Vaginal Prostate Specific Antigen (PSA) Is a Useful Biomarker of Semen Exposure Among HIV-Infected Ugandan Women

Woolf-King, S.E., Muyindike, W., Hobbs, M.M. et al. AIDS Behav (2016). doi:10.1007/s10461-016-1433-7

Abstract

The practical feasibility of using prostate specific antigen (PSA) as a biomarker of semen exposure was examined among HIV-infected Ugandan women. Vaginal fluids were obtained with self-collected swabs and a qualitative rapid test (ABAcard^®p30) was used to detect PSA. Trained laboratory technicians processed samples on-site and positive PSA tests were compared to self-reported unprotected vaginal sex (UVS) in the last 48 h. A total of 77 women submitted 126 samples for PSA testing at up to three study visits. Of these samples, 31 % (n = 39/126) were PSA positive, and 64 % (n = 25/39) of the positive PSA samples were accompanied by self-report of no UVS at the study visit the PSA was collected. There were no reported difficulties with specimen collection, storage, or processing. These findings provide preliminary data on high levels of misreported UVS among HIV-infected Ugandan women using practically feasible methods for PSA collection and processing.

 

 

How women can help men spot symptoms of prostate cancer

From: Louisa Peacock. from the Telegraph

As male patients are being given false hope on prostate cancer, Louisa Peacock outlines how wives and girlfriends can help their male partners spot the disease.

Prostate cancer is very tricky to spot. In some cases, the symptoms may develop over a number of years. In other patients, by the time symptoms become noticeable, prostate cancer has already spread to their bones.

Most men with early prostate cancer do not have symptoms, the charity points out.

However, there are some warning signs for men,  because men routinely risk their health by failing to go and see the doctor, their partners can often encourage them to go and get symptoms checked before it's too late.

Symptoms to look out for:
- Having to get up in the night several times to empty your bladder, which you wouldn't normally do

- Having trouble starting to urinate
- Feeling as though the bladder isn't emptying properly
- Dribbling after urinating

Fear of the doctor
A recent study  by the National Pharmacy Association showed that nearly nine in 10 men don't like to trouble a doctor unless they have a "serious problem". This reticence has largely been attributed to men’s fear of the doctor, (white coat syndrome) and male machismo.
Partners, wives or girlfriends of men should encourage their loved one to get checked if they notice any unusual bathroom habits.
Historically, women have usually been the custodians of health in the family. Mums, grandmothers, sisters, aunts – have typically been the ones to make their men visit health professionals and sort any kind of ill health out proactively.
Women can help men quell the irrational fear of going to the doctor, so they can seek help before it's too late.
Where prostate cancer has already spread to the bones, the symptoms can include long standing pain in one area, such as the back or pelvic bones.
However, this could be a sign of another illness, such as arthritis.
Blood in semen or in urine could indicate prostate or urine infection, or prostate cancer, he adds. Either way, you're advised to check it out.

Prostate Specific Antigen Mass Ratio Potential as a Prostate Cancer Screening Tool

Purpose
Studies suggest lowering the threshold of the prostate specific antigen test in obese men due to the hemodilution effect but prostate specific antigen may be affected by prostate volume and insulin resistance, which also increase with obesity. Thus, we examined the combined effect of these factors on prostate specific antigen.

Materials and Methods
We analyzed 3,461 Korean men 30 to 80 years old with prostate volume data available who underwent routine evaluation. We examined the effect of plasma volume, homeostatic model assessment index, prostate volume and body mass index on prostate specific antigen, and prostate specific antigen mass and mass ratio (total circulating prostate specific antigen protein per prostate volume) by the trend test and/or ANOVA after adjusting for age and/or prostate volume.

Results
Body mass index had positive associations with plasma volume, the homeostatic model assessment index and prostate volume (p for trend <0.01). Prostate specific antigen had a positive association with prostate volume and a negative association with plasma volume (p for trend <0.01) but not with homeostatic model assessment index. The adjusted R2 of prostate volume vs prostate specific antigen was greater than for plasma volume vs prostate specific antigen while for body mass index vs prostate volume it was less than for body mass index vs plasma volume (0.0892, 0.0235, 0.1346 and 0.3360, respectively). Prostate specific antigen mass was not associated with plasma volume or body mass index but it was still associated with prostate volume after adjusting for plasma volume or body mass index (p for trend <0.01). Mean prostate specific antigen mass ratio did not change significantly across body mass index, plasma volume or prostate volume quartiles in men older than 55 years.

