Archive for the ‘General Cancer Research’ Category

As many as 1 million U.S. men have received treatment for prostate tumors that would have never threatened their lives

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Posted 02 Sep 2010 — by James Street
Category Prostate Cancer

NEW YORK (Reuters Health) – Adding to evidence that men with early prostate cancer can safely put off surgery, a new study finds that patients who delayed surgery by over a year had similar outcomes as those who opted for immediate treatment.

Using a national cancer database, Swedish researchers found that among 2,566 men with cancer confined to the prostate gland, there was no evidence that men who delayed surgery were in worse shape once they did have the procedure.

Their tumors, on average, were no more likely to have extended beyond the prostate or have abnormalities that indicate a more aggressive cancer than men who had surgery soon after diagnosis.

Moreover, their long-term survival was nearly the same, according to the study findings published in the Journal of Urology.

After eight years, 0.9 percent of men in the delayed-surgery group had died, versus 0.7 percent of those who’d had prompt surgery.

“Our findings show that if a man is diagnosed with a localized low-risk prostate cancer, there is no rush to decide which treatment choice (is) best,” lead researcher Dr. Benny Holmstrom, of Gavle Hospital in Sweden, told Reuters Health in an email.

He said the results add to evidence that some men can safely opt for what is called “active surveillance” — where prostate cancer treatment is deferred and the disease is instead monitored with regular PSA blood tests, digital rectal exams and possibly prostate biopsies.

The issue is important because increasingly, experts are calling for expanded use of active surveillance in managing prostate cancer.

Since the introduction of widespread prostate cancer screening with PSA tests, a growing number of men have been diagnosed with early-stage tumors. The problem with this is that prostate cancer is often slow-growing and non-aggressive, so many men may be diagnosed with tumors that would never have caused them problems had they gone undetected.

This means that for some men, prostate cancer treatment can do more harm than good, as treatment carries a risk of side effects — including long-term urinary incontinence and erectile dysfunction.

In general, active surveillance (also known as “watchful waiting”) is an option for men with cancer confined to the prostate gland that has a low risk of rapid progression; “low risk” is determined by factors such as a relatively low PSA level and an absence of abnormalities in the prostate tumor that indicate a more aggressive cancer. According to the National Cancer Institute, about half of the more than 190,000 U.S. men diagnosed with prostate cancer in 2009 would fall into this low-risk group.

For the current study, Holmstrom’s team used the Swedish Cancer Register to identify 2,344 men who underwent prompt surgery for low-risk cancer between 1997 and 2002, and 222 men who underwent surgery after a period of active surveillance. All had a radical prostatectomy, where the entire prostate gland and some surrounding tissue are removed.

Men in the former group typically had surgery three months after their diagnosis, while those in the latter group had the procedure 19 months after diagnosis — most often prompted by a rise in their PSA levels or other signs of progression.

Overall, the researchers found no significant differences between the two groups as far as adverse tumor features at the time of surgery that could affect their long-term prognosis. And over a typical follow-up of eight years, there was no significant difference in their survival.

Holmstrom pointed out, however, that longer term studies are still needed to see whether choosing active surveillance does have an impact years down the road.

“Whether active surveillance represents an equally safe treatment approach as radical prostatectomy or radiation therapy in the aspects of prostate-cancer-specific mortality remains to be elucidated,” he said.

A limitation of this study, according to Holmstrom, is that during the study period, Sweden had no widely used criteria regarding active surveillance — so the findings reflect the typical clinical practice in Sweden. Since clinical practice varies by country, it is not clear how well the results might translate to other nations, like the U.S., according to the researchers.

A key difference between Europe and the U.S., Holmstrom said, is that active surveillance appears to be less commonly used in the U.S.

A study published last year in the Journal of the National Cancer Institute estimated that since 1986, as many as 1 million U.S. men have received treatment for prostate tumors that would have never threatened their lives.

SOURCE: link.reuters.com/kyf78n Journal of Urology, online August 18, 2010.

Unleashing the Immune System: New Insights Into Cancer

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Posted 30 Aug 2010 — by James Street
Category Immune System

This book-length report details the origin and development of a little-known treatment of cancer utilizing a system for filtering the blood in order to achieve a beneficial effect, even in late-stages. The report explains the rationale for this treatment: the removal of certain specific factors from the blood that block the activity of tumor necrosis factor (TNF). It details the theories and achievements of an American hematologist/oncologist, M. Rigdon Lentz, MD, who helped pioneer the use of therapeutic apheresis (TA) for cancer a quarter century ago. Lentz and his physician wife now administer this treatment to patients in a private outpatient clinic in Germany. He also works with industry to perfect the production of new commercial medical devices, such as his unique Oncosorb™ affinity column.
An early version of Lentz’s treatment, called UltraPheresis,™ was based on a modified kidney dialysis machine. This was tested in clinical trials at the University of California Medical Center, Irvine (where Lentz was a professor) and at the Kennedy Hospital in Indio, Calif. Using this prototype device, Lentz was able to achieve objective anti-tumor responses in several kinds of cancer. I first described these results in my newsletter in 1994.
His early results were consistent with results seen in a dozen small clinical trials using TA as a cancer treatment in the 1970s and early-to-mid 1980s. But with the development of adsorption columns in the 1990s, Lentz was able to advance the art and science of TA for cancer beyond what was possible in earlier decades.
I visited Lentz in Germany in 2008, shortly after his Oncosorb device received the CE mark of conformity in the European Union. I returned several times afterwards, most recently in May 2010, to gain a better understanding of his methods and results. Needless to say, I think this is a very promising technique. Like most TA, it is minimally invasive (although it does require implantation of an indwelling catheter), and its effects depend on removal of two specific blocking factors from the blood, rather than adding toxic substances.
Although not a “magic bullet,” at least in the cases of advanced disease where it has been studied, its beneficial effects are demonstrated in this report. It can sometimes achieve classically defined tumor regressions (and improvement in quality of life) in situations in which other more toxic modalities are no longer viable.
Telling this story in a fair and comprehensive manner has engaged much of my attention for the past two years. I give the entire history of TNF and blocking factors (dating back almost a century), of TA’s once-widespread use in cancer, including a description of the dozen clinical experiments using similar methods performed around the world in the 1970s and 1980s. I also give the first biographical account of Dr. Lentz’s life and career, including a detailed explanation of his troubles with the Food and Drug Administration (FDA).
This downloadable (pdf) report is 170 pages in length, including 20 pages of scientific references and a listing of Lentz’s main patents and publications.
Several leading immunologists read and commented on advance copies of “Unleashing the Immune System.”
“This report is extremely good, very detailed and well documented as well as very interesting historically,” said Prof. Jacques Miller, AC, FRS, the discoverer of the two major subsets of lymphocytes, T cells and B cells, and their function. “I did not know much about the treatment of Rigdon Lentz. I think it is a pity he had to go to Germany in order to pursue his work.”
Meanwhile, Peter Hersey, MD, the first person to publish a paper on the use of TA in cancer, commented, “Ralph Moss has uncovered another rich vein in medical history.“

Testosterone supplementation and prostate cancer

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Posted 26 Aug 2010 — by James Street
Category Diet and Prostate Cancer, Prostate Cancer

KIRKLAND, WASHINGTON.

