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NEXT MEETING

Tuesday, April 14, 2015 - 7:30PM

St. Andrews Presbyterian Church – Main St Markham

Rose Room (Downstairs)

(Free Parking off George St)

IN THIS ISSUE … .…Page 2

Study confirms genetic link between prostate and breast cancer .…Page 3

A New Screening Tool for Prostate Cancer .…Page 4

Improving Chemo Use in Prostate Cancer ….Page 6

Active surveillance 'may be appropriate' for intermediate-risk prostate cancer ….Page 8

Heart Disease Risk Higher With Androgen Deprivation Therapy in Prostate Cancer

Can fish oils help fight prostate cancer? Omega-3 may 'stop the growth of harmful cells' ….Page 10

Statins May Slow Prostate Cancer Progression Smokers at twice risk of prostate cancer recurring after surgery

….Page 11

SOCIAL MEDIA – VIDEOS UK scientists are finding new ways to 'starve' prostate cancer tumours to death

Prostate Cancer In The Family Increases Breast Cancer Risk ….Page 12 NOTABLE

"I received the call on my way to catch a flight last June…" (not just an old man’s disease!)

… Page 14 QUOTABLE

Contact Information

Group Discussion Have a question, a concern or not sure what’s next ? Attend our small group discussion and get feedback

from fellow survivors or just come and listen We’re here to share and support.

Spouses Always Welcome

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Study confirms genetic link between prostate and breast cancer KATHRYN DOYLE

Reuters Published Wednesday, Mar. 11 2015, 2:21 PM EDT

Women with close male relatives with prostate cancer are more likely to be diagnosed with breast cancer, a

new U.S. study confirms.

These findings, from the Women’s Health Initiative, reinforce the results of a 1994 study in the Journal of the

National Cancer Institute, the authors write.

“This is not the first study to examine this relationship, but it is one of the larger to date, if not the largest

study,” said lead author Dr. Jennifer L. Beebe-Dimmer of the Karmanos Cancer Institute in Detroit.

Cancer is a disease of the DNA, she said, and family clustering indicates that breast and prostate cancers

may have genes in common,

Beebe-Dimmer and her colleagues used data for more than 78,000 U.S. women in the Women’s Health

Initiative who were over age 50 and cancer-free when the study began in 1993. At the start they had

comprehensive physical exams and gave detailed personal and family medical histories.

Most women remained in the study for more than 10 years.

By 2009 there had been 3,506 new breast cancers in the original group.

Over all, more than 11,000 women had a first-degree relative – mother, sister or daughter – with breast

cancer, and this was more common for those who were eventually diagnosed themselves. Twenty per cent

of women with breast cancer had first-degree relatives with the disease, compared to nearly 15 per cent of

those who did not develop breast cancer.

There was a similar, but very slight, association with prostate cancer, the researchers reported in Cancer.

More than 11 per cent of women who developed breast cancer reported a first-degree relative with prostate

cancer, compared to about 10 per cent of women without the disease. Having a father, brother or son with

prostate cancer increased the risk of breast cancer by about 14 per cent.

Compared to women with no family history of breast or prostate cancer, those with a family history of both

were 80 per cent more likely to develop breast cancer, the authors found.

“We know that the major breast-cancer susceptibility genes BRCA1 and BRCA2 are also linked to prostate

cancer,” Beebe-Dimmer said. That may explain some of the clustering, she said.

Researchers have been reporting on familial links between breast and prostate cancer for 40 years, said Dr.

Mary-Claire King of the University of Washington School of Medicine in Seattle.

“It is good to see the link confirmed” in the Women’s Health Initiative, said King, who was not involved in

the new research.

“Both of these cancers are relatively common, so that it is possible when cancers are diagnosed in multiple

family members it may be due to chance,” Beebe-Dimmer said. “It may also be an exposure to something in

the environment.”

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The decision to increase breast-cancer screening will depend on how many male relatives have been

diagnosed with prostate cancer and at what age, she said, with more diagnoses at young ages being

particularly telling.

