As reported in an earlier Hot
Sheet, the surgical device CaverMap utilizes an intraoperative nerve
stimulator and a sensitive detector to determine the location and pathways of
nerves during radical prostatectomy surgery. A probe tip stimulates suspect
tissue and the product detects nerve involvement by monitoring minute penile
changes. Surgeons use such information to determine optimum dissection patterns
in each patient. CaverMap was tested by six clinical institutions across
Canada in a Randomized, Single Blinded, Multi-Center Clinical trial, presented
recently at the Annual American Urological Association meeting in Dallas, TX.
Doctors used the CaverMap tool to guide dissections and confirm nerve function
during and at the end of procedures.
When attempted, bilateral
nerve sparing was achieved in 73 percent of study patients, compared to only
56 percent of control patients. Also, CaverMap intraoperative
"confirmation" of nerve function proved a good indicator of return of
erectile function by a 12 months follow-up sexual function questionnaire.
Calling it a "promising
new technology," Laurence Klotz M.D., Professor of Urology at University
of Toronto says, "Until now, surgeons have relied solely upon anatomical
landmarks and experience to locate and
avoid damaging the cavernosal nerves responsible for erectile function. Use
of CaverMap... has potential...for
improved nerve-sparing radical prostatectomy results." Patients facing surgery should ask their
surgeons about this new technology.
Genetic Process Could be Reversible
A common genetic process that
could be reversible is linked to nearly 90 percent of prostate cancers,
according to Johns Hopkins researchers in a study appearing in Nature Medicine.
Most prostate cancers may involve a process called gene switching, which occurs
when certain members of a gene family switch "on" while others in
the family switch "off." Says molecular pathologist Gary Pasternack,
M.D., Ph.D., who led the research team, "Someday it's likely we can
reverse switching with drugs." Prostate cancer has the potential of being
corrected without using typical gene therapy, he says.
Scientists used molecular probes to highlight and compare
gene activity in cancer patients' normal prostate tissue with that of their
tumors and found clear evidence the gene pp32 was switched on in normal cells
but generally switched off in cancer cells. Earlier studies by the team showed
pp32 acts as a suppressor to keep cells from turning malignant. Close
relatives of the gene, pp32rl and pp32r2, encourage tumor growth and are
present and were turned on in perhaps 90 percent of the cases studied.
Switching could be a fundamental process in cancer,
researchers say; it has already been linked with common forms of breast
cancer.“If we can understand how the
switching works, what controls it, we can potentially reverse it,” Pasternack
says, “That’s our next task.”The team
hopes to screen and find drugs for the purpose within two years.
Model Explains Increased Incidence, Higher Mortality rate in Black Men
It has been noted for many
years that African American men suffer both a higher incidence and mortality
rate from prostate cancer. While genetic and environmental factors contribute
to disease causation in both races, a unifying theme is needed to explain many
unique observations regarding prostate cancer in blacks. A recent article in
Urology offers a conceptualization.
Although incidence rates rose
dramatically in both races in the early 1990's, the higher rate in blacks has
been documented for more than 20 years with differences most disparate in men
under 65 years old. The mortality rate is also greater in blacks, again with
greater disparity noted in younger men. Mortality rates are similar for blacks
and whites diagnosed after age 70.
One classic characteristic of prostate cancer in black men
is later stage. Delay in detection caused by cultural issues (i.e.: access to healthcare, knowledge of the disease, economic
factors, fear of therapy and distrust of a predominantly white medical
establishment) may lead to a higher stage at time of initial therapy and a
worse outcome for blacks. Data also suggests black
men eat more animal fat, which
is linked to greater prostate cancer risk. Recent autopsy studies show small,
latent cancers occur at similar frequency in both races between 20-80 years.
Yet more high grade prostatic intraepithelial neoplasia (PIN) has been identified
in blacks. Increasing data also confirms that blacks have a higher androgenic
stimulation as well as generally higher Gleason scores.
Two researchers hypothesize
that PIN is a precursor of Gleason grade 4 cancers: "The data support a
biologic etiology of increased incidence with epigenetic factors affecting
stage at diagnosis that could be circumvented by earlier detection. Cultural
issues alone in black men would tend to lower, not raise, detection and
incidence; thus, a biologic influence must be entertained. However, epigenetic
factors such as diet, detection practices or androgenic stimulation may explain
many other factors related to stage and presentation and mortality."
Normal prostatic epithelium can undergo malignant transformation
by at least two pathways, leading to either well-differentiated (Gleason
grades 2 and 3) latent carcinomas predominantly in older men or high-grade PIN
which, through additional mutations, could lead to morphologically high-grade
cancer, Gleason grade 4 and a higher frequency of Gleason score 7 or higher
cancers. Because of greater genetic instability of PIN, mutations occur at a
younger age. The growth of the cancer is under the epigenetic influence of
diet, androgenic stimulation, with cultural or detection issues contributing
to a delay in diagnosis. "In the case of prostate cancer in black men, an
increase of PIN establishes the setting for the sequence of events that explain
the epidemiological and pathologic findings," the authors write.
"There is opportunity for early detection to allow therapy before a
prolonged influence of epigenetic factors. Through earlier intervention,
advanced prostate cancer occurs less frequently and the disparity in
pathologic extent of disease between blacks and whites diminishes." The model
suggests pivotal issues for prostate cancer in blacks are higher incidence of
PIN and high-grade cancers. (Source:
'A Unifying Model to Explain the Increased Incidence and
Higher Mortality of Prostate Cancer in Black Men" by James Mon tie and
Kenneth Pienta.)