Conventional medicine wisdom has it that high levels of male sex hormones (androgens) are associated with an increased risk of prostate cancer and a more rapid tumour growth.

This has led to the use of chemical or physical castration in an attempt to reduce natural androgen production and thereby deprive the tumour of the androgen it supposedly requires to keep growing.

Unfortunately, the effect of castration is often temporary and subsequent tumours tend to be more virulent than the original one.

Now Dr. Richmond Prehn, MD of the University of Washington challenges the assumption that high androgen levels are a risk factor for prostate cancer.

Dr. Prehn points out that androgen levels decline with age whereas prostate cancer incidence rises sharply. He suggests that declining androgen levels may not only lead to benign prostate hyperplasia (BPH), but may also be the initiator of uncontrolled cell growth which may ultimately lead to cancer.

He further suggests that “androgen supplementation beginning early in the middle years might, among other possible benefits, largely prevent prostate cancer.”

Dr. Prehn cautions that androgen supplementation may be contra-indicated in older men who already have the seeds of prostate cancer. He also suggests that an alternating regimen of androgen deprivation and androgen supplementation should be evaluated as a therapy for prostate cancer.

Prehn, Richmond T. On the prevention and therapy of prostate cancer by androgen administration. Cancer Research, Vol. 59, September 1, 1999, pp. 4161-64

In the common cold, scientists find new hope for cancer treatment

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Posted 26 Aug 2010 — by James Street
Category Virus, genetic research



Posted by Laura Blue Thursday, August 26, 2010 at 5:34 pm
Submit a Comment • Related Topics: cancer medicine

New research on viruses may translate into new therapies to beat cancer, scientists say.

Molecular biologists at the Salk Institute have uncovered a previously unknown mechanism that allows adenoviruses – culprits behind the common cold as well as other illnesses — to beat the body’s immune system. Since adenoviruses and tumor growths both overcome our natural cellular defenses in a similar way, understanding one disease process can give us good clues for ways to fight the other, scientists hope.

Here’s how it works. Previous research has shown that the “p53″ protein is both a tumor suppressor, preventing cancer growth, and also important for keeping adenoviruses in check. When cancer invades one of the body’s cells, p53 will try to kill the cell outright to prevent the cell from being overrun. Adenoviruses also need to overcome p53 to replicate. Tumors and adenoviruses, therefore, have both adapted mechanisms of their own to knock out p53.

Scientists already knew about one mechanism by which adenoviruses can repress p53 function. But in the newly released research, published in the journal Nature, the Salk scientists analyzed adenoviruses with several induced mutations and discovered a second, previously unknown repressor of p53. That gives them a better idea of how adenoviruses overcome the body’s immune response to replicate successfully — and it hints at better ways to create new, genetically engineered viruses that would target and destroy tumors without otherwise causing harm to humans.

It sounds complicated. But Kevin Ryan, a molecular biologist and cancer researcher who was not involved with the study, explains why this finding is so important. Writing in an editorial published in the same journal issue as the original research, he says:

Undoubtedly, the greatest significance of this study will be its contribution to devising strategies to treat cancer. Adenoviruses must inactivate p53 so that they can replicate and subsequently induce the breakdown of the infected cell. Because many tumours lack p53 function, researchers have engineered viruses that lack E1B-55k [the previously known mechanism to wipe out p53] with the idea that these viruses would replicate selectively in tumour cells lacking p53 but not in normal cells, eventually leading to the death of the tumour cells.

In other words, scientists have already tried to engineer new viruses that would thrive only in tumors, killing off cancers. If cancer invades a healthy cell and wipes out the p53 function, then the lack of p53 allows the adenovirus to go in and take over the cell. With some genetic engineering to make sure that the adenovirus has no ability to repress p53 itself, the specially created virus should be of little threat to healthy cells — only a threat to the cancerous cells, where p53 function is suppressed.

Viruses like this have already been created. Ryan continues, however:

Although these engineered viruses have proven to be therapeutically beneficial, their replication does not seem to depend on the p53 ‘status’ of the cell.

They also weren’t as successful as treatments as people might have liked.

[The new] finding that [the second, newly uncovered p53 repressor] E4-ORF3 also, at least partly, inactivates p53 function provides an explanation for why this would be the case. Following on from these insights is the exciting prospect that adenoviruses lacking both [of the p53-blocking mechanisms] could be selective and even more potent anticancer agents than viruses lacking just E1B-55k.

Read more: http://wellness.blogs.time.com/2010/08/26/in-the-common-cold-scientists-find-new-hope-for-cancer-treatment/#ixzz0xmKrwIkM

New Drugs Offer ‘Extraordinary Hope’ in Skin Cancer Fight

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Posted 26 Aug 2010 — by James Street
Category genetic research

A new drug may change the landscape of melanoma treatment, offering patients a treatment option that goes beyond anything previously used against the skin cancer, new research shows. Tests in people whose melanoma had spread show the drug was able to shrink tumors in most patients and, in a few cases, even wiped the growths out, scientists report in the Aug. 26 New England Journal of Medicine. The compound targets the protein encoded by a mutated version of the BRAF gene that underlies melanoma in roughly half of all patients.

sciencenews“This demonstrates for the first time that a targeted therapy can work in melanoma,” says Richard Marais, a molecular biologist at the Institute of Cancer Research in London. “This is an enormous advance in the field. It’s just unparalleled.”

Early-stage melanoma that is confined to a spot on the skin can be surgically removed and in most cases stopped. But patients’ prospects take a deadly turn if the cancer metastasizes, or spreads, to other parts of the skin or to internal organs. Chemotherapy drugs benefit fewer than 20 percent of such patients. Survival outlook varies with the extent of the cancer’s spread and the age of the patient, but it is usually measured in months, not years.

The new drug is called PLX4032. Its impressive showing is actually the second dose of good news about melanoma to arrive this summer. In the Aug. 19 NEJM, scientists reported that another experimental drug, called ipilimumab, seems to extend survival in people with metastatic melanoma, and the Food and Drug Administration has fast-tracked its review of that drug.

A third study, published in 2008, found that melanomas arising from a much less common mutation — in a gene called C-kit — were susceptible to the leukemia-fighting drug Gleevec, or imatinib.