Conclusions
It is not logical to lower the prostate specific antigen threshold based on only the hemodilution effect since body mass index related prostate volume enlargement can increase prostate specific antigen in obese men. Another tool is needed and prostate specific antigen mass ratio may be an option.

Volume 184, Issue 2, Pages 488-493 (August 2010)

prostate Specific Antigen Mass Ratio Potential as a Prostate Cancer Screening Tool

Ho-Chun Choi, Jin-Ho Park, Be-Long Cho, Ki-Young Son, Hyuk-Tae Kwon

Prostate Cancer Treatments

Different types of treatment are available for prostate cancer. You and your doctor will decide which treatment is right for you. Some common treatments are—

•Active surveillance (watchful waiting): This consists of closely monitoring the patient's prostate cancer by performing the PSA and DRE tests regularly, and treating it only if and when the prostate cancer causes symptoms or shows signs of growing.
•Surgery (radical prostatectomy): Prostatectomy is surgery to remove the prostate completely. Radical prostatectomy removes the prostate as well as the surrounding tissue.
•Radiation therapy: Radiation destroys cancer cells, or prevents them from growing, by directing high-energy X-rays (radiation) at the prostate. There are two types of radiation therapy—
◦External radiation therapy: A machine outside the body directs radiation at the cancer cells.
◦Internal radiation therapy (brachytherapy): Radioactive seeds or pellets are surgically placed into or near the cancer to destroy the cancer cells.
•Hormone therapy: This treatment uses drugs, surgery, or other hormones to remove male sex hormones or block them from working, which prevents cancer cells from growing.
Other therapies used in the treatment of prostate cancer that are still under investigation include—

•Cryotherapy: Placing a special probe inside or near the prostate cancer to freeze and kill the cancer cells.
•Chemotherapy: Using special drugs to shrink or kill the cancer. The drugs can be pills you take or medicines given through an intravenous (IV) tube, or, sometimes, both.
•Biological therapy: This treatment works with your body's immune system to help it fight cancer or to control side effects from other cancer treatments. Side effects are how your body reacts to drugs or other treatments. Biological therapy is different from chemotherapy, which attacks cancer cells directly.
•High-intensity focused ultrasound: This therapy directs high-energy sound waves (ultrasound) at the cancer to kill cancer cells.
For more information, visit the National Cancer Institute's (NCI) Prostate Cancer Treatment Option Overview. This site can also help you find a doctor or treatment facility that works in cancer care. Visit Facing Forward: Life After Cancer Treatment for more information about treatment and links that can help with treatment choices.

Clinical Trials
If you have prostate cancer, you may want to take part in a clinical trial. Clinical trials are research studies that help find new treatment options. Visit the NCI and National Institutes of Health (NIH) sites listed below for more information about finding clinical trials.

•Introduction to Clinical Trials (NCI)
•Search for Clinical Trials (NCI)
•ClinicalTrials.gov (NIH)
Complementary and Alternative Medicine
Complementary medicine is a group of medicines and practices that may be used in addition to the standard treatments for cancer. Alternative medicine means practices or medicines that are used instead of the usual, or standard, ways of treating cancer. Examples of complementary and alternative medicine are meditation, yoga, and dietary supplements like vitamins and herbs.

Complementary and alternative medicine does not treat prostate cancer, but may help lessen the side effects of the cancer treatments or of the cancer symptoms. It is important to note that many forms of complementary and alternative medicines have not been scientifically tested and may not be safe. Talk to your doctor before you start any kind of complementary or alternative medicine.

For more information about complementary and alternative medicine, visit NCI's Complementary and Alternative Medicine.

Which Treatment Is Right for Me?
Choosing which kind of treatment is right for you may be hard. If you have prostate cancer, be sure to talk to your doctor about the treatment options available for your type and stage of cancer. Doctors can explain the risks and benefits of each treatment and their side effects.

Sometimes people get an opinion from more than one doctor. This is called a "second opinion." Getting a second opinion may help you choose the treatment option that is right for you.

Stage-specific cancer incidence: An artificially mixed multinomial logit model.

Takeda Global Research & Development Center, Inc., Analytical Sciences, 675 North Field Drive, Lake Forest, IL 60045, U.S.A.

