A retrospective cohort study showed that men who used statin drugs had a lower risk of prostate cancer but only with prolonged use or higher doses.

Men who had a history of treatment with statins was associated with a 15% reduction in the relative risk of low-grade prostate cancer and a 46% lower risk of developing high-grade disease. The association, however, was limited to men who took statins for at least 11 months or who had a specific defined daily dose of ≥121. This number is based on a reference dose of 20-mg simvastatin.

According to a report, lipophilic statins appeared to be more protective against prostate cancer than did hydrophilic drugs.

Researchers believe that mechanistically, statins have been found to reduce intracellular and serum cholesterol, and therefore may affect cell membrane organogenesis, steroidogenesis, and proliferation. Growth inhibition in prostate-derived cells lines was observed at clinically relevant statin concentrations.

This study adds to numerous others that preceded it, which collectively showed that statin use is associated with a lower risk of prostate cancer. The cumulative data does suggest only a modest effect on prostate cancer diagnosis.

Statins and Prostate Cancer

Over the past 15 years, statin use has increased dramatically, and as a class, the drugs are among the most widely prescribed medications in the world. It is thought that lowering serum and tissue levels of cholesterol may disrupt cellular lipid rafts, leading to reduced raft-dependent signaling and cell proliferation. And by extension, statins may have chemopreventive effects that reduce carcinogenesis, including prostate cancer carcinogenesis.

A recent study has found that eating dairy products has been linked to a higher chance of developing prostate cancer, and a plant-based diet appears to cut the risk.

In the past, some studies have found a link between consuming dairy products; such as milk and cheese; and prostate cancer. The disease is more prevalent in Western countries with the biggest consumption of calcium. The researchers in the study cited that prostate cancer is less common in Asian countries where such foods are consumed much less.

The team of Mayo Clinic researchers examined more than 47 existing scientific journal articles published between 2006 and February 2017, and involved more than 1 million participants in total.

The study results linked plant-based diets, such as vegetarian and vegan diets with a lower or unchanged risk of developing prostate cancer from the baseline.

Eating animal products, and dairy in particular, was associated with an increased or unchanged risk of being diagnosed with the disease.

Each year, approximately 175,000 new cases of prostate cancer are diagnosed, making it the most prevalent form of the disease among men other than skin cancer.

The disease is the second leading cause of cancer death in the U.S. after lung cancer, and kills around 31,620 people annually.

The study highlighted a cause for concern with high consumption of dairy products and the findings also support a growing body of evidence on the potential benefits of plant-based diets.

However, the study was limited because it included a range of different papers with varying methods. The researchers said that future research could test the validity of the findings by carrying out randomized control trials. Researchers would also like to look at the effects of other lifestyle factors like smoking and exercise.

A research team has been investigating the mechanisms driving prostate cancer progression and have been developing novel treatments and models to combat metastasis for the past 15 years. The team has mechanistically examined how cancer cells have been able to bypass immune cells and survive. The work initially started with the discovery that in advanced stages of prostate cancer, the cancer cells could not only escape immune system surveillance, but could also disable the immune system response.

The research found that the underlying mechanisms for these events came from the oncogenic stress-induced molecule called “MIC.” When found in healthy cells, MIC is not expressed on cell surfaces. However, the researchers discovered that during cancer development, and even at very early stages, prostate cells start to express MIC. MIC’s primary function is to “flag down” the immune cells, particularly the natural killer and cytotoxic T cells, to initiate their response in fighting cancer cells. However, it was found that in stages of advanced prostate cancer, the cancer cells have “chopped off” or eliminated the ability of MIC to “flag down” the immune cells.

Therefore, the cancer cells are able to bypass immune surveillance and roam free. Then, detrimentally, cancer cells release a soluble form of MIC, called sMIC, which shuts down the immune system and this allows for the cancer cells to “dodge” immune cells. When considered together, the research team reasoned that these mechanisms may explain the non-responsiveness to immunotherapy in patients with advanced prostate cancer.

The team developed a first-in-class monoclonal antibody to target sMIC. In preclinical models, the antibody has been found to “revive” immune system function and eliminate prostate cancer metastasis to solve this problem. The antibody has already shown promise in controlling metastasis of cancer cells when administered solo, and even in non-responders to immunotherapy. When it has been administered in combination with an immune checkpoint blockade, a synergistic anti-tumor effect occurred where both agents work to restore immune function.

The team is also working toward bringing this anti-sMIC antibody from preclinical to clinical use in humans. Plans are to conduct a preclinical safety assessment for clinical trials, examine how the antibody would work with current standards of care for prostate cancer, and investigate how to use the antibody to tackle neuroendocrine prostate cancer, the most lethal type prostate cancer.