“This creates extraordinary hope for many melanoma patients,” says Alan Spatz, a pathologist at McGill University in Montreal. “For the first time in 40 years we have accumulated three studies that show extremely promising results.”

In the new study, medical oncologist Keith Flaherty of Harvard Medical School and Massachusetts General Hospital in Boston and a team of U.S. and Australian researchers treated 48 patients who had BRAF-related metastatic melanoma with PLX4032, which was devised by scientists at the pharmaceutical company Plexxikon in Berkeley, Calif. The drug neutralizes the mutant BRAF protein and stops it from triggering cell growth.

Of the 48 patients, 37 experienced tumor shrinkage of at least 30 percent. In three patients, the tumors resolved completely. This tumor suppression lasted from three months to about two years. Some patients remain on the drug.

On average, the patients getting the treatment relapsed after nearly eight months, Flaherty says. That happens because the tumors develop ways to subvert the effects of PLX4032. Those changes are the target of study now.

But the relapse rate hasn’t discouraged observers. “Patients are very rarely cured with a single drug in cancer,” Marais says. “You typically need a cocktail.”

Keiran Smalley, a molecular pharmacologist at the H. Lee Moffitt Cancer Center & Research Institute in Tampa, Fla., notes that metastatic melanoma is exceptionally hard to treat anyway. “I think people in the field hadn’t really believed that these kinds of responses would even be possible,” he says.

The other two new approaches to fighting melanoma target other biological pathways. Early tests suggest Gleevec or similar drugs such as nilotinib (sold as Tasigna) could thwart melanoma stemming from a mutation in the C-kit gene by stopping its rogue protein from sending growth signals to cells. But the C-kit mutation is uncommon, and such patients typically don’t have the BRAF mutation. So combining those drugs with PLX4032 wouldn’t yield an additional benefit, Marais says.

Ipilimumab might offer the possibility of a one-two punch since it works by unfettering the body’s own T cells — immune shock troops — to fight cancer. As such, it may have an additive effect when used in combination with PLX4032, Marais says.

Flaherty says a trial is being discussed now that would use both drugs against BRAF-mutation melanoma — employing PLX4032 to catch the cancer in its early stages and ipilimumab to “improve immune surveillance” and mop up tumor cells that evade the effects of PLX4032. “You’d like to think these two things would complement each other,” he says.

“This is clearly a turning point” in melanoma treatment, says study coauthor Paul Chapman, a medical oncologist at Memorial Sloan-Kettering Cancer Center in New York City. “It’s the first time we’re actually treating the genetics of the tumor.” In the past, melanoma metastases were all treated about the same, he says. “Now we have the advantage of knowing their genetic differences and we are able to exploit that.”

Read More http://www.wired.com/wiredscience/2010/08/new-melanoma-drugs/#ixzz0xmIPSkEp

‘Hippo Man’ to Get Surgery to Remove Massive Nose Tumor

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Posted 26 Aug 2010 — by James Street
Category Finance and Politics of cancer research and treatment

Thursday, August 26, 2010

A 41-year-old man in China has been dubbed “Hippo Man” after a facial tumor grew so large it pushed his eyes to the side of his head, AOL News reported.

Fei Jianjun noticed a tiny, red bump on the tip of his nose last year, but he “didn’t pay much attention” to it at first, he said.

Fei’s tumor grew into the size of a human fist and it now covers half of his face, which has resulted in him not being able to breathe through his nose. He said he did not seek medical treatment when the tumor began to grow because he is so poor, but a local hospital in Changchun, Jilin province offered him free surgery.

“I try my best not to go out, as my family is too poor to compensate others if I scare them and make them sick,” Fei said.

Fei’s doctor said without surgery and medical treatment, he would likely die within six months.

“We will give him radiation therapy first to shrink the tumor underneath, and then we’ll perform plastic surgery on him,” said Dr. Zhang Jianjun, of Jilin Military

General Hospital.

TIP: Testosterone Inactivating Pharmaceuticals

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Posted 26 Aug 2010 — by James Street
Category General Cancer Research, Prostate Cancer

PCRI Insights • www.PCRI.org

Someday soon, a nontoxic treatment for prostate cancer is going to come along.
Perhaps the new treatment will be straightforward, similar to the way we treat
precancerous skin lesions by freezing them with liquid nitrogen.
When that day comes, all the controversies and conflicts about treating
prostate cancer will fade away. Everyone will know the best thing to do. Men will simply take the treatment and move on with their lives. The present reality, however, is that the potential side effects of surgery or radiation are intimidating. No one knows who will end up with irreversible impotence or incontinence. With surgery or radiation there is no going back. It’s impossible to undo any harm that may have occurred.

A MEDICINE TO TREAT PROSTATE CANCER?

What if there were a highly effective treatment with reversible side effects, a
treatment that not only worked inside the prostate but also had anticancer
effects covering the whole body? Believe it or not, there is such a treatment
presently available – blockade of the male hormone testosterone, the type of treatment that Ralph describes in chapter 7.
Another of my patients, Max Leiber, a gentle, self-effacing accountant, first consulted
me in May of 1997. He was sixty-four, with an elevated PSA of 12 detected during a
routine insurance examination. He had intermediate grade disease in the right base
of the prostate with areas of low grade disease in the right apex and right mid-gland.
Endorectal MRI showed early spread of cancer a few millimeters outside the surface of the prostate. He started a one-year course of treatment with testosterone inactivating pharmaceuticals (TIP) in November 1997 and his PSA dropped to undetectable levels within five months. A biopsy in September 1998 showed no residual cancer. Five years later, in August 2003, a color Doppler ultrasound
demonstrated a subtle, illdefined lesion in the right mid-peripheral zone, and a biopsy showed recurrence of intermediate grade disease. A second cycle of TIP was started in September 2003.

One year later, biopsy of the previously abnormal areas was clear and TIP was stopped. Max continued on observation, and as of 2009 had a stable PSA of 1.67.

TIP:

Testosterone Inactivating Pharmaceuticals

Excerpted from INVASION OF THE PROSTATE SNATCHERS
by Ralph H. Blum and Mark Scholz, MD.

Copyright (c) 2010 Ralph H. Blum and Mark Scholz.

To be published by Other Press LLC. Scheduled Release Date: August 24, 2010

“Wars are not won
by fighting battles:
Wars are won by
choosing battles.”
— George Patton

The Doctor’s Tract

Testosterone Inactivating Pharmaceutic als FROM PAGE 16

The Essence of Mojo

Testosterone is the hormone that causes masculinization at puberty. Prior to puberty the prostate gland exists as a vestigial nubbin the size of your fingernail.
When the teenage surge in testosterone occurs, the gland expands to the size of a walnut and begins producing semen.

