age
race and ethnicity
geography
family history
genetic changes
Age
A man’s risk of getting prostate cancer rises after age 50, with about 6 in 10 cases found in men over 65 years old.
Race and ethnicity
Prostate cancer happens more often in African-American and Afro-Caribbean men than men of other races. According to the American Cancer Society, black men are also more than twice as likely to die from prostate cancer than white men. Prostate cancer rates are lower in Asian and Hispanic men. Scientists don’t have a clear answer for these ethic and racial differences.
Geography
The highest rates of prostate cancer are seen in North America, northwestern Europe, Australia, and the Caribbean. The disease is less common in Africa, Asia, and Central and South America. Although the reasons are unclear, the American Cancer Society theorizes the gap in rates may exist due to differences in lifestyle and diet, and more intensive cancer screening.
Prostate cancer mortality rates around the world
Although incidence of prostate cancer is lower in Central and South America than in other areas, mortality rates are higher in those parts of the world than in other low-incidence countries.
Family history
Though most men who have prostate cancer do not have a family history of the disease, there may be an inherited or genetic factor for why prostate cancer runs in some families. Having a close relative, like a brother or father, with prostate cancer increases your risk for also developing the disease.
Gene changes
Prostate cancer can be caused by certain changes to DNA structure. These gene mutations can be hereditary or happen during a person’s lifetime. Lynch syndrome, as well as changes to the BRCA2 gene, can increase the risk of prostate cancer in men.
Additional factors
Some other factors have been loosely tied to an increase in prostate cancer risk:
Many studies have found a link between milk and prostate cancer rates, so if you can, it may be best to avoid milk or cut down on your intake. Studies are inconclusive, however, and more research is needed to better understand the link.
Survival rates for early-stage prostate cancer are high. According to the latest data available from American Cancer Society, the five-year survival rate for prostate cancer (relative to men without the disease) in the local or regional stage is 100 percent. The 5-year relative survival rate for advanced stage 4 cancer is only 28 percent, however. That’s why routine screenings are so important to treating prostate cancer. The earlier you’re able to catch the disease, the sooner you’re able to get treatment and go into remission.
Are there ways to reduce risk for prostate cancer?
You can’t eliminate your risk of getting prostate cancer, but you can lower it:
Change your diet. Add lots of fruits and vegetables to your daily meal plan.
Get active and stay fit. Go for walks, workout often, and maintain a healthy weight.
Screen regularly. Regular prostate screenings are important for prevention and early detection. By testing for the disease before you have symptoms, your doctor is more likely to catch prostate cancer in its early stages.
You may also consider eliminating dairy from your diet. Here are some dairy alternatives that you can incorporate into your diet if you want to cut down on your dairy intake:
Try rice, oat, soy, coconut, or almond milk to replace cow’s milk.
Try vegan cheese, yeast flakes, or crumbled tofu to replace dairy-based cheeses.
Choose soy-based yogurts and ice cream instead of products with cow’s milk.
Blood test may help create personalised treatments for advanced prostate cancer
A simple blood test could help doctors devise personalised treatments for men with advanced prostate cancer.
The new test, which costs less than £50, can predict which patients are likely to respond to new targeted drugs, and who might be better served by alternative therapies.
It looks for multiple copies of a gene for the androgen receptor, a hormone-sensitive molecule that helps many prostate cancers to grow.
Men with multiple copies of the gene were found to respond much less well to the drugs abiraterone and enzalutamide, both used to treat advanced prostate cancer.
The drugs are given to men whose cancer is no longer responding to traditional hormone therapy and has started to spread.
Lead researcher Dr Gerhardt Attard, from the Centre for Evolution and Cancer at The Institute of Cancer Research, London, said: " Abiraterone and enzalutamide are excellent treatments for advanced prostate cancer and some men can take these drugs for years without seeing a return of their cancer.
"But in other men, these drugs do not work well and the disease rapidly returns. Currently, there is no approved test to help doctors choose whether these are the best treatments for an individual.
"We have developed a robust test that can be used in the clinic to pick out which men with advanced prostate cancer are likely to respond to abiraterone and enzalutamide, and which men might need alternative treatments.
"Our method costs less than £50, is quick to provide results, and can be implemented in hospital laboratories across the NHS. We are now looking to assess our test in prospective clinical trials and would hope it can become part of standard patient care."
For the study, published in the journal Annals of Oncology, scientists took blood samples from patients taking part in three different clinical trials.
In the primary trial of 171 patients, men found to have multiple copies of the androgen receptor gene were four times more likely to die than those who had a negative test result.
Men with multiple copies of the gene from a second group of 94 patients responded to abiraterone and enzalutamide for an eight-fold shorter time than those with only one or two copies.
The androgen receptor was already known to play an important role in cancers becoming resistant to the two drugs.
Dr Iain Frame, director of research at Prostate Cancer UK, which part-funded the study, said: " To stop prostate cancer from being a killer, we need to move away from a one-size-fits-all approach to treatment.
"This test could be a significant step towards that and we'll be watching its development very closely."
Dr Emma Smith, from Cancer Research UK, which also contributed funding, said: " If further studies confirm this test is reliable, it could also help doctors choose better options for men whose prostate cancer is unlikely to respond to standard treatments."
Each year around 41,000 men in the UK are diagnosed with prostate cancer and 11,000 die from the disease.
Assay Shown to Help Detect Prostate Cancer Patients at Risk of Metastasis
An assay may help to determine those prostate cancer patients at risk of metastasis, a study reports. It works by identifying a molecular subgroup of primary prostate cancer to detect patients who might have metastatic recurrence following radical prostatectomy.
“An unbiased discovery approach was used to identify a molecular subtype of primary prostate cancer that demonstrated metastatic biology,” Richard Kennedy, vice president and medical director of Almac Group Diagnostics, which developed the assay, said in a news release.
“This approach has created a very robust assay with excellent performance, independent of clinical factors such as Gleason and CAPRA,” added Kennedy, who is also a professor of Medical Oncology at Queen’s University Belfast. “We believe it will play a significant role in aiding clinicians to select the most appropriate therapy regimen for their patients.”
While prognosis for localized prostate cancer patients following radical prostatectomy is very good, evidence has shown that up to 25 percent of patients — dependent upon disease stage and use of population-based PSA screening — will develop metastatic disease within 15 years.
The researchers used a molecular assay to identify a subgroup of prostate cancers with metastatic potential. Patients whose cancer was included in this subgroup had a high risk of recurrence following radical prostatectomy.
They performed an independent assay validation using 322 radical prostatectomy samples. They found that patients who scored positive in the metastatic assay had 62 percent higher risk of having their cancer return after surgery, and a 3.2-fold increased risk of developing metastatic disease.
Next, the researchers tested the potential their assay (called Prostate Cancer Metastatic Assay used in combination with the Cancer of the Prostate Risk Assessment post surgical (CAPRA-S). CAPRA-S is a prognostic model that uses PSA at presentation, age, Gleason score, cancer stage, invasion of the seminal vesicle, lymph node invasion, and surgical margins to predict recurrence, metastasis, and cancer-specific survival after radical prostatectomy.
The combination was superior in identifying patients at an increased risk of biochemical and metastatic recurrence, when compared to either model alone.
“The publication of this manuscript … represents a significant milestone in the assay’s development and with two additional manuscripts being prepared for submission,” said professor Paul Harkin, president and managing director, Almac Diagnostics.