After presenting the results of a new study, researchers have called for immediate action to recommend screening for prostate cancer for men with BRCA2 mutations over the age of 40.

It is widely known that BRCA mutations greatly increase the risk of breast and ovarian cancer in women with the disease. However they also increase the risk of several types of cancer in men, including prostate and breast.

Scientists have also determined that BRCA2 mutations are likely to increase the chance of a type of childhood cancer called non-Hodgkin lymphoma.

The sturdy research looked at almost 3,000 men aged 40-69, with just over half carrying inherited mutations in either BRCA1 or BRCA2, while the others were healthy controls. These men were screened with a common test for prostate cancer called the PSA (prostate-specific antigen) test.

The researchers found that the incidence of prostate cancer in men with BRCA2 mutations was significantly higher than in men with no BRCA mutations. They also determined that BRCA2 carriers were typically diagnosed when younger and had more substantial disease. However, there were no differences observed in men who carried BRCA1 mutations, compared to healthy controls.
The researchers feel that the study shows very clearly that men with the BRCA2 gene fault are at increased risk of aggressive prostate cancer and that regular PSA testing could go some way to improving early diagnosis and treatment.

The research indicates that men over the age of 40 who carry a mutation in the BRCA2 gene should undergo an annual PSA test as a way of identifying prostate cancer which in their case may be more aggressive.

1. If you are a man who has an inherited BRCA gene there is a possibility that if you develop prostate cancer, it will be at a younger age, and have a higher mortality rate.

2. Men who have been found to have a BRCA mutation have an increased risk for developing prostate cancer (3 – 8 times) compared to men without the BRCA mutation. Those men who have a family history of prostate cancer should talk with their doctor about whether genetic tests should be considered.

3. If you are a man who has been diagnosed with prostate cancer and also have a BRCA mutation, you are more likely to have an aggressive form of cancer. Knowing your BRCA status may be a key tool in helping your doctor anticipate the aggressiveness of your disease and evaluate treatment and management options.

4. In some cases a BRCA gene mutation may not be present when a man’s prostate cancer is first diagnosed, however it can occur over time. This is a reason why many doctors may discuss genetic testing at different times throughout the course of the disease.

5. Many experts suggest that men get tested to learn more about their genetic composition and BRCA status. Men who know their status can prevent misleading management options if diagnosed with prostate cancer and it can be determined whether they are at a higher risk of an aggressive form of cancer if diagnosed.

There are lots of spouses who will say that cancer didn’t just hit the husband, it hits the spouse/partner as well.

Like all cancer diagnoses, telling a man he has prostate cancer can force him — and his loved ones — to confront his mortality for the first time. But unlike many other cancers, prostate cancer often has a direct effect on the significant other, particularly in the form of erectile dysfunction, a common side effect of treatment, according to the Prostate Cancer Foundation.

The diagnosis can influence a man’s mental health and, in turn, his relationship. A 2014 review of 27 studies published in the journal BMJ Open concluded that the prevalence of depression and anxiety in men with prostate cancer, across the treatment spectrum, is relatively high. The diagnosis of cancer has a psychological impact on the body and mind.

Some side effects of treatment like incontinence can also influence a man’s behavior. Men may not feel comfortable socializing, and so spouses will believe he must be depressed but he may actually just anxious and doesn’t know how to deal with it.

On the upside, it’s possible for the mental health and relationships of survivors to actually improve after prostate cancer. Most men that go through treatment end up on the other side with a great quality of life, and their relationship is the same — sometimes even better because they have a new perspective on the important things in life.

In many countries rates of prostate cancer cases and deaths have declined or stabilized. The United States had the largest recent decrease in disease incidence, a recent study says.

Previous studies have indicated significant variation in prostate cancer rates, due to factors including detection practices, availability of treatment, and genetic factors.

By comparing rates from different countries, the differences in detection practices can be assessed and improvements in treatment can be determined.

The researchers examined long-term and short-term data from 44 countries with incidence data and 71 countries with prostate cancer death data.

There were 44 countries assessed for incidence. Prostate cancer rates rose in four countries and fell in seven, with the United States with the biggest decrease. In the other 33 countries rates remained stable.

Of the 71 countries assessed for prostate cancer death rates, there were decreases in 14, increases in three, and no change in 54.

As of 2012, prostate cancer was the most commonly diagnosed cancer among men in 96 countries and the leading cause of death in 51 countries, according to the study.