This remarkable transformation occurs because the cells of the prostate gland are uniquely sensitive to the presence or absence of testosterone. And because prostate cancer cells are derived from the prostate gland, the cancer cells retain the same dependency on testosterone for survival. Cancer cells can grow and proliferate
when testosterone is present; they shrivel up and die when testosterone is absent. When testosterone levels in the blood drop, the cancer cells literally commit suicide through a cellular process called apoptosis.

Ever since Charles Huggins discovered the beneficial effects of surgical castration for treating prostate cancer, urologists have followed a policy of reserving anti-testosterone therapy until the development of metastatic bone cancer. Since irreversible castration was the only means for lowering testosterone, a hesitation
to use such draconian means was understandable.

As repugnant as castration is, the anticancer results are undeniable. Doctor Huggins
was given the Nobel Prize for his discovery that castration could cause metastatic prostate cancer to go into remission. Today, thankfully, there are medications that
achieve similar or better results.

TIP Gets No Respect

When TIP was invented in the 1980s, doctors continued to adhere to the same old policy – they persisted in withholding treatment until the onset of bone metastasis. TIP for earlier-stage disease was scarcely considered. Bearing in mind that the main interest of urologists is surgery, this is hardly surprising. However, there is another reason the idea of TIP for newly diagnosed cancer has been very slow to catch on.

The medical community has wrongly assumed that remission in men with early-stage disease will be just as brief as in men with bone metastasis, lasting only three to six years.

This lack of understanding about TIP’s effectiveness in early-stage disease might have been understandable in the 1990s, before studies using TIP in early-stage disease were published. Now, however, we know that men who start TIP before the
onset of bone metastasis respond well for more than ten years before developing resistance to TIP.1

Long-Term Results With TIP

Being  medical  oncologists rather than surgeons, and being more impressed
by the toxicity of surgery than by its effectiveness, my partners and I hypothesized in
the early 1990s that medications powerful enough to reverse metastatic disease should be even more effective against less entrenched, early-stage disease.

Our initial experience bore out these suppositions. Jim Taylor, a podiatrist, came to our office in 1992 for his newly diagnosed prostate cancer.  His PSA was substantially elevated to 34 and his prostate biopsy showed Gleason 6 disease. Even though his scans were clear, his high PSA made us concerned about possible microscopic cancer outside the gland. Using TIP as primary therapy in that era was highly unorthodox.
Nevertheless we decided to proceed, encouraged by the knowledge that treatment could be stopped.

After two months Jim’s PSA was down to 0.3. A repeat prostate biopsy in June 1993 showed no evidence of any residual cancer! We decided to stop his TIP in February 1994 and by June of 1995 his testosterone blood levels were backto normal. As of 2009, Jim, now seventy-eight, continues to be under surveillance with periodiccolor Doppler ultrasound and PSA testing.He has never required any additional therapy and his PSA has been stable between 4 and 5.
Over the years we have seen hundreds of men with excellent responses to TIP. Larry McCoy is a professional musician diagnosed in May of 1996 at age seventy-five.
His PSA was 14 with a doubling time of fourteen months. Endorectal MRI in August 1996 showed a small prostate with bilateral tumor in the mid-gland and possible
early spread of cancer outside the capsule. At the end of a sixteen month course of TIP, his PSA was undetectable. A year later, an endorectal MRI showed marked
improvement. To this day, Mr. McCoy continues on Proscar as his sole form of therapy, with a stable PSA of 3 and a normal testosterone level of 381.
Tom Fox was first diagnosed with prostate cancer in January of 1997 at the age of seventy-eight. His initial PSA was 33. The prostate examination showed extensive
palpable disease. He started an eighteen-month course of TIP in February of that year. After he stopped, his testosterone recovered quickly. He has never required
any additional therapy other than Proscar. His last prostate ultrasound in September 2007 showed stable lesions in the left base and right mid-gland. In mid-2008, at the age of ninety his PSA was only 0.6.
We recently submitted for publication a scientific article detailing the twelve-year outcome for seventy-three men who embarked on TIP as primary therapy in the
mid 1990s. The average age of this group was sixty-seven. The average PSA was 9 with a Gleason score of 7 (intermediate grade). In most of the participants, the cancer was large enough to be felt by digital rectal examination prior to treatment. All
the men were treated with TIP and all seventy-three of them recovered their testosterone when TIP was stopped. Twenty-one of these men (29%) never needed any further therapy; a single course of TIP kept their PSA low indefinitely. Twentyfour men (33%) required periodic retreatment with TIP to keep their PSA levels under 5. Twenty-eight men (38%), rather than continuing on intermittent TIP, decided to have local therapy such as surgery, seeds or radiation. Their local therapy was performed, on average, five and a half years after the first cycle of TIP. Of these twenty-eight men who had delayed local therapy, only three developed a cancer relapse and none have developed metastasis.

TIP, A Totally Unique Form Of Cancer Treatment
Prostate cancer is the only type of cancer so exquisitely sensitive to hormone
blockade. Although women with breast cancer also benefit from hormonal manipulation, TIP for prostate cancer is approximately five times more effective than the best breast cancer therapy. Compared to other medical treatments such
as chemotherapy, TIP works much better and is far less toxic. Other than breast cancer, all the other types of cancer, such as colon, lung or stomach cancer, are completely immune to hormonal treatments. Almost all men treated with TIP
experience sharp declines in PSA down to undetectable levels.2

If they have a palpable abnormality on digital rectal examination, the nodule usually disappears within three to four months. We know that TIP does not completely eradicate every last prostate cancer cell. Microscopic evaluation of surgically removed prostate glands after eight months of TIP shows that total eradication
of cancer occurs only in a small minority of cases.3 However, studies done in our office show that after twelve months of TIP the amount of residual cancer is usually too small to be detected with a careful lesion directed biopsy using color Doppler
ultrasound.

Our belief is that using TIP as a primary therapy is eminently reasonable considering how well men with Low-Risk disease fare on active surveillance. If biopsy-positive Low-Risk disease can be safely monitored, why not use the same surveillance techniques to monitor men with TIP induced, biopsy-negative disease?
Criticisms of using TIP as primary therapy for Intermediate-Risk or High-Risk disease seem to be based more on an unwillingness to deviate from “the way things have always been done” than justifiable logic.

Some Basic Practicalities The medications that make up testosterone inactivating
pharmaceuticals fall into three different chemical categories: LHRH agonists,  anti-androgens and 5-alpha reductase inhibitors. Medicines in the first category such as Lupron, Zoladex, Eilgard and Vantas are administered as quarterly or annual shots. They work by sending a false hormonal message to the testicles via the pituitary gland, which turns off testosterone production.

