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Prostate cancer is the second leading cause of cancer-caused fatalities in men, and within a man's lifetime, one in six men will have the disease. [104] Alterations in histone acetylation and DNA methylation occur in various genes influencing prostate cancer, and have been seen in genes involved in hormonal response. [105]
The PI3K pathway is a major source of drug resistance in prostate cancer. This is particularly true in castration-resistant prostate cancer, where tumours become resistant to androgen-deprivation therapy, which block the tumours ability to utilise the hormone androgen to grow. [17]
Prostate cancer is the most diagnosed cancer in men in over half of the world's countries, and the leading cause of cancer death in men in around a quarter of countries. [91] Prostate cancer is rare in those under 40 years old, [92] and most cases occur in those over 60 years, [2] with the average person diagnosed at 67. [93]
There are several reasons why PIN is the most likely prostate cancer precursor. [3] PIN is more common in men with prostate cancer. High grade PIN can be found in 85 to 100% of radical prostatectomy specimens, [4] nearby or even in connection with prostate cancer. It tends to occur in the peripheral zone of the prostate.
ONCE PROSTATE CANCER is diagnosed, doctors determine what stage the cancer is in and how aggressive it is—and then recommend the most appropriate treatment, says Sunil Kakadia, M.D., a medical ...
They can cause cancer by turning the receptor permanently on (constitutively), even without signals from outside the cell. Ras is a small GTPase that hydrolyses GTP into GDP and phosphate. Ras is activated by growth factor signaling (i.e., EGF, TGFbeta) and acting as a binary switch (on/off) in growth signaling pathways.
Tissue can be organized in a continuous spectrum from normal to cancer. Often, the multiple genetic changes that result in cancer may take many years to accumulate. During this time, the biological behavior of the pre-malignant cells slowly changes from the properties of normal cells to cancer-like properties.
The authors describe how tumor progression proceeds via a process analogous to Darwinian evolution, where each genetic change confers a growth advantage to the cell. These genetic changes can be grouped into six "hallmarks", which drive a population of normal cells to become a cancer. The six hallmarks are: self-sufficiency in growth signals