Men’s cancer risk is climbing: what can we do about it?

reposted from: CancerResearchUK

crabsallover highlights, key points, comments / links.

Posted on December 19, 2012 by Oliver Childs @ Cancer Research UK

If current trends continue, half of UK men born in 2027 will develop cancer

A boy born in 2027 in the UK will have a one in two chance of developing cancer over the course of his lifetime, according to new figures we released today.

In other words, 50 in every 100 UK men in the future are likely to hear the words “you have cancer” at some point in their lifetime. However you say it, that’s clearly not a positive headline.

But crucially, this increasing lifetime risk of cancer is balanced by another powerful force – that of increasing survival rates. Against a backdrop of increasing cancer risk over the past 40 years,survival rates have doubled in the UK.

This is thanks to our greatest weapon against cancer – research, be it new treatments or new ways to prevent people getting cancer in the first place.

Read on for more in-depth analysis of today’s report, and for the visually-minded, this short animation has the key facts:

What is lifetime risk?

Today’s projections don’t mean one in every two men will have cancer by 2027. Instead the lifetime risk of cancer estimates the chance that a newborn child has of developing cancer at some point during their life. The projected lifetime risk is based on predicted population and all cause mortality data, along with incidence and death rates, both in the past and projected into the future. (You can read more about the methods used to predict lifetime risk on our website.)

What’s driving this increase?

Lifetime risk accounts for a person’s overall risk over their whole life. It doesn’t say anything about when a person might develop cancer. But our risk of cancer doesn’t stand still during our lifetime – just as our baby-soft skin starts to accumulate wrinkles as we get older, our risk of developing cancer builds up as we age.

That’s because, as well as wrinkles, we accrue more and more genetic damage over our lives, which is the underlying cause of cancer. And as time passes, cancer-linked genetic factors we may have inherited from our parents have more chance of kick-starting cancer.

Age is one of the biggest risk factors for cancer. In other words, the older we get, the more likely we are to develop cancer. That’s one reason why – thankfully – childhood cancer is rare, accounting for less than 1 per cent of all cancers.

And because of advances in general medicine and improving living conditions, people are living longer on average. The result is more cancer.

As the following chart shows, the projection of one in two men in the future developing cancer is disproportionally down to our ageing population. In fact, based on current trends, a boy born in 2027 will be at least 75 before his risk of cancer starts to exceed that of a man in 2010. But many more people will be living into their 80s, 90s and beyond, so the burden of cancer will increase.

So in many ways we’re a victim of our own medical successes – the conditions that used to kill great numbers of people, such as infections like polio, are no longer as big a threat. But chronic diseases such as cancer, diabetes and heart disease are fast replacing the diseases of old. We’re living longer, but are not necessarily healthier.

Which cancers are increasing?

The men’s cancers set to increase the most over the next 15 years include prostate andbowel cancer and malignant melanoma, the most dangerous form of skin cancer.

• The lifetime risk for prostate cancer is predicted to increase from around 132 in 1,000 men now to 162 in 1,000 men born in 2027. A large reason for the increase in prostate cancer is because of the use of a test called prostate specific antigen (PSA), which is leading to more men being diagnosed with the disease. But we don’t yet have a reliable way to work out which men have life-threatening disease, and which don’t. In other words, working out who will die from their prostate cancer, as opposed to with their disease is still beyond us.
• The lifetime risk for bowel cancer is predicted to increase from around 72 in 1,000 men to 84 in 1,000 men by 2027. Beyond our ageing population, the increase in lifetime risk of bowel cancer is down to lifestyle factors such as an increase in red meat consumption, obesity, low-fibre diets, alcohol and tobacco.
• The lifetime risk for malignant melanoma is predicted to increase from around 18 in 1,000 men to 27 in 1,000 men by 2027. Malignant melanoma is the most deadly skin cancer, and around 10,200 men in the UK in 2027 are predicted to be diagnosed with the disease.

But these are areas we’re actively researching. You can read highlights of our current research on skin, prostate and bowel cancer on our website.

What can men do to reduce their risk?

