Prostate cancer is the most common form of cancer in men and the second most common cause of cancer death after lung cancer. This year, an estimated 217,730 men will be diagnosed with the disease, and 32,050 men will die from it, reports the American Cancer Society. Moreover, prostate cancer is the most common malignancy among older men: 64 percent of new cases in the United States this year were diagnosed in men older than 65, and 23 percent in men above 75.

Yet most studies delving into optimal treatment options focus on men younger than 75. The new UCSF study is among the first to explore the relationship between age, disease risk and survival among prostate cancer patients.

The researchers studied men in the Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE) database, a longitudinal, observational disease registry of men with prostate cancer who were recruited from urology practices throughout the United States. At the time of the study, the database contained information on 13,805 patients. The scientists found that older patients are more likely to have high-risk prostate cancer at the point of diagnosis, and less likely to receive potentially curative local therapy. Yet when older, high-risk men received more aggressive treatment, they had a 46 percent lower death rate compared with patients treated more conservatively with hormonal therapy or watchful waiting.

Older men with high-risk prostate cancer frequently are offered fewer – and less effective – choices of treatment than younger men, potentially resulting in earlier deaths, according to a new UCSF study.

The scientists found that men above age 75 with high-risk prostate cancer often are under-treated through hormone therapy or watchful waiting alone in lieu of more aggressive treatments such as surgery and radiation therapies. Instead, say the researchers, old age should not be viewed as a barrier to treatments that could lead to potential cures.

“There is a disconnect between risk and treatment decisions among older men,” said senior investigator Matthew R. Cooperberg, MD, MPH. “Patient age is strongly influencing treatment decisions, so we sought to understand whether age plays a role in risk of the disease and survival. We found that under-treatment of older-men with high-risk disease might in part explain higher rates of cancer mortality in this group. There is also pervasive over-treatment of low-risk disease in this age group. Overall, treatment needs to be selected more based on disease risk and less based on chronologic age.”

Prostate cancer is one of the most common cancers diagnosed in the US and Europe, and the most common way to test for it non-invasively is the PSA blood test, which is routinely done in some countries for men aged 50 and over.

However, while generally speaking the higher the level of PSA, the more likely it is that the patient has prostate cancer, PSA can also be raised for other reasons, such as due to an enlarged but benign prostate or an infection. The result would still have to be confirmed with a biopsy of the prostate, which is invasive, and not without risk.

A study recently concluded that DNA mutations throughout the mitochondrial genome seemed to be linked to increased levels of prostate specific antigen (PSA) and prostate cancer itself. This suggests that perhaps screening men’s mitochondrial genome as part of annual checks could increase the accuracy of the PSA test itself.

The study appeared online in the journal American Journal of Human Genetics on 2 December 2010. In the report Austrian researchers outlined how they compared mitochondrial DNA from cancerous tissue with that of benign tissue for each of 30 Austrian men with various stages of prostate cancer. They found 41 mutations in cancerous cells that were totally absent in healthy prostate or blood cells.

Mitochondria could be likened to tiny “batteries” inside each cell that create the energy needed by the cell. Mitochondria have their own DNA which is quite separate from the DNA found in the cell nucleus itself.
Other research published last year showed that mitochondrial DNA (mtDNA) mutations were linked to prostate cancer, but senior author Dr Anita Kloss-Brandstätter, of Innsbruck Medical University, and colleagues, wanted to take this further and look across the whole mitochondrial genome, comprising over 16,500 base pairs.

Kloss-Brandstätter told the press this was the first study to target the “entire mitochondrial genome in prostate cancer and benign tissue from the same patient with a superior sequencing strategy”. She and her colleagues found that the men with the more advanced cancers had more mutations, suggesting these could be used as markers of cancer progression and spread.

They wrote that “sequencing of selected mitochondrial regions will likely result in a mutation spectrum useful for prognosis. These findings will potentially help others monitor malignant transformation, tumor progression, and metastasis,” said Kloss-Brandstätter.

Adding mitochondrial DNA sequencing to the PSA test could lead to more precise prostate cancer diagnosis for patients, said Kloss-Brandstätter.