“Knowledge of breast-cancer family history is still extremely important,” Beebe-Dimmer said. She would

not recommend BRCA1 or 2 genetic testing for women with a family history of prostate cancer but no

history of breast or ovarian cancer. http://www.theglobeandmail.com/life/health-and-fitness/health/study-confirms-genetic-link-between-prostate-and-breast-cancer/article23406355/

A New Screening Tool for Prostate Cancer MARCH 05, 2015

“Often, one biopsy is not enough to definitively rule out prostate cancer,” says study researcher Jonathan

Epstein, M.D., director of the Division of Surgical Pathology and a professor of pathology, urology and

oncology at the Johns Hopkins University School of Medicine. “Our research finds that by looking for the

presence or absence of cancer in a different way, we may be able to offer many men peace of mind without

putting them through the pain, bleeding and risk of infection that can come with a repeat biopsy.”

The new research, called the Detection of Cancer Using Methylated Events in Negative Tissue

(DOCUMENT) study, suggests that an initial biopsy complemented with an epigenetic diagnostic test

accurately rules out the existence of cancer up to 88 percent of the time. The test, developed by MDxHealth,

which paid for the study, was described online in April in The Journal of Urology.

The test specifically captures the presence of chemical modifications to non-nuclear DNA sequences within

cells that commonly appear when prostate cancer is present. These so-called epigenetic changes, which add

a methyl group to the biochemical makeup of the DNA, alter the way genes function without changing their

foundational DNA sequence. The researchers analyzed tissue from biopsies from 320 men with elevated

prostate-specific antigen (PSA) levels whose results were negative for prostate cancer. The men were

patients at The Johns Hopkins Hospital; the University of California, Los Angeles; the Cleveland Clinic;

Eastern Virginia Medical School; and Lahey Hospital & Medical Center.

The epigenetic biomarkers the test detects reflect a process called DNA hypermethylation, in which a

methyl group is chemically attached to DNA — in this case, to genes called GSTP1, APC and RASSF1. These

genes are known to play prominent tumor suppressive roles in key cancer-related pathways. When these

genes are hypermethylated, they are commonly silenced, which can lead to a loss of this tumor-suppressing

function and the emergence of cancer.

Specifically, the GSTP1 gene acts as a detoxifying agent, preventing genomic damage by carcinogens.

Studies find that GSTP1 is methylated in up to 90 percent of prostate cancer cases, making it a strong

indicator of the disease.

For the study, pathologists compared methylation levels between the subjects’ initial tissue biopsies and

later tissue samples taken from each man done within 24 months of the first biopsy. They found that

average levels of APC and RASSF1 were about twice as high in the 92 subjects whose second biopsies

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yielded positive results, as compared to the 228 with two negative biopsies. For GSTP1, the levels were more

than eight times higher in the cancerous biopsies.

“It turns out as many as 20 percent of men have prostate cancer, even if their first biopsy results are

negative,” says Epstein, the Rose-Lee and Keith Reinhard Professor of Urologic Pathology. Approximately

40 percent of men with a negative biopsy go on to receive a second biopsy. Many high-risk men fear

sampling errors in their initial biopsy, which often leads to a high rate of follow-up procedures to merely

confirm the absence of the disease.

Initial biopsies are typically performed when men receive abnormal results on PSA screenings or digital

rectal exams. But an initial biopsy can sometimes miss cancer if none of the biopsy needles pass through the

cancer, leading to the false-negative results.

“With prostate biopsies, there is often very little cancer, which makes it difficult to perform molecular

prognostic and predictive tests,” says Epstein. “The DOCUMENT study overcomes this problem, because it

looks at benign tissue, not just the cancer. There is a lot of benign tissue, which is why we think it performs

so well.”

“Overall, if there is an absence of methylation in all three biomarkers, there is an 88 percent likelihood you

don’t have cancer,” Epstein says. “The test isn’t 100 percent of an assurance, but it is a major step forward.”