Early detection of prostate cancer using the prostate-specific antigen test led to a sharp spike in the incidence of the disease accompanied by an equally sharp improvement in patient prognoses as evaluated at the point of advanced diagnosis. Observed outcomes represent age at diagnosis and stage, a categorical prognostic variable combining the actual stage and the grade of tumor. The picture is summarized by the stage-specific cancer incidence that represents a joint survival-multinomial response regressed on factors affecting the unobserved history of the disease before diagnosis (mixture). Fitting the complex joint mixed model to large population data is a challenge. We develop a stable and structured MLE approach to the problem allowing for the estimates to be obtained iteratively. Factorization of the likelihood achieved by our method allows us to work with only a fraction of the model dimension at a time. The approach is based on generalized self-consistency and the quasi-EM algorithm used to handle the mixed multinomial part of the response through Poisson likelihood. The model provides a causal link between the screening policy in the population and the stage-specific incidence. Copyright (c) 2009 John Wiley & Sons, Ltd
Stat Med. 2009 May 19.

Prostatic Acid Phosphatase Adversely Affects Cause-Specific Survival in Patients with Intermediate to High-Risk Prostate Cancer Treated with Brachythe

Objectives
To perform a retrospective analysis to assess the utility of pretreatment serum prostatic acid phosphatase (PAP) as a predictor of cause-specific survival (CSS) in patients with higher risk prostate cancer treated with palladium-103 (103Pd) brachytherapy and supplemental external beam radiotherapy (EBRT).

Methods
From 1992 to 1996, 193 patients with clinically localized prostate adenocarcinoma, a pretreatment PAP level, and Gleason score 7 or more, and/or a prostate-specific antigen (PSA) level of 10 ng/mL or more were treated with 103Pd brachytherapy and supplemental EBRT. The patients underwent EBRT of 41.4 Gy to a limited pelvic field and 103Pd brachytherapy with a prescribed minimum 103Pd dose of 80 Gy. Multivariate analysis was performed to analyze the predictive value of PAP, PSA, and Gleason score on CSS.

Results
The 10-year CSS rate for patients with a PAP level of less than 1.5, 1.5 to 2.4, and 2.5 U/L or more was 93%, 87%, and 75%, respectively (P = 0.013). The 10-year CSS rate for patients with a PSA level of less than 10, 10 to 20, and greater than 20 ng/mL was 92%, 76%, and 83%, respectively (P = 0.393). The 10-year CSS rate for patients with a Gleason score of 6, 7, 8, and 9 was 90%, 89%, 70%, and 68%, respectively (P = 0.002). On Cox multivariate regression analysis, PAP (hazard ratio 1.31, P <0.0001) and Gleason score (hazard ratio 2.37, P = 0.0007) were associated with CSS. PSA was not predictive of CSS (P = 0.393).

Conclusions
The results of this study demonstrated that PAP is a stronger predictor of CSS than PSA or Gleason score in men with higher risk prostate cancer treated with 103Pd brachytherapy and EBRT. Given the findings of this analysis, the use of PAP should be reconsidered in these patients.

Body Mass Index and Prostate-Specific Antigen Failure Following Brachytherapy for Localized Prostate Cancer.

PURPOSE:
Increasing body mass index (BMI) is associated with prostate-specific antigen (PSA) failure after radical prostatectomy and external beam radiation therapy (EBRT). We investigated whether BMI is associated with PSA failure in men treated with brachytherapy for clinically localized prostate cancer.

PATIENTS AND METHODS:
Retrospective analyses were conducted on 374 patients undergoing brachytherapy for stage T1c-T2cNXM0 prostate cancer from 1996-2001. Forty-nine patients (13%) received supplemental EBRT and 131 (35%) received androgen deprivation therapy (ADT). Height and weight data were available for 353 (94%). Cox regression analyses were performed to evaluate the relationship between body mass index (BMI) and PSA failure (nadir + 2 ng/ml definition). Covariates included age, race, preimplantation prostate-specific antigen (PSA), Gleason score, T category, percent of prescription dose to 90% of the prostate, use of supplemental EBRT, and ADT.