The anti-androgens, pills such as Casodex, Eulexin and Nilutamide, work at the molecular level by interposing themselves between the testosterone molecule and the androgen receptor. This deactivates the androgen receptor and inhibits cell growth. The 5-alpha-reductase inhibitors, pills such as Proscar or Avodart, block the chemical conversion of testosterone into dihydrotestosterone, a substance five times
more potent than testosterone. Generally, a combination of these medications is used – one from each class – to attain the most potent anticancer results.

As you can tell, I have seen a lot of men benefit from TIP. One of the advantages is how easily the anticancer effects can be monitored with PSA. Within the first few
months of starting treatment, the degree of PSA decline reveals how well treatment is progressing. More than 95% of men with newly diagnosed disease see a drop in their PSA to less than 0.05 within eight months of starting therapy.2

Fortunately, it’s a rare cancer that continues to produce PSA above a threshold of 0.05 after six months of TIP therapy. However, when that is the case, additional treatment with radiation is required. These unusual types of prostate cancer are known to be much more dangerous.4

Even if the disease is not arrested altogether, TIPs usually delay cancer progression for many years.

Reading The Fine Print

So what’s the catch? Up to this point TIP sounds like a decidedly superior type of treatment. Basically, there are two problems. First is it may be hard to find a qualified
doctor who is familiar with up-to-date methods for administering TIP. Second, even though the side effects of TIP are manageable, they are not trivial. Adverse side effects like Ralph’s are all too common.

Without attention to diet, notable weight gain occurs. Without regular resistance training and weight lifting, significant muscle weakness will ensue. And perhaps most important of all, while on treatment, the majority of men have a total loss of
sex drive.

A loss of sex drive is different than impotence. With medications such as Viagra and Cialis most men on TIP can have erections sufficient for intercourse. 5 The problem is apathy, a low libido. Sex can be enjoyed, but it is not sought with the usual
male verve. Unfortunately, there is no known way to rejuvenate libido other than stopping TIP.  These issues – weight gain, muscle loss and low libido – are the biggest concerns. However, there is also the potential for additional side effects such as breast enlargement, osteoporosis, hot flashes and anemia. As dire as these side effects sound, they are preventable with proper medical management (chapter 16).

What About Heart Attacks?

Of even greater concern are claims from retrospective studies stating that TIP causes more heart attacks.6,7 The weakness of these retrospective studies is their failure
to account for the well-known fact that urologists generally reserve TIP for men who can’t have surgery, those most likely to have preexisting heart problems. However, there is a single prospective study that also argues for an increased risk of heart attacks with TIP.8  Offsetting this are higher quality prospective studies that either show no increased risk9,10,11 or an actual reduction in the risk of heart attacks.12 The question arises as to why researchers would be suspicious that TIP could induce
heart attacks in the first place. The reason is the weight gain that so commonly accompanies treatment with TIP. Putting on weight exacerbates diabetes, a condition
that is well known to be associated with an increased incidence of heart attacks.13,14
How then can we explain studies that report a reduction in heart attacks? The mechanism is the very same one that enables women to live five years longer than men. Women have fewer heart attacks because their blood is thinner and flows more freely, creating less trauma to the vasculature. Testosterone in men thickens the  blood by increasing the number of red blood cells, putting a greater strain on their hearts and blood vessels. The advantage of having greater numbers of red cells is that physical performance and endurance are enhanced. Nevertheless, at the same time, this thicker blood creates excess wear and tear on the walls of the blood vessels, leading to hardening of the arteries and more heart attacks and strokes at a younger age. When TIP lowers the testosterone levels, it thins the blood down into the female range.15

The controversies raging about TIP’s potential cardiac effects are rooted in the undeniable fact that weight gain and secondary diabetes significantly increase the risk for heart problems. However, the best prospective study evaluating this question shows that the net effect of TIP is an overall reduction in heart attacks by about 10%.

The beneficial effect of thinning the blood is apparently sufficient to offset the known increased risks from gaining weight.

Final Thoughts

There has been no incentive among surgeons and radiation therapists to support research into the viability of TIP as a treatment option for men with newly diagnosed prostate cancer. After all, it competes directly with surgery, their preferred method  of treatment. TIP is rarely presented or even discussed as a treatment alternative. Like all forms of prostate cancer treatment, it has undesirable side effects. However, at least men can “test the water” and determine its effectiveness and tolerability  without risking irreversible lifelong impotence or incontinence. If after starting treatment, a man feels that the side effects are excessive, therapy can be stopped and another form of treatment implemented.

The Patient’s View

By Ralph H. Blum

It amazes me that, even to this day, testosterone inactivating pharmaceuticals are still primarily utilized as a “salvage technique” for advanced cancers – meaning, you have been through surgery or radiation and the cancer has returned. Now, however, thanks in good measure to Mark’s unwavering commitment, that is changing. TIP is slowly becoming recognized by physicians – and even more to the point, by patients – as a viable, noninvasive alternative to surgery or radiation. Yes, there are the side effects we could do without, but that’s small potatoes compared with the advantages.And almost all of those side effects are reversible. So TIP has been my treatment of choice. It has bought me and my tortoise of a cancer time to wait for less toxic treatments to become available. I ended TIP in May 2004. Since then I have been taking Avodart and monitoring the cancer. But if at any point I need to start treatment again, then I can revisit TIP if Mark and I agree that it’s the best option.

Resources.

1. Judd Moul, Early versus delayed hormonal therapy for prostate specific antigen only recurrence of prostate cancer after radical prostatectomy. The Journal of Urology, March 2004.
2. Mark Scholz, Prostate cancer-specific survival
and clinical progression-free survival in men
with prostate cancer treated intermittently with
testosterone inactivating pharmaceuticals.
UROLOGY, September 2007.
3. Martin Gleave, Randomized comparative study
of 3 versus 8-month neoadjuvant hormonal
therapy before radical prostatectomy: Biochemical
and pathological effects. The Journal
of Urology, August 2001
4. Paddy Niblock, Rising prostate-specific antigen
values during neoadjuvant androgen deprivation
therapy: The importance of monitoring.
International Journal Radiation Oncology Biology
Physics. May 2006.
5. Mark Scholz, Re: Recovery of spontaneous
erectile function after never-sparing radical
prostatectomy with and without early intracavernous
injections of alprostadil: Results of a
prospective randomized trial. Journal of Urology
Letter, June 1999.
6. Nancy Keating, Diabetes and cardiovascular
disease during androgen deprivation therapy
for prostate cancer. Journal of Clinical Oncology,
September 2006.
7. Christopher Saigal, Androgen deprivation therapy
increased cardiovascular morbidity in men
with prostate cancer. Cancer, October 2007.
8. Anthony D’Amico, Influence of androgen suppression
therapy for prostate cancer on frequency
and timing of fatal myocardial infarctions.
Journal of Clinical Oncology, June 2007.
9. Michel Bolla, Duration of androgen suppression
in the treatment of prostate cancer. The
New England Journal of Medicine, June 2009.
10. Fritz Schroder, Early versus delayed endocrine
treatment of T2-T3 pN1-3 M0 prostate cancer
without local treatment of the primary tumor:
Final results of European organization for
the research and treatment of cancer protocol
30846 after 13 years of follow-up. European
Urology, January 2009.
11. Jason Efstathiou, Cardiovascular mortality
after androgen deprivation therapy for locally
advanced prostate cancer: RTOG 85-31. Journal
of Clinical Oncology, January 2009.
12. Urs Studer, Immediate or deferred androgen
deprivation for patients with prostate cancer
not suitable for local treatment with curative
intent: European organization for research
and treatment of cancer (EORTC) trial 30891.
Journal of Clinical Oncology, April 2006.
13. Payam Hakimian, Metabolic and cardiovascular
effects of androgen deprivation therapy.
British Journal of Urology International, August
2008.
14. Jennifer Yannucci, The effect of androgen deprivation
therapy on fasting serum lipid and
glucose parameters. The Journal of Urology,
August 2006.
15. Stephen Strum, Anemia associated with androgen
deprivation in patients with prostate
cancer receiving combined hormone blockade.
British Journal of Urology, June 1997