The findings confirm the benefits of prostate-specific antigen (PSA) screening. In the United States, incidence rates rose from the 1980s to the early 1990s, then declined from the mid-2000s through 2015, largely due to increased use of PSA screening.

This type of screening is less available in poorer nations, meaning that men there are more likely to be diagnosed at later stages of prostate cancer and more likely to die.

Some nations plan to scale back recommendations for PSA screening due to fears about possible overtreatment of prostate cancer that would never cause symptoms.

The U.S. Preventive Services Task Force recommends that men aged 55 to 69 undergo periodic screening after they’ve discussed the risks and benefits with their doctor.

“The screening recommendations were changed recently after further analysis of the U.S. data and we are now seeing more high-risk prostate cancer diagnoses that require treatment.

Future studies may monitor trends in mortality rates and late-stage disease to assess the impact of reduction in PSA testing in several countries.

A 29-year follow-up of the Scandinavian Prostate Cancer Group Study Number 4 (SPCG-4) trial has shown that radical prostatectomy is associated with a lower risk of prostate cancer–specific mortality vs. watchful waiting in men with clinically detected localized prostate cancer.

Investigators stated, “Radical prostatectomy reduces mortality among men with clinically detected localized prostate cancer, but evidence from randomized trials with long-term follow-up is sparse.

Study Details

IN THE TRIAL, 695 men with localized disease from 14 centers in Sweden, Finland, and Iceland were randomly assigned to radical prostatectomy or watchful waiting between October 1989 and February 1999. Follow-up data were collected through 2017. The cumulative incidence and the relative risks for death from any cause, death from prostate cancer, and metastasis were estimated, as were the numbers of years of life gained. The median follow-up was 23.6 years; the maximum observed follow-up time was 28.0 years, and the maximum potential follow-up time was 29.3 years.

By December 31, 2017, 294 men in the radical prostatectomy group (85%) had undergone a radical prostatectomy, and 52 men in the watchful waiting group (15%) had undergone curative treatment.

Treatment Outcomes

By Decmber 31, 2017, a total of 261 of the 347 men in the radical prostatectomy group and 292 of the 348 men in the watchful waiting group had died in the intention-to-treat population. Prostate cancer was the cause of death in 71 vs 110 patients. In the intent-to-treat analysis, the cumulative incidence of death from prostate cancer was 19.6% with radical prostatectomy and 31.3% with watchful waiting (absolute difference = 11.7 percentage points) at 23 years, with the relative risk for the complete follow-up period being 0.55 (P < .001) in favor of radical prostatectomy. The mean years of life gained in the radical prostatectomy group at 23 years was 2.9 years.

The cumulative incidence of death from any cause at 23 years was 71.9% in the radical prostatectomy group and 83.8% in the watchful waiting group (absolute difference = 12.0 percentage points), with the relative risk for the complete follow-up period being 0.74 (P < .001). The number needed to treat to avert 1 death from any cause was 8.4.

Men with clinically detected, localized prostate cancer and a long-life expectancy benefited from radical prostatectomy, with a mean of 2.9 years of life gained.

Distant metastases were diagnosed in 92 men in the radical prostatectomy group and 150 men in the watchful waiting group. The cumulative incidence of distant metastases at 23 years was 26.6% vs 43.3% (absolute difference = 16.7 percentage points), with the relative risk based on data from the complete follow-up period being 0.54 (P < .001).

The beneficial effect of radical prostatectomy was greater among men younger than age 65 vs 65 years of age or older at diagnosis, with the risk of overall mortality being 15.0 percentage points lower, prostate cancer mortality being 15.1 percentage points lower, and distant metastasis being 18.6 percentage points lower in the radical prostatectomy group than in the watchful waiting group. Among men 65 years of age or older, between-group differences were smaller for all 3 outcomes.

A per-protocol analysis was performed involving all patients who survived at least 1 year and based on treatments given during the first year. In this analysis, for radical prostatectomy vs watchful waiting, the relative risks were 0.70 (95% confidence interval [CI] = 0.59–0.83) for death from any cause, 0.45 (95% CI = 0.33–0.61) for prostate cancer death, and 0.43 (95% CI = 0.33–0.57) for distant metastases.

Radical prostatectomy vs. watchful waiting

Compared with watchful waiting, radical prostatectomy was associated with a reduced risk of prostate cancer–specific mortality.

Radical prostatectomy was associated with improved overall survival and a reduced risk of distant metastasis.