RESULTS:
Median age, PSA, and BMI were 66 years (range, 42-80 years), 5.7 ng/ml (range, 0.4-22.6 ng/ml), and 27.1 kg/m(2) (range, 18.2-53.6 kg/m(2)), respectively. After a median follow-up of 6.0 years (range, 3.0-10.2 years), there were 76 PSA recurrences. The BMI was not associated with PSA failure. Six-year PSA failure rates were 30.2% for men with BMI less than 25 kg/m(2), 19.5% for BMI of 25 or greater to less than 30 kg/m(2), and 14.4% for BMI of 30 kg/m(2) or greater (p = 0.19). Results were similar when BMI was analyzed as a continuous variable, using alternative definitions of PSA failure, and excluding patients treated with EBRT and/or ADT. In multivariate analyses, only baseline PSA was significantly associated with shorter time to PSA failure (adjusted hazard ratio, 1.12; 95% confidence interval, 1.05-1.20; p = 0.0006).

CONCLUSIONS:
Unlike after surgery or EBRT, body mass index (BMI) is not associated with prostate-specific antigen (PSA) failure in men treated with brachytherapy for prostate cancer. This raises the possibility that brachytherapy may be a preferred treatment strategy in obese patients.

Prostate specific antigen versus prostate specific antigen density as a prognosticator of pathological characteristics and biochemical recurrence foll

PURPOSE: The usefulness of prostate specific antigen (PSA) density for predicting pathological stage and biochemical recurrence after radical prostatectomy has not been well defined. We investigated whether prostate specific antigen density yielded an advantage over total prostate specific antigen for predicting adverse pathological characteristics and disease recurrence following radical prostatectomy.

MATERIALS AND METHODS: A total of 13,434 men who underwent radical prostatectomy for clinically localized prostate cancer between 1984 and 2006 were included in this study. The study population was stratified by Gleason score (6 or less, 7, and 8 or greater), and the clinical and pathological characteristics of each group were compared. We constructed ROC curves and determined the ROC AUC and concordance index to specifically investigate the accuracy of prostate specific antigen (PSA) and prostate specific antigen density for predicting pathological stage and biochemical recurrence.

RESULTS: Prostate specific antigen density was better than prostate specific antigen (PSA)for predicting extraprostatic extension and biochemical-free recurrence in patients with a biopsy Gleason score of 6 or less (each p <0.001). In patients with a biopsy Gleason score of 7 prostate specific antigen was more predictive than prostate specific antigen density for seminal vesicle involvement (p <0.001), lymph node involvement (p = 0.017) and biochemical-free recurrence (p <0.001). In men with a biopsy Gleason score of 8 or greater there was no statistical difference between prostate specific antigen and prostate specific antigen density in terms of prognostic value for pathological or clinical outcomes.

CONCLUSIONS: Prostate specific antigen density is highly associated with pathological stage and biochemical-free survival following radical prostatectomy. In lower grade prostate cancers prostate specific antigen density is significantly more accurate for predicting extraprostatic extension and biochemical-free recurrence compared to total prostate specific antigen. It should be considered when counseling patients on outcomes following radical prostatectomy.

Hierarchical Changepoint Models for Biochemical Markers Illustratedby Tracking Postradiotherapy Prostate-Specific Antigen Series inMen With Prostate

PURPOSE: Biomarkers provide valuable information when detecting disease onset or monitoring diseaseprogression; examples include bone mineral density (for osteoporosis), cholesterol (for coronary artery diseases), or prostate-specific antigens (PSA, for prostate cancer). Characteristics of markers series can then beused as prognostic factors of disease progression, such as the postradiotherapy PSA doubling time in mentreated for prostate cancer. The statistical analysis of such data has to incorporate the within and be-tween-series variabilities, the complex patterns of the series over time, the unbalanced format of thedata, and the possibly nonconstant precision of the measurements.

METHODS: We base our analysis on a population-based cohort of 470 men treated with radiotherapy forprostate cancer; after treatment, the log2PSA concentrations follow a piecewise-linear pattern. We illustrate the flexibility of Bayesian hierarchical changepoint models by estimating the individual and popula-tion postradiotherapy log2PSA profiles; parameters such as the PSA nadir and the PSA doubling time wereestimated, and their associations with baseline patient characteristics were investigated. The residual PSA variability was modeled as a function of the PSA concentration. For comparison purposes, two alternativemodels were briefly considered.

RESULTS: Precise estimates of all parameters of the PSA trajectory are provided at both the individualand population levels. Estimates suggest greater PSA variability at lower PSA concentrations, as well as anassociation between shorter PSAdts and greater baseline PSA levels, higher Gleason scores, and older age.