Treatment Choices for Early (Localized) Prostate Cancer

No Comments
Posted 26 Aug 2010 — by James Street
Category Prostate Cancer

6 PCRI Insights • www.PCRI.org
Updated Information and Insight
for Some Common Questions…

Grace Lu-Yao, Ph.D. and Siu-Long Yao, M.D.

Treatment Choices
for Early (Localized)
Prostate Cancer

Over the last two decades, prostate specific antigen (PSA) testing has
been able to diagnose prostate cancer at a much earlier stage, and we
have witnessed tremendous changes in the characteristics of prostate
cancer. This phenomenon was discussed in detail in the November, 2009
issue of Insights entitled, The Great Prostate Cancer Stage Migration (1). PSA
testing may find prostate cancer 6-12 years earlier than previous methods
(2, 3). This fact raises the possibility that previous data based on men
diagnosed at a later stage of cancer, through means other than PSA testing,
may not be applicable to patients who are diagnosed today. Using outdated
information may limit the accuracy and appropriateness of subsequent
decisions. Below are some common questions about this issue.
There seems to be a lot of controversy about whether to treat prostate
cancer that has not spread beyond the prostate (i.e., localized disease).
Some doctors and organizations say that this type of cancer should be
treated, while others say it should be monitored closely, and treated only if
needed. What is the basis of this controversy?

Because of screening, most prostate cancers diagnosed today (~93%) are
found at early stage and have not spread to other parts of the body (4). In
addition, we have known for a long time that this early type of prostate
cancer is extremely common. For example, in autopsy studies, approximately
50% of men in their 50s and more than 75% of men in their 80s have been
found to have early prostate cancer (5, 6).

No one would have known about this cancer if an autopsy had not been performed. These men all died of something other than prostate cancer, so treating their prostate cancer would not have been beneficial.

If so many men have prostate cancer (about 1 of every 6 men will be
diagnosed with prostate cancer), but relatively few die of prostate
cancer (about 1 of every 30 men will die of prostate cancer), who
should be getting treated, and who should be monitored closely?
Several studies (7, 8) have shown that men with low-risk disease
characterized by a Gleason score <7 (the Gleason score is a measure of
the aggressiveness of a cancer and ranges from 2 – 10, with 10 being
the most aggressive), who delay treatment until it is necessary, live
as long as men without prostate cancer. This makes some sense
because about 29 – 84% of prostate cancers would never have been
discovered (and would never bother or hurt these men) in the
absence of contemporary screening (e.g., PSA and rectal exam) (9-11).

When considering treatment, surgery (radical prostatectomy)
is one of the most common approaches, and the approach for
which much of the data exists. One of the best studies of surgery was
the Scandinavian Prostate Cancer Group 4 study (SPCG-4) which
randomly assigned men with early prostate cancer to surgery or no
surgery (12). In this study, surgery reduced overall deaths from 30%
to 24%, and deaths due to prostate cancer from 15% to 10% (12).

However, these survival benefits did not seem to occur in patients
over age 65 years. In addition, most of the patients in the study
(~95%) had disease that was somewhat more advanced than
that currently diagnosed through contemporary screening (12).
This is important because cancer diagnosed through contemporary
screening is much less likely to cause death in a patient compared
to disease diagnosed in earlier eras (such as the era when the SPCG-4
trial was conducted).

The Table below shows that prostate cancer diagnosed in the contemporary era (and treated only when necessary) has more favorable survival experience (about 94%- 98% survival at 10-year after diagnosis) than the same cancer diagnosed in earlier eras before the advent of PSA screening (about 77% – 85% survival at 10-year after
diagnosis).
Table.

Ten-Year Risk of Dying of Prostate Cancer according to
Cancer Risk Group for Men under 70 Years of age without Initial
Attempted Curative Therapy Author Year of Diagnosis

Risk Group 10-Year Risk of Death Due to Prostate Cancer Contemporary PSA Era
Stattin (13) 1997 – 2002 One lobe of prostate affected & PSA <10 & Gleason score <7
2% Stattin( 13) 1997 – 2002 Both lobes of prostate affected or PSA ≥10 or Gleason score ≥7 5%

Lu-Yao (8) 1992 – 2002 One lobe of prostate affected
2%

Lu-Yao (8) 1992 – 2002 One or two lobes of prostate affected
6%

Pre-PSA Era Albertsen (14) 1971 – 1984 One or two lobes of prostate
affected
21%

Johansson (15) 1977 – 1984 One or two lobes of prostate affected
15%

Lu-Yao (7) 1983 – 1992 One or two lobes of prostate affected
23%

Because early-stage low-risk disease is less likely to harm a patient, the risk of unnecessary treatment correspondingly increases. Taken together, this information suggests that there may not be reasonable proof of benefit from surgery in cancers
with Gleason score <7, or men who are >65 years of age. Information about the potential benefits of other treatment approaches is more difficult to find. For example, thereare no definitive studies (i.e., randomized trials) that have evaluated
primary androgen deprivation (hormonal therapy), radiation therapy,
brachytherapy (seeds), cryotherapy (freezing), robotic radical prostatectomy,
photon-beam or intensitymodulated radiation therapy compared to delaying treatment until it is necessary (16).