Jonathan Epstein, M.D., and Alan Partin, M.D., Ph.D., of Johns Hopkins contributed to the research, as well

as researchers from Maastricht University Medical Center, the Glickman Urological and Kidney Institute,

the UCLA Urology Department, Lahey Hospital & Medical Center, Eastern Virginia Medical School,

MDxHealth Inc. and Ghent University. Lead researcher Leander Van Neste, Ph.D., a consultant for

MDxHealth, may have stock or stock options. http://robbreport.com/health-and-wellness/prevention-treatment/johns-hopkins/new-screening-tool-prostate-cancer

Improving Chemo Use in Prostate Cancer Tue, 02/17/2015 - 12:21pm Thomas Jefferson University

Prostate cancer is the second leading cause of cancer for men in the United States. Only one class of

chemotherapy called taxanes is effective against the disease. A study published online in Clinical Cancer

Research, researchers have found that a newer member of the taxane family called cabazitaxel, an FDA

approved drug, has properties that could make it more effective for some patients - a hypothesis currently

being tested in clinical trials. Researchers also found a genomic marker that could help physicians identify

which patients might benefit most from cabazitaxel.

"It was surprising to find that cabazitaxel functions differently than docetaxel in killing cancer cells, even

though they're both taxanes," says senior author Karen Knudsen, Ph.D., Interim Director of the Sidney

Kimmel Cancer Center and a professor of cancer biology at the Sidney Kimmel Medical College at Thomas

Jefferson University. "It shows that we may not be taking full advantage of this next generation taxane in the

clinic."

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For years, docetaxel has been the only effective chemotherapy for men whose cancer was no longer

responding to hormone treatments. The next generation drug in the taxane family, cabazitaxel, was

approved in 2010, but only for patients whose cancer no longer responded to hormone therapy or docetaxel

treatment.

Knudsen and colleagues explored how cabazitaxel worked and demonstrated that it might be more effective

sooner in treatment. The researchers showed that cabazitaxel worked better than docetaxel in human

prostate cancer cells lines that were resistant hormone treatment, both in terms of slowing cancer-cell

growth and in its ability to kill cancer cells. Analysis of the tumor genes affected by the two drugs revealed

that cabazitaxel had a greater effect on cellular division and regulation of chromatin - a spool for DNA that

helps control which genes are in use and when - whereas docetaxel has a greater impact on DNA

transcription and repair. "This difference in mechanism suggests that we should treat these two drugs less

like members of the same family, and more like two distinct therapies that may each have distinct benefits

for certain patients," says first author Renée de Leeuw, a postdoctoral researcher in the department of cancer

biology at Thomas Jefferson University.

In order to test their hypothesis in a model that more closely mimicked human disease, the researchers also

tested the two drugs side-by-side on slices of tumors removed from patients during radical prostatectomy.

The tissues were grown on a 3D gelatin sponge, and two portions of the same tumor were treated with

either cabazitaxel or docetaxel. The results confirmed that cabazitaxel was more effective at killing tumor

cells than docetaxel. "The ability to test our ideas in tumor tissues removed from patients underscores the

unique and multi-disciplinary nature of our Prostate Cancer Program, one of only eight Prostate Cancer

Programs of Excellence in National Cancer Institute Designated Centers," said Dr. Knudsen. "Notably, key

contributors to the study included leaders in Urology, Medical Oncology and Radiation Oncology, Drs.

Leonard Gomella, W. Kevin Kelly, and Adam Dicker."

The collaborative research team also found a molecular marker that would help identify patients most likely

to benefit from cabazitaxel treatment. Knudsen and colleagues showed that tumors whose retinoblastoma

(RB) gene no longer worked were likely to become hormone resistant, but remarkably were more likely to

respond to cabazitaxel. "This gene could give us a way to identify patients who would benefit from

cabazitaxel earlier and reduce the trial and error of treating a cancer patient," says Dr. Knudsen.