CONCLUSIONS: The use of Bayesian hierarchical changepoint models accommodates multiple com-plex features of longitudinal data, permits realistic modeling of the variability as a function of the markerconcentration, and provides precise estimates of all clinically important parameters. This type of modelshould be applicable to the study of marker series in other diseases.

CARINE A. BELLERA,PHD, JAMES A. HANLEY,PHD, LAWRENCE JOSEPH,PHD,AND PETER C. ALBERTSEN,MD

PSA velocity does not aid long-term prediction of prostate cancer incidence

Elevated serum prostate-specific antigen (PSA) levels can indicate the presence of prostate cancer, although PSA levels are also elevated in some nonmalignant conditions, which affects the reliability of prostate cancer prediction. PSA levels rise sharply in patients with aggressive prostate cancer, and a recent study suggested that the rate of increase (PSA velocity) could predict life-threatening prostate cancer 10–15 years before diagnosis. Ulmert and colleagues evaluated data from the Malmö Preventative Medicine population-based study to compare the accuracy of a single PSA measurement versus PSA velocity in the long-term prediction of prostate cancer diagnosis.

Nature Clinical Practice Oncology (2008) 5, 302

Using spectral moments of spiral networks based on PSA/mass spectra outcomes to derive quantitative proteome–disease relationships (QPDRs) and predict

In prostate cancer (PCa), prognostic (predictive) factors are particularly important given the marked heterogeneity of this disease at clinical, morphologic, and biomolecular levels. Blood contains a treasure of previously unstudied biomarkers that could reflect the ongoing physiological state of all tissue. The serum prostate-specific antigen (PSA) measurement is a very good biomarker for PCa, but the percentage of bad classification is somewhat high. The blood proteome mass spectra (MS) represent a potential tool for detection of diseases; however the identification of a single biomarker from the complex output from MS is often difficult. In this paper, we propose a general strategy, based on computational chemistry techniques, which should improve the predictive power of PSA. Our group adapted the square–spiral graph to represent human serum-plasma–proteome MS for healthy and PCa patients. These graphs were previously applied to DNA and/or protein sequences. In this work, we calculated different classes of connectivity indices (CIs), and created various models based on the spectral moments. The best QPDRs model found showed accuracy values ranging from 71.7% to 97.2%, and 70.4% to 99.2% of specificity. This methodology might be useful for several applications in computational chemistry.

Giulio Ferinoa, Humberto González-Díaza b, Giovanna Delogua, Gianni Poddaa, and Eugenio Uriarteb

ARTICLE

Gene Linked to Deadly Prostate Cancer

Prostate cancer is common. It's also deadly. About 220,000 men in the United States will learn that they have prostate cancer this year. Despite tests to detect it early and several effective treatments, the disease kills about 27,000 men in the United States each year.

On the other hand, many men with prostate cancer have tiny tumors that pose no significant threat to their health. For these men, early detection and treatment provides no benefit. So, it's a big challenge to learn how to detect the dangerous tumors while leaving the others alone. That's not easy.

To make matters worse, non-cancerous enlargement of the prostate, a nearly universal part of aging for men, may mimic prostate cancer . For example, the prostate-specific antigen (PSA) blood test may be high. This can raise concern about prostate cancer even when no cancer is present.

Clearly, we need better ways to identify men who have early prostate cancer requiring treatment. That's why the results of a new research study from Iceland are notable. The study links a gene mutation to an increased risk of aggressive prostate cancer. Interestingly, the mutation is located on a gene – called BRCA2 – known to increase the risk of cancers of the breast and ovary among women.

In this new research, scientists reviewed cases of prostate cancer in Iceland from the last 50 years. They selected study subjects with prostate cancer who also had female relatives with breast cancer. Researchers discovered that men who carried a particular BRCA2 gene mutation tended to have the worst forms of prostate cancer.

For example, men with the BRCA2 mutation had:

· Onset of prostate cancer at a younger age

· More advanced prostate cancer

· Shorter survival

The effect on survival was particularly striking. On average, those with the mutation lived just 2 years from the time of diagnosis. Non-carriers of the mutation survived more than 12 years.

It's hard to know whether these results will have a big impact on prostate cancer detection or treatment. The mutation was found in less than 6% of study subjects with prostate cancer. The rate might have been lower if these men did not have relatives with breast cancer. This mutation might be even rarer outside Iceland.