Yes, age is the biggest risk factor for cancer, but this doesn’t mean we should be complacent or fatalistic. The predicted rise in the number of cancer cases isn’t inevitable, there are things we can do to reduce the risk – because more than four in ten cancers could be prevented by lifestyle changes.

If more men start making changes to their lifestyles, such as not smoking, keeping a healthy weight, cutting back on alcohol, eating a healthy, balanced diet, being physically active and staying safe in the sun, then some of these cancers would never develop.

Research is the answer

Everyone has their part to play in the fight against cancer, and we’re at the frontline of the battle. Because, as our new TV ad says, cancer’s biggest enemy is research.

History proves that research is a formidable enemy – it’s thanks to advances in the prevention, detection and treatment of cancer that more people are surviving their disease than ever before. And our recent figures show that the rates of people dying from cancer are predicted to fall by 17 per cent in the UK by 2030.

But today’s lifetime risk projections in men – and equally sobering statistics in women – clearly show there is more to do.

With the continued help of the public we’ll continue to support lifesaving research; continue to lobby government to make the right choices when it comes to cancer, such as supporting the plain packaging of cigarettes; and continue to encourage people to make the lifestyle choices that research shows can help cut their cancer risk.

Research has already beaten diseases like smallpox. And one day, research will beat cancer.

Dedicated to John Head, aged 80+, who is being treated for Prostate Cancer.

reposted from: http://www.nhs.uk/news/2011/03March/Pages/new-prostate-cancer-test-studied.aspx

crabsallover highlights, key points, comments / links.

“Thousands of lives could be saved by a new cancer test,” the Daily Express reported today. It said that the new test for prostate cancer “detects twice as many cases as the current method”.

This story is based on a study in 288 men with and without prostate cancer, which assessed whether a urine test that measures levels of a protein called EN2 could detect the disease. Cases of prostate cancer had been confirmed through biopsy. The study found that testing for the protein could accurately identify 66% of men with prostate cancer, and correctly rule out the disease in almost 90% of men without the disease.

This study has identified a potential new marker for prostate cancer. The results are promising, but the research is at an early stage, and much further study is needed. The performance of the test will need to be confirmed in larger samples of men from the general population. After this, studies would need to examine how the test affects outcomes such as the numbers of men dying from prostate cancer, and those having unnecessary biopsies. Newspaper estimates that the test will be ready within months are probably overly optimistic.

Where did the story come from?

The study was carried out by researchers from the University of Surrey and other research centres in the UK. It was funded by Cancer Research UK and the Prostate Project Foundation. The authors were also supported by The University of Cambridge, Hutchison Whampoa Limited, the NIHR Cambridge Biomedical Research Center, the Department of Health, and the Medical Research Council.

The study was published in the peer-reviewed medical journal Clinical Cancer Research.

The Daily Express, Daily Mail, Mirror, and The Daily Telegraph covered this research. The papers vary in their predictions of how soon the test might be available; the Mail suggests it could be in general use within months, while the Telegraph claims “within 18 months”. The Express suggests that the test could cost less than £100. However, the test’s performance is still being assessed in the laboratory. It is too early to say if it is reliable and accurate enough to be put into general use, when that may be, or how much it might cost. It is much too early to know whether the test “could save thousands of lives” as some papers suggest.

What kind of research was this?

This laboratory research investigated whether testing for a protein called engrailed-2 (EN2) might detect prostate cancer. This protein belongs to a family of proteins that are usually produced in cells in the embryo but are also switched back on in cancerous cells. The researchers wanted to test whether this protein was produced by prostate cancer cells, and whether it might be a good marker for prostate cancer.

Currently, prostate cancer is detected by measuring the levels of prostate specific antigen (PSA) in the blood. PSA levels are also used to monitor the effects of treatment. PSA is made by normal prostate cells as well as cancerous prostate cells, and men vary in their natural levels of PSA. Raised PSA levels may indicate the presence of prostate cancer, but can also occur in men with non-cancerous enlargement of the prostate. This means that the PSA test misses some cancers (false negatives), and it may suggest that cancer is present in some men who do not have the disease (false positives). The performance of the test depends on the level of PSA selected as the “threshold” for indicating the possible presence of cancer. It also depends on the population tested. Different studies have reported that the PSA test detects between 15% and 44% of prostate cancers.