Drs. Kelly and Knudsen are testing their hypothesis in a phase II clinical trial (ABICABAZI NCT02218606),

currently recruiting patients. The study is funded by Sanofi and conducted as a collaboration between

Sidney Kimmel Cancer Center and Memorial-Sloan Kettering Cancer Center. Patients with metastatic

prostate cancer who have not yet been treated with chemotherapy will be given either the second-line

hormone therapy abiraterone, or abiraterone in combination with cabazitaxel. In addition, researchers will

scan the tumors for their RB gene expression to test whether low levels of RB correlate with strong

responses to cabazitaxel.

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"These results from our laboratory research give us a strong reason to believe that this drug could be more

useful to some men earlier in their course of treatment," says Dr. Knudsen. "The ABICABAZI trial puts these

ideas to the test in humans, and if we are correct, has the capacity for the first time to tell us what patients

might most benefit from chemotherapy." Source: Thomas Jefferson University

http://www.dddmag.com/news/2015/02/improving-chemo-use-prostate-cancer

Active surveillance 'may be appropriate' for intermediate-risk prostate cancer Written by James McIntosh

Last updated: Sunday 22 February 2015 at 12am PST

Researchers have suggested that patients with favorable intermediate-risk prostate cancer could be treated

with active surveillance, similar to the way in which patients with low-risk prostate cancer currently can be.

Prostate cancer is one of the most commonly diagnosed tumors in the US, with an estimated 233 000 new cases diagnosed in 2014.

Active surveillance (AS) is a treatment method whereby the course of the cancer is monitored carefully, with

an expectation to start treatment immediately if the cancer is found to progress. AS is currently considered

for prostate cancer patients who have a life expectancy of at least 10 years and whose disease is considered

to be low-risk.

In the study, published in JAMA Oncology, the researchers state that no direct comparison has been made

between low-risk prostate cancer and favorable intermediate-risk prostate cancer pertaining to rates of

prostate cancer-specific and all-cause mortality following courses of high-dose radiotherapy.

Such a comparison is relevant, according to the study authors, as AS is currently only considered

appropriate for patients with low-risk prostate cancer per the guidelines of the National Comprehensive

Cancer Network (NCCN).

If patients with favorable intermediate-risk prostate cancer have rates of prostate cancer-specific and all-

cause mortality comparable to those experienced by patients with low-risk prostate cancer then AS could

also be an appropriate form of treatment for them, allowing these patients to avoid the clinical risks that

come with brachytherapy - a form of high-dose radiotherapy.

Currently, radiation therapy is the most common form of treatment for patients with all forms of prostate

cancer. Another new study, also published in JAMA Oncology, reports that around 57.9% of prostate cancer

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cases are treated with radiation therapy, whereas only 9.6% of cases are treated with watchful waiting or

AS.

"There remains an increased use of treatments in men diagnosed as having prostate cancer and underuse of

active surveillance in men with low-risk disease. There is an increased use of radiotherapy among all risk

groups and in particular patients with indolent disease with limited correlation according to tumor

biological characteristics and patient health," state the authors.

'Similarly low mortality estimates' observed following brachytherapy

For the study concerned with the implications for AS in men with favorable intermediate-risk prostate

cancer, Dr. Ann C. Raldow and colleagues analyzed data for 5,580 men with localized prostate cancer that

were treated at the Prostate Cancer Foundation of Chicago from 1997-2013.

They calculated the estimated risks of prostate cancer-specific and all-cause mortality following

brachytherapy and compared findings for patients with low-risk prostate cancer with those for patients with

favorable intermediate-risk prostate cancer.

A total of 605 patients (10.84%) died during the follow-up period. Among these, 34 patients (5.62% of total

deaths) died specifically due to prostate cancer. Overall, the authors report that the men with favorable

intermediate-risk prostate cancer did not have a significantly greater risk of mortality compared with men

with low-risk prostate cancer.