All cancer therapies are associated with substantial side effects. For example, urinary leakage is  more common with radical prostatectomy (35%) than with radiation
therapy (12%) or androgen deprivation (11%) (16). Erectile dysfunction (ability to maintain an erection) occurs frequently after all treatments (radical prostatectomy,
58%; radiation therapy, 43%; androgen deprivation, 86%) (16, 17). Adjuvant hormone therapy was associated with worse outcomes across multiple qualityof-
life domains among patients receiving brachytherapy or radiotherapy (18). Patients treated with brachytherapy often report having long-lasting urinary system
irritation, bowel and sexual symptoms, and transient problems with vitality or hormonal function (18).
Many of these treatment-related adverse events are worsened by obesity, a large prostate size, a high PSA value, and older age (18).

In summary, the choice of treatment approach is truly a personal matter. Cancer doctors like to see the good, even in very challenging situations. We like to say that the glass is half full. Others can look at the same situation and say that the
glass is half empty. Each person’s focus will be different depending on whether he feels that he needs to fight the cancer and risk side effects from treatment, or whether living with the cancer (and its side effects if it progresses) will be OK. We have
entered a new era and it is safe to say that many patients can now live with their cancer just like patients with diabetes or heart disease or other chronic diseases can live with their ailments. People do die of these diseases, but many more can
make peace, and live with them.

Should I get a second opinion to help me with my treatment decision?
Yes. Second opinion and multidisplinary approach may provide different perspectives and more comprehensive information. As researchers, healthcare providers, and scientists, we try to provide clear and objective information. However, each of us believes strongly in what we do, and each of us anxiously
wants to help. Sometimes, during all the confusion following a new diagnosis of cancer, both healthcare providers and patients can inadvertently mix up fact and
opinion.

Siu-Long Yao, MD
Executive Director, Oncology Clinical Research
Merck Research Laboratories
Clinical Assistant Professor
Medical Oncology
Cancer Institute of New Jersey

Dr. Yao is responsible for Phase I-III clinical development of numerous
oncology drugs and biologics at Merck Research Laboratories. He is also a
clinical assistant professor at the Cancer Institute of New Jersey where he specializes in genitourinary oncology.

Dr. Yao holds a B.A. in chemistry and a B.A. in biochemistry, both from the University of Pennsylvania. He attended Yale University School of Medicine and completed Internal Medicine internship and residencies at Dartmouth-
Hitchcock Medical Center in Hanover, NH. Following residency, Dr. Yao completed subspecialty fellowship training in hematology, and oncology, both at Johns Hopkins. He is a Board certified internist, hematologist, and oncologist.

For example, although specialists may present various options, most overwhelmingly “recommend” the therapy that they themselves deliver (19). In a national survey of physicians, 93% of urologists chose radical prostatectomy as the preferred
treatment option, while 72% of radiation oncologists believed surgery and external beam radiotherapy were equivalent treatments (19). In addition, healthcare professionals tend to recommend particular types of treatment in specific regions of
the country (20, 21). For example, in the late 1980s and early 1990s, the
rate of radical prostatectomy in the Northwest region was more than five times that in the Northeast region (20). Getting a second opinion can help. Hearing things a second
time, after the initial shock of the diagnosis, can help you make that distinction. A different specialist may have a different preference, and you can hear another side of the story. Don’t be dismayed if you hear something different each time you talk to someone else. I often tell my patients that doctors in the US are amongst the most tested in the world. We have to constantly pass a test every few years to get, and
maintain, licensure and certification.
If there was a single correct answer for everyone, we would have had to provide that same answer over and over again on each test, and each patient would get the same answer every time the situation arose. The fact is, though, that there is no one
correct answers. The art of medicine is finding the answer that is best for
each patient.
References
1. Cavanagh WA. The great prostate cancer stage migration.
In: Insights. Los Angeles, CA: Prostate Cancer Research
Institute; 2009. p. 12-15.
2. Draisma G, Boer R, Otto SJ, van der Cruijsen IW, Damhuis
RAM, Schroder FH, et al. Lead Times and Overdetection
Due to Prostate-Specific Antigen Screening: Estimates From
the European Randomized Study of Screening for Prostate
Cancer. J Natl Cancer Inst 2003;95(12):868-878.
3. Brawley OW. Prostate cancer screening: Clinical
applications and challenges. Urol Oncol 2004;22(4):353-7.
4. Shao YH, Demissie K, Shih W, Mehta AR, Stein MN, Roberts
CB, et al. Contemporary Risk Profile of Prostate Cancer in
the United States. J Natl Cancer Inst 2009.
5. Sakr WA, Haas GP, Cassin BF, Pontes JE, Crissman JD. The
frequency of carcinoma and intraepithelial neoplasia of
the prostate in young male patients [see comments]. J Urol
1993;150(2 Pt 1):379-85.
6. Gronberg H. Prostate cancer epidemiology. Lancet
2003;361(9360):859-64.
7. Lu-Yao GL, Yao SL. Population-based study of long-term
survival in patients with clinically localised prostate cancer
[see comments]. Lancet 1997;349(9056):906-10.
8. Lu-Yao GL, Albertsen PC, Moore DF, Shih W, Lin Y, DiPaola
RS, et al. Outcomes of localized prostate cancer following
conservative management. Jama 2009;302(11):1202-9.
9. Draisma G, Etzioni R, Tsodikov A, Mariotto A, Wever E,
Gulati R, et al. Lead time and overdiagnosis in prostatespecific
antigen screening: importance of methods and
context. J Natl Cancer Inst 2009;101(6):374-83.
10. Schroder FH, Hugosson J, Roobol MJ, Tammela TLJ,
Ciatto S, Nelen V, et al. Screening and Prostate-Cancer
Mortality in a Randomized European Study. N Engl J Med
2009:NEJMoa0810084.
11. McGregor M, Hanley JA, Boivin JF, McLean RG. Screening
for prostate cancer: estimating the magnitude of
overdetection. CMAJ 1998;159(11):1368-72.
12. Bill-Axelson A, Holmberg L, Ruutu M, Haggman M,
Andersson SO, Bratell S, et al. Radical prostatectomy versus
watchful waiting in early prostate cancer. N Engl J Med
2005;352(19):1977-84.
13. Stattin P, Holmberg E, Johansson J-E, Holmberg L, Adolfsson
J, Hugosson J, et al. Outcomes in Localized Prostate Cancer:
National Prostate Cancer Register of Sweden Follow-up
Study. J. Natl. Cancer Inst. 2010:djq154.
14. Albertsen PC, Hanley JA, Fine J. 20-year outcomes following
conservative management of clinically localized prostate
cancer. Jama 2005;293(17):2095-101.
15. Johansson J-E, Andren O, Andersson S-O, Dickman PW,
Holmberg L, Magnuson A, et al. Natural History of Early,
Localized Prostate Cancer. JAMA 2004;291(22):2713-2719.
16. Wilt TJ, MacDonald R, Rutks I, Shamliyan TA, Taylor BC,
Kane RL. Systematic Review: Comparative Effectiveness
and Harms of Treatments for Clinically Localized Prostate
Cancer. Ann Intern Med 2008;148(6):435-448.
17. Stanford JL, Feng Z, Hamilton AS, Gilliland FD, Stephenson
RA, Eley JW, et al. Urinary and sexual function after radical
prostatectomy for clinically localized prostate cancer: the
Prostate Cancer Outcomes Study. Jama 2000;283(3):354-60.
18. Sanda MG, Dunn RL, Michalski J, Sandler HM, Northouse
L, Hembroff L, et al. Quality of Life and Satisfaction with
Outcome among Prostate-Cancer Survivors. N Engl J Med
2008;358(12):1250-1261.
19. Fowler FJ, Jr., McNaughton Collins M, Albertsen
PC, Zietman A, Elliott DB, Barry MJ. Comparison of
recommendations by urologists and radiation oncologists
for treatment of clinically localized prostate cancer. JAMA
2000;283(24):3217-22.
20. Lu-Yao GL, McLerran D, Wasson J, Wennberg JE. An
assessment of radical prostatectomy. Time trends,
geographic variation, and outcomes. The Prostate Patient
Outcomes Research Team. Jama 1993;269(20):2633-6.
21. Potosky AL, Harlan LC, Stanford JL, Gilliland FD, Hamilton
AS, Albertsen PC, et al. Prostate Cancer Practice Patterns
and Quality of Life: the Prostate Cancer Outcomes Study. J
Natl Cancer Inst 1999;91(20):1719-1724
Dr. Grace Lu-Yao is a cancer epidemiologist whose primary research
interest includes study of the epidemiology of prostate cancer and
outcomes assessment of prostate cancer therapies. She received her
graduate training in health services research and epidemiology at
Yale University. After her doctoral training, Dr. Lu-Yao received a
faculty appointment at Dartmouth Medical School and worked with
Dr. John E. Wennberg, the founding father of outcomes research and
evidence-based medicine. Many of her research findings have been incorporated in guidelines and
featured in highly respected medical journals with wide media coverage.
Grace Lu-Tao, Ph.D.
Cancer Institute of New Jersey
Robert Wood Johnson Medical School

