A Medical Device Daily

The Diagnostic Center for Disease (Sarasota, Florida) reported that it has identified “a previously underestimated risk” indicating that routine prostate biopsy to evaluate prostate cancer spreads cancer cells and may be the reason that men have a recurrence of disease many years after the prostate was removed.

Traditionally, an ultrasound and prostate biopsy is commonly recommended and performed when a patient presents with a prostate specific antigen (PSA) of 2.5 ng/ml or above.

Men have been told for years that the biopsy is safe and the only way to diagnose prostate cancer, but DCD said “this paradigm ... exposes far too many men to needless biopsies; as the number one reason PSA rises is prostatitis, not prostate cancer.”

It said that an issue often not discussed between physician and patient is the possibility of “needle tracking,” offering the potential for spreading cancer cells beyond the prostate when a biopsy is performed. When the needle is withdrawn from the targeted organ, the chance of spreading cancer cells establishes itself, and every puncture of the prostate adds to this risk.

A recent evaluation of data from patients with a positive MRI-S scan at the DCD found 75% of biopsies performed yielded a cancer, allowing men without cancer to avoid a biopsy procedure.

DCD called this “a quantum leap from the blind biopsy approach.”

The facility said it used a 3.0 Tesla MRI spectroscopy (MRI-S) scan which predicted and confirmed the presence of prostate cancer. It sasid MRI-S “represents the most sensitive and specific diagnostic modality for the prostate evaluation” and is superior to PET scans, CAT scans and Prostascint scans.

It says that MRI-S at 3.0 Tesla allows imaging of the entire prostate, thereby, creating a roadmap and allowing selective targeting of specific areas of interest for biops.

DCD estimates that “needle tracking” takes place from 20% to 30% of the time, suggesting that 70%-80% of biopsies are performed unnecessarily. It says that despite this risk physicians generally fail to acknowledge a process that allows cells to lie dormant or incubate for up to 10 years or more regardless of the treatment rendered.

BPA studied for prostate cancer risk

Does exposure of baby boys — in utero or in infancy — to bisphenol A (BPA), a man-made chemical which mimics natural estrogens, predispose them to prostate cancer later in life? A five-year, $2.6 million grant to a University of Illinois at Chicago researcher and her colleague aims to shed light on the mechanism by which this might occur.
Gail Prins, professor of urology at the UIC College of Medicine and the lead investigator, and her colleague Shuk-Mei Ho, professor and chair of environmental health at the University of Cincinnati, established in earlier studies in animals that perinatal exposure to BPA at very low doses results in increased sensitivity to estrogen as the male animal ages and an increased risk of developing prostate cancer.

Demonstrating a similar link in humans in an epidemiological study is difficult because of the small dosages and long lag time between exposure and effect. With the new grant, from the National Institute of Environmental Health Sciences, Prins and Ho will attempt to unravel the genetic mechanism by which the dose-response effect in animals is thought to occur.

BPA is a key chemical in the production of polycarbonate plastic and epoxy resins and is found in products ranging from baby bottles to tin can linings. BPA may break down and leach into food or beverages when it is heated. More than a billion pounds of BPA is produced in the U.S. each year, and the Centers for Disease Control and Prevention (Atlanta) has found BPA in 92% of Americans age six or older.

Scientists think that sensitization to estrogen due to a much earlier exposure to an estrogen-like compound is “epigenetic,” a heritable change in gene function that occurs without a change in the DNA sequence, as in mutation.

In this model, the early environment of the fetus causes chemical changes in DNA, called imprinting, which may cause later changes in gene expression. These changes can impact an organisms’ development of an organism, Prins said, and may be implicated in the origin of a number of adult diseases, like prostate cancer.

“We hypothesize that early ‘imprinting’ of the prostate gland by exposure to small doses of BPA is the result of specific modifications which permanently affect gene expression in the gland,” Prins said. “As men age, they produce less testosterone and relatively more estrogen. Our work with animals has shown that exposure of the ‘BPA-imprinted’ prostate gland to this more estrogen-rich environment is the key to the heightened risk of developing cancer.”
The study will work with both an animal model and human prostate-like structures and is designed to characterize the dose-response and the period of susceptibility in the developing male, to determine which genes are modified and turned on or off as a result. The researchers also plan to test directly whether the epigenetically modified genes play an active role in the later development of cancer of the prostate gland.

The study may also lead to improved methods of screening men who may already be at risk, Prins said, and could lead to the identification of new biomarkers “for identifying men at higher risk for prostate cancer as a result of environmental exposures.”