Specifically, 8-year estimates for prostate cancer-specific mortality were 0.48% for men with favorable

intermediate-risk prostate cancer, compared with 0.33% for men with low-risk prostate cancer. Similarly, for

all-cause mortality, the estimate was 10.45% for men with favorable intermediate-risk prostate cancer and

8.68% for men with low-risk prostate cancer.

"Despite potential study limitations, we found that men with low-risk prostate cancer and favorable

intermediate-risk prostate cancer have similar and very low estimates of PCSM [prostate cancer-specific

mortality] and ACM [all-cause mortality] during the first decade following brachytherapy," report the

authors.

The authors urge that their findings should be interpreted with caution as they are based on data taken from

a single institution and were not obtained from a randomized clinical trial. However, they also note that a

randomized trial of AS against treatment is currently being conducted in the UK.

In a related commentary, Dr. Fred Saad of the University of Montreal, Canada, suggests that these findings

require careful reflection:

"Although I am a urologist who has been practicing active surveillance for most of my low-risk patients for

many years, I suggest that we continue to be very cautious, and extremely selective, in offering AS to

patients with any features of intermediate-risk prostate cancer."

At the end of last year, Medical News Today reported on a study suggesting that physical activity is linked to

a lower risk of death in patients with localized prostate cancer. http://www.medicalnewstoday.com/articles/289788.php

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Heart Disease Risk Higher With Androgen Deprivation Therapy in Prostate

Cancer (HealthDay News) — March 14, 2015

For men with prostate cancer, the risk for incident cardiovascular disease (CVD) is increased with androgen

deprivation therapy, according to a study published in the Journal of Clinical Oncology.

Sean O'Farrell, from King's College London, and colleagues used data on filled drug prescriptions in

Swedish national health care registers to examine the risk for CVD associated with androgen deprivation

therapy in men with prostate cancer.

Data were collected in a cohort of 41,362 men with prostate cancer on androgen deprivation therapy and an

age-matched prostate cancer-free comparison cohort of 187,875 men. Overall, 10,656 men were on

antiandrogens ; 26,959 were on gonadotropin-releasing hormone (GnRH) agonists; and 3,747 underwent

surgical orchiectomy from 2006 to 2012.

Compared with the comparison cohort, the researchers found that the risk for CVD was increased in men on

GnRH agonists (HR for incident CVD=1.21) and in those who underwent orchiectomy (HR=1.16). The risk

for incident CVD, however, was decreased for men on antiandrogens (HR=0.87).

Men who experienced two or more CV events before therapy had the highest CVD risk during the first 6

months of androgen deprivation therapy vs. the comparison cohort, with HRs of 1.91 for GnRH agonist

therapy; 1.60 for antiandrogens; and 1.79 for orchiectomy.

"There should be a solid indication for [androgen deprivation therapy] in men with [prostate cancer] so that

benefit outweighs potential harm," the researchers wrote.

Several authors disclosed financial ties to Ferring.Reference O'Farrell S et al. J Clin Oncol. 2015;doi:10.1200/JCO.2014.59.1792.

http://www.endocrinologyadvisor.com/cardiovascular-disease-androgen-deprivation-therapy/article/402940/

Can fish oils help fight prostate cancer? Omega-3 may 'stop the growth of harmful

cells' Omega-3 fatty acids 'prevent growth and spread of prostate cancer cells'

Finding could pave the way for more effective cancer drugs, say experts

Omega-3s also found to reduce inflammation in the body and diabetes risk By Anna Hodgekiss for MailOnline

Published: 15:44 GMT, 18 March 2015 | Updated: 15:49 GMT, 18 March 2015

Fish oils could help in the battle against prostate cancer, new research suggests.

Scientists have discovered a mechanism by which omega-3 fatty acids prevent the growth and spread of

prostate cancer cells.

However the findings are at odds with a 2013 study asserting that omega-3s increase the risk of prostate

cancer.

Despite this, the new research 'points the way to more effective anti-cancer drugs,' the researchers claim.