Among the men who underwent radical prostatectomy, a factor predictive of poorer prostate cancer survival was extracapsular extension (relative risk = 5.21, 95% CI = 2.42–11.22). Compared with a Gleason score of 3 to 6, the risk of prostate cancer mortality was increased in men with a Gleason score of 3 + 4 (relative risk = 5.73, 95% CI = 1.59–20.67) and among men with a Gleason score of 8 or 9 (no patient had a score of 10; relative risk = 10.63, 95% CI = 3.03–37.30).

A positive surgical margin was associated with a poorer prognosis in a model adjusting for age alone; however, after adjustment was made for extracapsular extension, prostate-specific antigen level, and Gleason score, the relative risk of death from prostate cancer for positive vs clear margins was no longer statistically significant (1.16, 95% CI = 0.62–2.15).

The investigators concluded: “Men with clinically detected, localized prostate cancer and a long-life expectancy benefited from radical prostatectomy, with a mean of 2.9 years of life gained. A high Gleason score and the presence of extracapsular extension in the radical prostatectomy specimens were highly predictive of death from prostate cancer.”

New research has found that prostate cancer cells change the behavior of other cells around them, including normal cells, by ‘spitting out’ a protein from their nucleus.

The researchers in the study believe that these tiny pieces of protein are taken up by the other cells, provoking changes that promote tumor growth and help the cancer hide from the body’s immune system.

This process has been captured on video by researchers at the University of Bradford and University of Surrey. The research was published in Scientific Reports.

For tumors to survive, grow bigger and spread they need to control the behavior of cancer cells and the normal cells around them and we’ve found a means by which they do this. Researchers think that blocking this process may be a potential target for future cancer therapy.

The researchers focused on a protein called EN2 that has a role in early development of the brain. This protein has also been found at high levels in many types of cancer cells.

The team highlighted the protein using a green florescent tag. The researchers then studied its activity in human prostate cancer cells, normal prostate cells and in bladder cancer, melanoma and leukemia cells. They found that both cancer and normal cells took up the protein from other cells.

The researchers also did time lapse photography of prostate cancer cells, taking pictures every five minutes for 24 hours. The resulting video shows the cells eject small parts of themselves containing the green florescent protein that are then taken up by otherwise dormant cancer cells, causing them to reactivate, changing shape or fusing together.

These findings may be significant because cell fusion in cancer is relatively unusual and is associated with very aggressive disease. It may lead to new and unpredictable hybrid cells that are frequently better at spreading to different sites and surviving chemotherapy and radiotherapy.

Molecular analysis of the normal prostate cells showed that take up of EN2 caused them to express a gene called MX2 that generates an anti-viral response.

It is thought that the cancer may be trying to minimize the chances of the cells around it being infected by a virus, to avoid scrutiny by the immune system. This could undermine the effectiveness of immunotherapy treatments, which try to use viruses to kill cancer by stimulating the immune system to attack it.

The researchers were surprised to find that the EN2 protein in the cell membrane as well as in the nucleus – which is very unusual for this type of protein. This provides an opportunity to block its action. The team was able to identify that part of the protein that was accessible at the cell surface to be a potential target for treatment.

Findings of a recent study suggest that drinking coffee may help delay risk of prostate cancer.

If the findings of a latest study can be believed, drinking coffee may help delay risk of prostate cancer. According to researchers, the findings could help pave way for treating drug-resistant cancer.

The recent study was performed by scientists from Kanazawa University in Japan who identified kahweol acetate and cafestol- hydrocarbon compounds naturally found in Arabica coffee — which may inhibit growth of prostate cancer.

The pilot study presented at the European Association of Urology Congress in Barcelona, suggested that kahweol acetate and cafestol may possibly play a role in inhibiting growth in cells that are resistant to common anti-cancer drugs like Cabazitaxel.

“We found that kahweol acetate and cafestol inhibited growth of cancer cells in mice, but the combination seemed to work synergistically, leading to a significantly slower tumour growth than in untreated mice,” said the lead author Mr. Iwamoto.

The study team tested six compounds that are naturally found in coffee, on proliferation of human prostate cancers cells in vitro (i.e. in a petri-dish). Their findings revealed that cells treated with kahweol acetate and cafestol grew more slowly than controls. The team then tested these compounds on prostate cancer cells, transplanted to 16 mice.

“After 11 days, the untreated tumors had grown by around three and a half times the original volume (342 per cent), whereas tumors in the mice treated with both compounds had grown by just over one and a half (167 per cent) times the original size,” Mr. Iwamoto said.

The growth reduction in transplanted tumor cells were much prominent that in native tumor cells.

Even though these are promising findings, they should not make people change their coffee consumption because it can have both positive and negative effects. More research is needed to find out more about the mechanisms behind these findings before anyone can consider clinical applications.