Therefore, researchers are looking into whether they can develop a better test for prostate cancer. This study aimed to test the diagnostic accuracy of the EN2 urine test (its sensitivity and specificity) and to define a useful threshold for the test, i.e. what a ‘normal’ and ‘abnormal’ level for the protein might be.

What did the research involve?

The researchers first tested whether the EN2 protein was produced by prostate cancer cells and non-cancerous prostate cells grown in the laboratory. They also tested for EN2 in normal and cancerous prostate tissue samples from men with prostate cancers. Prostate tissue samples from men with the non-cancerous condition “benign prostatic hyperplasia” were also tested, as were tissue samples from men with the pre-cancerous condition “high-grade prostatic intraepithelial neoplasia”.

In the next part of their study, the researchers compared the levels of EN2 in urine samples from 82 men with biopsy-confirmed prostate cancer, with 102 men without the disease.

Some of the urine samples were collected from men who had been referred to their specialist Uro-Oncology clinic. These men were referred because they had urinary symptoms that could be a sign of prostate cancer, or had no symptoms but were concerned that they might have prostate cancer (due to a family history of prostate cancer, for example) or had an abnormal PSA test. These men had been referred for testing to determine whether they did or did not have prostate cancer. Of these men, 82 had prostate cancer confirmed on biopsy. Fifty-eight had negative biopsies and were included in the control group of men without prostate cancer.

The researchers also collected urine samples from additional control men aged over 40, who had normal levels of PSA (below 2.5 nanogrammes per mL). These men either had blood in their urine but had no malignancies in their urinary system (urothelial malignancy) detected on testing (17 men), or they had no symptoms or family history of prostate cancer (27 men). The researchers also had urine samples from 10 men with the pre-cancerous condition “high grade prostatic intraepithelial neoplasia”.

Men already being treated for known prostate cancer, or with any known cancer in the past 10 years, or with a urinary tract infection, were not eligible to take part in the study. Urine samples were collected from the first passage of urine of the day. They were taken before any biopsies were performed or any hormone therapy received, and at least 24 hours after any digital rectal examination.

The researchers testing the urine samples did not know which men had cancer. Blood samples for PSA testing were also collected before the urine samples were collected. The researchers looked at whether the levels of EN2 in a man’s urine were related to the levels of PSA in his blood.

To confirm their results, another research centre tested urine from a further 81 patients with prostate cancer and 13 men without prostate cancer.

What were the basic results?

The researchers found that the EN2 protein was being made and secreted by prostate cancer cells grown in the laboratory, but not in normal prostate cells.

They also found EN2 protein in 92% of 184 prostate cancer tissue samples, but in none of the 20 normal prostate tissue samples. The EN2 protein was not detected in prostate tissue samples from men with “benign prostatic hyperplasia”, nor in prostate tissue samples from men with “high grade prostatic intraepithelial neoplasia”.

The urine tests showed that 66% of the men with prostate cancer had EN2 protein in their urine. About 12% of men without prostate cancer had EN2 protein in their urine. The researchers report that using a cut-off value of 42.5 ng/mL of EN2 protein in the urine appeared to be optimal, giving a sensitivity of 66% and specificity of almost 90%. This suggests that in combination with other tests it may be useful at ruling out disease in normal men and confirming disease in those with cancer.

On average, levels of EN2 protein in the urine of men with prostate cancer were 10.4 times higher than those in men without prostate cancer. Independent testing of urine samples from another 94 men at another laboratory found that 58% of the prostate cancer patients in this sample had EN protein in their urine, compared with 15% of control men without the disease.

Of the 10 men with the pre-cancerous condition “high grade prostatic intraepithelial neoplasia”, three had EN2 protein in their urine. A second biopsy taken within six months of the first found that two of these three men had prostate cancer.

The level of EN2 in the men’s urine was not related to the level of PSA in their blood.

How did the researchers interpret the results?

