Prostate cancer is the most common form of cancer in men.
The cancer usually develops in the sixth or seventh decade of life and is often silent. A rising PSA (Prostate-Specific Antigen test) is the most common diagnostic tool, but controversy surrounding the PSA as a screening technique has arisen, as many patients with indolent (slow growing) disease undergo biopsies and even surgeries.
Prostate cancer appears more common in developed societies and this may reflect exposures, diet, or lifestyle.
There is a higher incidence in men whose family history is strong for prostate cancer.
While over 200,000 men are diagnosed each year with prostate cancer, the death rate from this malignancy remain comparatively low with only approximately 30,000 deaths per year attributed to this diagnosis.
Again, this reflects the relatively indolent nature of this disease and its tendency to be diagnosed later in life.
A number of genetic factors are associated with prostate cancer.
These include mutations in the BRCA-1 and 2 genes, associated with ovarian and breast cancer in women. There are hereditary prostate cancer genes, changes in androgen receptor, and of interest, alternations in vitamin D metabolism. There is a well-established association between a gene fusion known as TMPRSS2 and the ETS family.
Prostate cancer is managed entirely based on stage.
Early stage disease can be removed surgically, either by open prostatectomy or by laparoscopic procedure. There is a growing reliance upon robotic procedures, which may spare patients hospital stays and complications.
Once the disease has spread, it can be managed with radiation. Metastatic disease is uniformly managed with hormonal ablation.
As hormones are a principal part of the drivers for prostatic carcinoma, deprivation of male testosterone leads to prompt and dramatic improvement in most patients.
Unfortunately, hormonal therapies last for only several years and hormone resistance is common.
Newer therapies have been developed that can confront hormone refractory patients utilizing agents that further block testosterone synthesis or block testosterone at the level of DNA.
In addition, chemotherapeutic drugs have activity against this disease with Docetaxel and Cabazitaxel, both active and widely used in late-stage disease.
It is recognized that many patients who develop hormone resistant disease may do so by up-regulating other signal pathways.
Among the abnormalities identified in prostate cancer are vascular endothelial growth factor (VEGF), C-Met, K-Ras, PI3-K, and PTEN.
Each of these pathways may be a candidate for treatment with small molecules.
We have studied many patients with prostate cancer and often explore the more advanced presentations as lymph node involvement, metastatic disease to the liver or other sites, provides tissue for functional profiling analysis.
We have previously identified many unexpected findings, including the use of the newest classes of drugs, the PARP inhibitor, in select patients found positive for BRCA mutation. In addition, patients may respond to VINCA alkaloids, antimetabolites, alkylating agents, platins, and other classes of drugs.
As hormonal therapies can provide durable benefit, we often do not find it necessary to conduct studies on prostate cancer patients until late in the disease process.
Nonetheless, active treatments can be identified and patients who present with lymph node and soft tissue involvement, progressive disease to liver, who are undergoing surgical procedures for other indications such as bone stabilization, can be evaluated for drugs and combinations.
We have the good fortune of having many active treatments for prostate cancer and many active hormonal agents that provide very good benefit. It is fortunate that prostate cancer remains a responsive disease and can be often managed successfully for decades.
Call us at 800-542-4357 or email us via our Contact Us page to find out how we can test your cancer cells which enables us to identify those drugs and combinations most likely to be effective for treating your prostate cancer.