Still, the findings suggest that looking for mutations in genes with known links to cancer could provide valuable information. It's easy to imagine that genetic testing could someday be a routine part of screening for prostate cancer (and other cancers). Perhaps the results could be used to predict the need for aggressive treatment.

by Harvard Publications

Link Between Severe Acne and Prostate Cancer

(Ivanhoe Newswire) A higher risk of prostate cancer may be linked to severe acne.

New research from Johns Hopkins Bloomberg School of Public Health in Baltimore finds men who took tetracycline -- an antibiotic used to treat severe acne -- for four years or longer were 70 percent more likely to develop prostate cancer over a 10-year period than men who had taken the drug, or had taken it for a shorter time.

But the studys authors urge caution in interpreting their findings. They note the small number of participants who had used tetracycline for at least four years -- 0.5-percent of the 34,629 men in the study -- the indirect assessment of severe acne, and the fact that acne can have several causes.

The research looked at the link between severe acne and prostate cancer because recent studies found the acne-related bacterium Propionibacterium acnes in one third of prostate samples taken from men with prostate cancer. The tissue containing P. acnes was more likely to be inflamed. Inflammation is believed to be an important part of the development of prostate cancer.

Researchers say it is unlikely tetracycline itself would raise the risk of prostate cancer . They believe one possible explanation for the acne-prostate cancer link is that men who develop severe acne may be more likely to have stronger inflammatory immune responses when P. acnes goes into the prostate.

SOURCE: International Journal of Cancer, 2007;121:2688-2692

Prostate Specific Antigen

A prostate-specific antigen (PSA) test measures the amount of prostate-specific antigen in the blood. PSA is released into a man's blood by his prostate gland . Healthy men have low amounts of PSA in the blood. The amount of PSA in the blood normally increases as a man's prostate enlarges with age. PSA may increase as a result of an injury, a digital rectal exam , sexual activity ( ejaculation ), inflammation of the prostate gland ( prostatitis ), or prostate cancer .

Prostate cancer often grows very slowly, without causing major problems. Detecting prostate cancer early and treating it may prevent some health problems and reduce the risk of dying from the cancer. However, some treatments for prostate cancer can cause other problems, such as controlling urination (incontinence) or erection problems (erectile dysfunction). Some men may choose not to have a PSA test or treat prostate cancer if it is detected. For example, a man older than age 75 who has no bothersome symptoms of prostate cancer may choose not to treat the cancer if it is found, so he would not need a PSA test.

Biology of Prostate Specific Antigen

Prostate-specific antigen (PSA) is an androgen-regulated serine protease produced by both prostate epithelial cells and prostate cancer (PCa) and is the most commonly used serum marker for cancer . Prostate specific antigen (PSA) is a protein produced by the cells of the prostate gland. Prostate-specific antigen is present in small quantities in the serum of normal men, and is often elevated in the presence of prostate cancer and in other prostate disorders.

PSA is a major protein in semen , where its function is to cleave semenogelins in the seminal coagulum. Prostate Specific Antigen is secreted into prostatic ducts as an inactive 244–amino acid proenzyme (proPSA) that is activated by cleavage of seven N-terminal amino acids. PSA that enters the circulation intact is rapidly bound by protease inhibitors, primarily alpha1-antichymotrypsin, although a fraction is inactivated in the lumen by proteolysis and circulates as free PSA

A PSA blood test is the most effective test currently available for the early detection of prostate cancer. Higher than normal levels of PSA are associated with both localized and metastatic prostate cancer (CaP).

Prostate-specific antigen (PSA), also known as kallikrein III, seminin, semenogelase, γ-seminoprotein and P-30 antigen is a 34 kD glycoprotein manufactured almost exclusively by the prostate gland ; PSA is produced for the ejaculate where it liquifies the semen and allows sperm to swim freely. PSA is also believed to be instrumental in dissolving the cervical mucous cap, allowing the entry of sperm.

In addition to measuring human Prostate Specific Antigen in blood, tissue samples can be stained for the presence of PSA in order to determine the origin of maligant cells that have metastasized.

Source:
Steven P. Balk, Yoo-Joung Ko, Glenn J. Bubley
From the Cancer Biology Program, Hematology-Oncology Division, Beth Israel Deaconess Medical Center , Harvard Medical School , Boston, MA.