The researchers concluded that EN2 protein in the urine is a good candidate marker for the presence of prostate cancer. They say that a larger study across multiple centres “to further evaluate the diagnostic potential of EN2 is justified”.

Conclusion

This study has identified a potential new marker for prostate cancer. This research is at an early stage, and much further research is needed. The test’s accuracy will need to be confirmed in larger samples of men from non-specialist settings to show how effective it is at screening for prostate cancer in the general population. After this, studies would need to examine how the test affects outcomes such as the numbers of men dying from prostate cancer, and those having unnecessary biopsies.

Though promising, these findings also need to be considered with some pragmatism. Even if the EN2 test performs well in larger scale testing, the test would not necessarily replace PSA testing. The authors suggest that the tests could be used together in prostate cancer diagnosis. Also, if the combined tests did indicate that cancer might be present, the results would still need confirmation by prostate biopsy.

There is a need for improved prostate cancer tests, particularly those that can detect early prostate cancer accurately. There is a lot of research going on in this area. More research will be needed to determine how well these newer tests perform when compared with current tests, and which of them performs the best.

Links to the headlines

Thousands of lives could be saved by a new cancer test. Daily Express, March 2 2011

Prostate cancer test is 'twice as good', say researchers. BBC News, March 2
2011

Accurate new prostate cancer test could save thousands of lives. Daily Mirror, March 2 2011

Urine test for prostate cancer 'in 18 months'. The Daily Telegraph, March 2 2011

New test to spot prostate cancer could be in use in surgeries within months. Daily Mail, March 2 2011

Links to the science

Morgan R, Boxall A, Bhatt A,et al.Engrailed-2 (EN2): A Tumor Specific Urinary Biomarker for the Early Diagnosis of Prostate Cancer.Clinical Cancer Research 2011, Published OnlineFirst March 1

Further reading

Ilic D, O'Connor D, Green S, Wilt TJ. Screening for prostate cancer.Cochrane Database of Systematic Reviews 2006, Issue 3

(Another) urine test for prostate cancer

reposted from: http://www.bbc.co.uk/blogs/thereporters/ferguswalsh/2011/03/another_urine_test_for_prostate_cancer.html

crabsallover highlights, key points, comments / links.

Fergus Walsh (BBC News) Tue Mar 01 2011 16:19:39 GMT+0000 (GMT Standard Time) Share

An encouraging development in the diagnosis of prostate cancer - the most common cancer in men. Scientists at the University of Surrey have developed a urine test which - in an early trial - was at least twice as good at detecting prostate cancer than the current test.

Last October, Cancer Research UK scientists in Cambridge also announced early results of a prototype urine test. The CRUK researchers looked at levels of a protein found in urine called MSMB, and in a small study were able to diagnose prostate cancer from urine samples with about 50% accuracy.

The team at the University of Surrey focussed on another protein, Engrailed-2 (EN2) which is made by prostate cancers and secreted into urine. In a study of nearly 300 men published in the US journal Clinical Cancer Research, they found the test was able to detect prostate cancer with 66% accuracy, and with few so-called "false positives" - where cancer was supposedly detected when the patient was free of the disease. The research was funded by the University of Surrey and The Prostate Project charity.

The standard blood test checks prostate-specific antigen (PSA) levels. Among many problems with the blood test are that PSA levels can vary widely between men and at different time. Furthermore, a raised level may indicate other prostate conditions which are not cancerous.

False positives are a significant problem with the PSA test. A raised level may prompt a significant period of anxiety for patients and mean that they undergo a needle biopsy. Here the problem can be false negatives - so a cancer may be missed if the needle does not sample the right area.

Professor Malcolm Mason from CRUK said: "There is a desperate need for a better prostate cancer test than PSA, and this latest candidate, EN2, is very welcome. However, more work needs to be done to find out whether or not EN2 is capable of distinguishing between aggressive prostate cancers that need treatment, and non-aggressive ones that don't. Almost certainly, this new marker would be used as part of a combination of several markers, including PSA.

Both the Surrey and Cambridge urine tests are promising. Indeed there are frequent research papers showing the potential of biomarkers in blood and urine for detecting cancer and other diseases. But most still have a long way to go. A blog in the Guardian last year discussed the problems involved with using these "biological fingerprints" for detecting disease.