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Scientists have discovered a mechanism by which omega-3 fatty acids (found in oily fish such as salmon)

inhibit the growth and spread of prostate cancer cells.

Scientists have long known that omega-3s reduce inflammation and have anti-diabetic effects, and some

recently discovered how this happens.

'But we're the first to show that they work this way in cancer,' said Kathryn Meier, a professor of pharmacy

at Washington State University.

'The attention has mostly been on inflammation and diabetes but there has always been an interest in

cancer, and we were the first to show this mechanism in any cancer cell at all.

And we're using prostate cancer, which is the most controversial subject in omega-3s.'

A 2013 study in the Journal of the National Cancer Institute found that men with higher levels of omega-3

fatty acids in their blood had a greater risk of developing prostate cancer.

It was not clear if the fatty acids came from food - certain fish, seeds and nuts are high in omega 3s - or

supplements like fish oil.

Working with prostate cell cultures, Professor Meier and two students found the fatty acids bind to a

receptor called FFA4, for 'free fatty acid receptor 4.'

Rather than stimulating cancer cells, the receptor acts as a signal to prevent growth factors, suppressing

proliferation of the cancer cells.

'This kind of knowledge could lead us to better treat or prevent cancer because now we know how it works,'

Professor Meier said.

The researchers said it's still unclear if the effect can be obtained by taking dietary supplements like fish oil

The study also found that a drug mimicking the action of omega 3s can work as well or better than fatty

acids in suppressing the cancer cells.

The study appears in the Journal of Pharmacology and Experimental Therapeutics.

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Professor Meier said it is still unclear if the effect can be obtained by taking dietary supplements like fish

oil.

Some people don't tolerate fish oil very well, she said.

Moreover, the effect of fish oil could fade as it is digested, while data from this study suggest that an omega-

3 drug needs to be in a cancer cell all the time to have an effect.

'It's very difficult in dietary studies to tell how much to take or what form to take,' Professor Meier said.

'Should you be eating fish?

'Should you be taking pills? But now we have a potential drug.

'Once you have a drug you can test very precisely whether it works or not in a certain disease and you

would know exactly how much to give people.' Read more: http://www.dailymail.co.uk/health/article-3000857/Can-fish-oils-help-fight-prostate-cancer-Omega-3-stop-growth-harmful-

cells.html#ixzz3UptKCfbR Follow us: @MailOnline on Twitter | DailyMail on Facebook

Statins May Slow Prostate Cancer Progression March 10, 2015

Statins may slow down prostate cancer in men who are also on androgen deprivation therapy, according

to new research.

The study's findings were presented recently at the American Society of Clinical Oncology's annual

Genitourinary Cancers Symposium, held in Orlando, Fla.

Lauren Christine Harshman, M.D., an assistant professor at the Dana-Farber Cancer Institute and Harvard

Medical School in Boston, and colleagues reviewed medical data from 926 prostate cancer patients being

treated with androgen deprivation therapy.

About 31% of the men were taking a statin at the time they began prostate cancer treatment. The researchers

noted that statin users were less likely to be initially diagnosed with aggressive prostate cancer.

Tracking the men's progress, researchers found that statin users had about 27.5 months of progression-free

survival on androgen deprivation therapy.

Men not taking statins had about 17 months of progression-free survival, according to the study. The link

remained statistically significant even after accounting for other factors.

"Patients on a statin have a significantly longer time to progression," Harshman told HealthDay. http://www.cancertherapyadvisor.com/prostate-cancer-progression-statin-effect-treatment/article/402676/

Smokers at twice risk of prostate cancer recurring after surgery Current smokers, and those who have quit smoking less than 10 years previously, have twice the risk of a

recurrence of prostate cancer after surgery, according to new research presented at the European

Association of Urology conference in Madrid.

