Download September Kick Off Meeting

PCCN Markham
Volume 16 Issue 8
Newsletter
April, 2015
NEXT MEETING
Tuesday, April 14, 2015 - 7:30PM
St. Andrews Presbyterian Church – Main St Markham
Rose Room (Downstairs)
(Free Parking off George St)
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
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
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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 allcause 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 omega3 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-harmfulcells.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-prostatecancer/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
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PCCN Markham
Volume 16 Issue 8
Newsletter
April, 2015
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)
PCCN Markham
Prostate Cancer Support Group
Meets the 2nd Tuesday
Every month
September – June
St. Andrew’s Presbyterian Church
143 Main St Markham
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 [email protected]
We look forward to your feedback and thoughts. Please email suggestions to [email protected]
Website www.pccnmarkham.ca
Twitter https://twitter.com/pccnmarkham
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