Men hoping to benefit from the Surrey research may have to wait some time at the prostate cancer urine test is still experimental. Dr Richard Morgan, senior lecturer in Molecular Oncology at the University of Surrey said: "We are preparing several large studies in the UK and in the US and although the EN2 test is not yet available several companies have expressed interest in taking it forward."

Prostate cancer mutations identified

reposted from: http://www.nhs.uk/news/2011/02February/Pages/mutations-behind-prostate-cancer.aspx

crabsallover highlights, key points, comments / links.

The genetic map of prostate cancer has been “cracked”, The Daily Telegraph reported. The newspaper said that new research into prostate cancer has provided a “breakthrough that could transform our understanding of the disease”.

The research scanned the entire genetic sequences of prostate tumours and compared them to the genetics of healthy cells from the same patient. The research identified a range of mutations and genetic patterns that showed the way that the DNA is sometimes rearranged in these tumours. The researchers suggest that these patterns may be unique to prostate cancer and may have a role in initiating it.

Such research helps to further our understanding of the complex genetic reasons why some men may develop prostate cancer while others do not. However, it will be some time before this knowledge can be used in diagnosis or treatment as several thousand mutations were identified in each tumour and it is unclear what effect each mutation has. The study also looked at only seven tumours, so further research must verify the presence of these mutations in more samples.

Where did the story come from?

Numerous researchers from several research institutions across the US contributed to this research. The study was funded by several US organisations, including the Prostate Cancer Foundation Movember campaign, the Howard Hughes Medical Institute, the National Human Genome Research Institute, the Kohlberg Foundation, the National Cancer Institute and the National Institutes of Health. It was published in the peer-reviewed scientific journal Nature.

The newspapers generally reported the study clearly, although the Daily Mail did not highlight that this study has limitations due to the small number of samples tested. Given that the research only studied samples from seven men, it needs to be repeated on a larger scale.

What kind of research was this?

This genetic study set out to sequence the entire DNA code of prostate cancer cells. Prostate cancer is a major disease and the second most common cause of cancer deaths in men in the UK. Previous research, through genome-wide association studies, has identified that certain single-letter variants within the DNA code are associated with an increased risk of cancer. In fact, nine such variants were identified by four studies covered by Behind the Headlines in September 2009, where it was concluded that many regions in the DNA appear to contribute to the risk of prostate cancer and that further variants are likely to be discovered.

The methods of this research differed from those employed in genome-wide association studies, which look at associations that may exist between specific DNA variations traits and the risk of developing a particular disease. In this current study, researchers “read” (sequenced) the entire genetic code of a person’s prostate cancer cells and compared it with the genetic sequence of that person’s healthy prostate cells. Using this method, the researchers could see what genetic changes and mutations occurred in these cells as they became cancerous.

What did the research involve?

The researchers used DNA extracted from prostate tumour samples from seven men given a radical prostatectomy (removal of the prostate and related tissue). They also had blood samples from these men. DNA extracted from the blood was used as a control in the experiments, to show what the men’s DNA was like in non-cancerous cells.

The researchers sequenced the entire genome of the prostate cancer cells, looking for mutations and variations that did not exist in normal cells from the same patient. They looked for small differences in the sequence of the DNA, larger-scale changes in the chromosome arrangements and instances where part of one chromosome had broken off and attached to another chromosome to form a hybrid. The DNA was sequenced using established methods in this field and the information was processed by complex software that could identify the presence of mutations in the DNA.

A portion of the mutations detected were checked using different methods to validate the original process. The researchers reported how many mutations they detected in the tumour cells and their observations on the common types of genetic rearrangements. They then discussed how certain variations may increase the risk of prostate cancer developing.

What were the basic results?

The researchers found about 3,866 single-letter mutations of the genetic code in each tumour, a rate of mutation that they say is similar to that seen with acute myeloid leukemic and breast cancer but lower than that seen in small cell lung cancer and skin cancer.