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Prostate cancer is the third most common male cancer in Europe, accounting for over 92,000 deaths in 2012

(9% of male deaths). Around 30% of all prostate cancer patients treated with radical prostatectomy

experience biochemical recurrence (defined by an increase in PSA, prostate specific antigen) within 10 years

after surgery

An international group of scientists and clinicians from the USA and Europe retrospectively looked at

biochemical prostate cancer recurrence - in 7191 men who had had their prostate removed by radical

prostatectomy. Of these men, roughly a third were never smokers (2513, or 34.9%), a third were former

smokers (2269, or 31.6%) and a third were current smokers (3409, or 33.5%). These patients were followed

up for an average of 28 months.

The results showed that after a median of 28 months, current smokers had around double (HR 2.26) the

chance of the cancer recurring than did patients who had never smoked (see abstract below for full results).

Even those who had quit smoking within the last 10 years still had a significantly higher risk of cancer

recurrence, at about the same level (HR 2.03) as that for current smokers. It wasn't until 10 years after a

patient had quit smoking that the risk of cancer recurrence dropped significantly.

According to lead researcher Dr Malte Rieken (University Hospital, Basel, Switzerland):

"This is a new analysis, but it seems to confirm results we have seen in many other types of cancer: basically,

smoking increases the risk of cancer recurrence after initial treatment. Prostate cancer mortality varies

widely throughout Europe. The fact that cancer recurrence can vary so dramatically due to smoking is

probably one of the factors which may contribute to differences in prostate cancer mortality. It's just another

reason not to smoke at all, but the fact that the risk drops after 10 years means that anyone who has prostate

cancer, would be well advised to quit immediately."

Commenting former EAU Secretary-General, Per-Anders Abrahamsson (Malmo, Sweden) said:

"Prostate cancer is a leading cause of cancer death for man in the western world. A number of studies have

addressed how diet and environmental factors affect the risk of prostate cancer. This is the first report that

clarifies that smoking increases the risk of prostate cancer recurring after surgery and, therefore, a major

step forward to advise our patients to stop smoking when diagnosed with prostate cancer." http://medicalxpress.com/news/2015-03-smokers-prostate-cancer-recurring-surgery.html

SOCIAL MEDIA – VIDEOS UK scientists are finding new ways to 'starve' prostate cancer tumours to death http://www.theglobeandmail.com/life/life-video/video-cutting-off-the-blood-supply-to-prostate-

cancer/article23046385/

Prostate Cancer In The Family Increases Breast Cancer Risk https://www.youtube.com/watch?v=QKxMtxtnupw

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NOTABLE

Ed.note: You don’t need to be 50, 60 or older to get prostate cancer, Todd was less than 40!!

"I received the call on my way to catch a flight last June…" I was in the airport parking lot when my doctor called to deliver the news that I feared the most – I had

prostate cancer. I remember sitting there, stunned. Several things began running through my mind, over

and over: My kids. My wife. My loved ones. And death. I was too young to die. I wanted to be there for my

family. I wanted to see my children grow up.

I debated whether or not to call my wife, as I sat there. When I finally decided to call her, as soon as I heard

her voice, I started to cry. It was a tough day. Later I went from fear, to disbelief. I thought: This can’t be

right. I played in the NFL. I work out all the time. I’m in excellent shape. And I’m not even 40 yet. How

can this be happening?

But it was true. Prostate cancer can affect anyone. And every man is susceptible – old or young, married

or single – men from every walk of life have to know their risk for this disease, and they have to be

accountable for it! That’s why I want to reach as many men as I can to encourage them to be proactive

about their health. I want them to know that a simple PSA blood test can save their lives.

My father had prostate cancer many years ago, and knowing that critical piece of information made a

huge difference – because I knew I had to be on guard. That meant I got regular PSA blood tests, even in

my 30s.

Todd McMillon, his wife and 3 children

In January 2013, one of those PSA tests found an irregularity. It showed that my PSA levels were elevated,

and prompted my doctor to keep an eye on them. He asked that I return in 6 months for a follow-up. When

I did, the test revealed an even higher PSA level, and a biopsy was scheduled. The results of that biopsy

confirmed that I had prostate cancer.