Greyhounds and bone cancer research

1 Comment
Posted 25 Aug 2010 — by James Street
Category Dog Osteosarcoma

Lisa Stone’s 7-year-old greyhound was bred for the racetrack, but it was another facet of Tex’s breed that determined his fate.

Greyhounds are more likely than most dogs to die of osteosarcoma, a bone cancer. The disease robbed Tex of his right front leg. It also took the lives of Stone’s other greyhounds, causing her to ask why certain breeds are more susceptible to the disease.

Researchers may soon have answers, thanks to a study that may well have implications for human sufferers as well.

Phoenix-based Translation Genomics Research Institute recently launched a $5.3 million canine-cancer project to study the genetic link between cancers and specific breeds of dogs, including greyhounds and osteosarcoma.

TGen has partnered with the Van Andel Research Institute in Grand Rapids, Mich., to create the Canine Hereditary Cancer Consortium. The project will analyze DNA samples from thousands of dogs in the hopes of unlocking the genetic secrets to types of cancers called sarcomas.

For Stone, the research is a godsend. The founder of a Scottsdale law firm treats Tex and her two Ridgebacks, Layla and Larry, like her children.

“I’m the crazy dog parent,” she said, offering proof: When Tex was in the hospital after his amputation, she stayed at his bedside for eight to nine hours a day.

And when her first greyhound had his hindquarters amputated due to osteosarcoma, she slept on the living-room floor with him for more than a year because he couldn’t climb the stairs to her bedroom.

While aimed at canines, TGen’s research may benefit people as well. Jeffery Trent, president and research director at TGen, said dogs and humans suffer the same types of cancers. However, some forms that are rare in humans are extremely common in certain breeds of dogs.

His hope is that collecting canine samples will help researchers learn more about these rare human cancers.

Mark Neff, the geneticist directing the study, said findings may aid in the treatment of such cancers, which occur in numbers that draw comparatively little in research funding.

The bulk of the canine project’s funding comes from a two-year, $4.3 million federal stimulus grant. An additional $1 million was donated by Phoenix-based PetSmart as well as Hill’s Pet Nutrition.

More than 30 researchers at nearly a dozen institutions, including the National Cancer Institute, will be involved with the project.

Trent, who has a Labrador named Honey Bear, said no dogs would be harmed (or housed by TGen) during the harvesting of DNA.

“To collect the DNA, we just need a little slobber, and trust me, with my Labrador, you can get plenty of it,” Trent said.

Veterinarians across the country are assisting the effort, collecting DNA samples from their patients.

Among them is Betsy Hershey, who is Tex’s oncologist at Integrative Veterinary Oncology in Phoenix. While treatments have improved – Tex has been cancer-free for 25 months, thanks to chemotherapy – she hopes TGen’s research will shed light on the illness and its correlation to certain breeds.

Hershey is not alone in her hopes. Other veterinary oncologists believe research could lead to improved treatments, for humans as well as their four-legged friends.

“There is a lot to be gained from this research,” said Jennifer Arthur, a radiation oncologist at Arizona Veterinary Specialists. “We could potentially use the data gained to improve the drugs we use and to get them on the market for humans sooner.”

Many characteristics of dogs make them a genetic researcher’s best friend: a compressed life span, selective breeding and fewer privacy constraints.

Valana Wells, a dog breeder in Scottsdale, said that centuries of selective breeding have created canine populations with very similar DNA.

And her interest in the project is personal as well. Wells raises Clumber spaniels, a breed that suffers a high rate of hemangiosarcoma, a soft-tissue cancer.

“This breed has a very small gene pool, so there’s not a lot of genetic variation,” Wells said. That similarity among Clumber spaniels makes it easier to identify what variation is likely causing the cancer among the breed.

Wells is keeping a close eye on her 10-year-old spaniel, because roughly half of dogs 10 and older die of cancer-related causes, according to Trent. However, with proper treatment, some dogs are able to enjoy a high quality of life after being diagnosed with cancer, according to Arthur.

Greyhound aficionado Stone is happy that Tex has survived so long and has not been slowed by the loss of a leg. Though he hops more than runs, Tex loves to play fetch and simply run in spurts.

But Stone anticipates the day the cancer may return, when she will try to make him as comfortable as possible and try to put aside her grief.

“At that point, it’s not about you anymore,” she said.

Still, Stone is encouraged by TGen’s project.

“It gives people hope, and the way they translate the research to humans is incredible,” she said.

Read more: http://www.azcentral.com/arizonarepublic/arizonaliving/articles/2010/08/26/20100826dogcancer0826.html#ixzz0xgRQnabt