Two of the seven tumours tested had mutations within two genes called SPTA1 and SPOP. In three of seven tumours, there were mutations in three genes called CHD1, CHD5 and HDAC9, which are responsible for producing chromatin modifier proteins. These proteins are known to play a role in suppressing tumours, regulating how genes are switched on and off, and stem cells’ capacity to develop into different body cells. Three of seven tumours also had mutations in HSPA2, HSPA5 and HSP90AB1, a set of genes linked to cells’ response to environmental stress and damage. Other genes were mutated in only one of the seven tumours.

The researchers identified 90 chromosome rearrangements in each tumour and noted that this number was similar to that seen in breast cancer cells. The rearrangements showed a distinctive pattern that had reportedly not been seen in other solid tumours before.

Some of the rearrangements involved genes that were affected by single-letter mutations in other tumours, including the chromatin modifier gene CHD1. A number of rearrangements also occurred  near multiple known cancer genes.

Overall, sixteen genes affected by a rearrangement mutation were found in at least two tumours.

How did the researchers interpret the results?

The discovery of many mutations in the genetic code of prostate cancers, some of which are associated with known genes, led the researchers to conclude that these mutations may contribute to the development of tumours in the prostate.

They also say that the high number of “recurrent gene fusions” suggests that rearrangements in the DNA may be critical events in initiating prostate cancer. These are complex rearrangements and the researchers note that a “whole-genome approach”, looking at the whole of a tumour cell’s genetic code, is necessary to profile them.

Conclusion

This important study looked at the entire genetic sequence in a sample of prostate tumour cells and compared this with that of normal tissue. It has revealed that there are many mutations and rearrangements of DNA, which the researchers suggest could increase the risk of this cancer type. Importantly, only seven tumour samples were used in this analysis, and the mutations identified were not present in all tumour samples. This confirms what is already suspected about the disease, that factors affecting prostate cancer are complex, particularly the genetic elements.

The methods of this study will need to be replicated in a larger sample of individuals, a process which is likely to be extensive and time consuming. Such research will also need to confirm the extent to which each mutation or DNA rearrangement increases the risk of the disease and the normal function of the genes around the mutation sites. Such information could be critical in the development of screening or treatment approaches in the future.

While this study has importantly applied a whole genome approach to understanding the genetics of prostate cancer, this now needs to be applied to more samples. Only then can the full implications of the genetic changes found through this research be appreciated.

Links to the headlines

Genetic map of prostate cancer cracked. The Daily Telegraph, February 10 2011

Prostate cancer's genetic code cracked by U.S. scientists in breakthrough set to transform treatment of the disease. Daily Mail, February 10 2011

Links to the science

Berger MF, Lawrence MS, Demichelis F et al. The genomic complexity of primary human prostate cancer. Nature: 470, 214–220 February 10 2011

Is mitochondrial DNA the secret of prostate cancer?

reposted from: http://www.newscientist.com/article/dn19894-is-mitochondrial-dna-the-secret-of-prostate-cancer.html?DCMP=OTC-rss&nsref=online-news

• 16:15 20 December 2010 by Wendy Zukerman

Fresh insight into prostate cancer has come in a study that shows the mitochondrial DNA of human prostate cancer cells are riddled with mutations.

The findings could shake up prostate cancer research, providing targets for treatment, diagnosis and monitoring of one of the most prevalent cancers in the west.

Most such research focuses on mutations in the DNA of chromosomes within the cellular nucleus. But although most DNA in a cell is located in the nucleus, mitochondria – the power plants of cells – have their own genome.

Last year, mutations in mitochondrial DNA (mtDNA) were linked to development of the cancer. To investigate further, Anita Kloss-Brandstätter of Innsbruck Medical University, Austria, and colleagues compared the entire mitochondrial genome – some 16,569 base pairs – of cancerous and non-cancerous tissue from 30 men with prostate cancer.

In total, 41 mutations were found in cancerous cells that were not observed in healthy prostate or blood cells. This suggests the mutations are specifically associated with prostate cancer development, says Kloss-Brandstätter.

More mtDNA mutations were found in more advanced cancers, she says, indicating that the mutations could be used to track cancer progression and metastasis.