When I next spoke with my doctor to arrange a consultation, he suggested that I bring my wife, Erin, with

me to the appointment. He said it was important that we come in together. Throughout the whole ordeal,

she was there to support me. When I was down, she picked me up.

After careful consideration, we decided that surgery was the best way to go. And that was the only time I

ever saw Erin cry, on the day of my surgery. When I asked her what was wrong, she said “we’re just finally

here”. It made me realize how incredibly strong she had been – and just how tough prostate cancer is on

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the entire family.

I underwent surgery that required ten small incisions in my abdomen to remove the prostate. I was in the

hospital only for a day, but it was difficult coming home, and seeing the look of concern on my children’s

faces. I’d always been so strong in their eyes – and prostate cancer had temporarily sidelined me.

A few days after the surgery, we found out that the cancer had been contained entirely within the prostate.

It had been a success. And we got through it together.

I think one of the biggest challenges for me was overcoming the embarrassment I initially felt when I was

diagnosed. I didn’t want to tell anyone, and I didn’t want word to get around. I was afraid people would

look at me differently; that now they weren’t going to see the man that I was – they would only see the

prostate cancer.

Standing up and saying “I had prostate cancer, and I’m a survivor” was even tougher than playing in the

NFL. There was no helmet – there was nothing to hide my face as I said those words to people.

But you know what? As I began to tell people, I realized just how unaware men are about this disease.

People had so many misconceptions about prostate cancer – and about the PSA blood test. And the more I

talked about it, the more men were going to the doctor and taking charge of their health.

I realized I could reach even more people if I worked with organizations like Prostate Cancer Canada (PCC)

because donor support helps PCC to fund the most innovative prostate cancer research, so that new

methods of diagnosis and treatment are always being developed. And it helps them spread the word about

prostate cancer, so that men will get that critical PSA test.

Together, we’ll encourage all men to be proactive and to “own their health”. That means men everywhere

– of all ages and backgrounds – can hear the message, face prostate cancer and overcome it. I applaud your

dedication to fighting this disease, and I hope you’ll send in your generous gift to Prostate Cancer Canada

today.

Sincerely,

http://www.prostatecancer.ca

PPCCCCNN MMaarrkkhhaamm

NNeewwsslleetttteerr

Volume 16 Issue 8 April, 2015

14 | P a g e

QUOTABLE

“If we had no winter, the spring would not be so pleasant: if we did not sometimes taste of adversity,

prosperity would not be so welcome.” Anne Bradstreet (1612 - 1672),

“Do not anticipate trouble, or worry about what may never happen. Keep in the sunlight”. Benjamin Franklin (1706 - 1790)

The Markham PCCN Prostate Support Group is generously supported by Dr John DiCostanzo, PCCN, Janssen Pharmaceuticals, St. Andrews

Presbyterian Church, and the Canadian Cancer Society.

The group is open to all; survivors, wives, partners, relatives and those in our community who are interested in knowing about prostate health.

Drop by St Andrews Presbyterian Church 143 Main Street Markham at 7:30PM, the 2nd Tuesday every month from September to June. The information

and opinions expressed in this publication are not endorsements or recommendations for any medical treatment, product, service or course of action by

PCCN Markham its officers, advisors or editors of this newsletter.

Treatment should not be done in the place of standard, accepted treatment without the knowledge of the treating physician.

The majority of information in this newsletter was taken from various web sites with minimum editing. We have recognized the web sites and authors

where possible.

PCCN Markham does not recommend treatment, modalities, medications or physicians. All information is, however, freely shared.

Email markhampccn@gmail.com

We look forward to your feedback and thoughts. Please email suggestions to markhampccn@gmail.com

PCCN Markham

Prostate Cancer Support Group Meets the 2nd Tuesday

Every month September – June

St. Andrew’s Presbyterian Church

143 Main St Markham

Website www.pccnmarkham.ca

Twitter https://twitter.com/pccnmarkham