Mutations drive metabolism

Several mutations were found in genes coding the machinery that makes mitochondrial proteins, and so would probably hinder mitochondria's ability to make the chemical fuel called ATP, which is used by normal cells.

Phillip Nagley of Monash University in Melbourne, Australia, who was not involved in the work, says this could contribute to the changed metabolism typical of cancer cells. Many cancers get energy from glycolysis, which occurs in the liquid inside cells, rather than via aerobic respiration from mitochondria. Ordinary cells use glycolysis for energy only if they are short of oxygen, because it is inefficient.

Despite this, glycolysis is thought to benefit cancer cells because it also produces the chemical building blocks for making cells, and enables cancer cells to rapidly grow.

According to Juergen Reichardt at the University of Sydney, Australia, it's also possible that mtDNA mutations trigger nuclear DNA mutations. Mitochondrial dysfunction could lead to the release of free radicals, which are by-products of aerobic respiration. Free radicals could then lead to nuclear DNA mutations. Reichardt points out, however, that it has not been shown that free radicals released in the mitochondria can enter into the nucleus.

Precise prognosis

Prostate cancer is currently diagnosed by elevated levels of prostate-specific antigen (PSA). However, the test is far from perfect: PSA levels increase in men with enlarged, but not cancerous prostates. "Additional mtDNA sequencing could lead to a more precise prognosis for the patient," says Kloss-Brandstätter.

Journal reference: The American Journal of Human Genetics, DOI: 10.1016/j.ajhg.2010.11.001

crabsallover PSA test for Prostate cancer

crabsallover tested Twin Oaks - Nigel Savage, blood tested: 15-Jul 2010, report no: 52588-280541315
test: 0.7 ug/L = 0.7ng/ml = normal

ug/L=ng/mL

Levels under 4 ng/mL are usually considered “normal.”
Levels over 10 ng/mL are usually considered “high”
Levels between 4 and 10 ng/mL are usually considered “intermediate.”
http://www.pcf.org/site/c.leJRIROrEpH/b.5802071/k.C620/PSA__DRE_Screening.htm

www.labtestsonline
The 'normal' value for total PSA varies with age and is generally considered to be under 3.0 nanograms (ng) per millilitre (mL) in men under 60 years of age of blood, under 4.0 ng per mL in men 60 - 69 years of age, and under 5.0 ng per mL in men over 70 years of age. Total PSA levels greater than 10.0 ng/mL may indicate a high probability of prostate cancer. Increased levels of PSA in those with a small prostate gland volume (which can be measured using ultrasound at the time of biopsy) indicate a higher probability of cancer. Levels between 4.0 ng/mL and 10.0 ng/mL may be due to BPH, a non-cancerous swelling of the prostate which occurs most frequently in elderly men. Increased total PSA levels may also indicate a condition called prostatitis, which is caused by an infection.

There is some evidence that the free PSA ratio (the percent of total PSA not bound to proteins) can help predict the probability of cancer, especially in patients with total PSA levels in the 'grey-area’ range of 4.0 to 10.0 ng/mL. This test may also be useful in early diagnosis of disease when values are between 2.5 and 4.0. A free-PSA test result above 25% is thought to suggest a lower risk of cancer, whereas a lower percentage suggests a higher probability of disease. This ratio may help reduce the number of unnecessary biopsies. A recent study also suggests that very low ratios of free PSA to total PSA (less than 14%) might be seen with a more aggressive form of the disease. Further studies are now being undertaken.

In most cases, test results are reported as numbers rather than as "high" or "low", "positive" or "negative", or "normal". In order for the doctor to properly understand laboratory results it is necessary for them to know what the reference range (or ‘normal value’ range) is for the laboratory where the test is performed. However, reference ranges can be influenced by the patient's age and sex and, amongst other things, by what drugs they are receiving, the time of day and what they have eaten. Reference ranges can also influenced by the test method and instrument used by laboratory. To learn more about reference ranges, please read the article, Reference Ranges and What They Mean. 
source: http://www.labtestsonline.org.uk/understanding/analytes/psa/test.html#what