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Castration-resistant prostate cancer (CRPC) is prostate cancer that progresses despite extremely low testosterone in the body often due to medical castration. [4] Unlike many other types of prostate cancer, CRPC do not need normal testosterone levels, but they still require regular androgen receptors (AR).
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]
Eventually cancer cells can grow resistant to this treatment. This most-advanced stage of the disease, called castration-resistant prostate cancer, is treated with continued hormone therapy alongside the chemotherapy drug docetaxel. Some tumors metastasize (spread) to other areas of the body, particularly the bones and lymph nodes.
PC3 cells have been utilized to research aggressive and castration-resistant forms of pancreatic cancer. The androgen-independence of these cells during cell division makes them invaluable for studying the molecular mechanisms embedded in studying advanced prostate cancer. [13] PC3 cells have been involved in research regarding the prevention ...
Bicalutamide is used primarily in the treatment of early and advanced prostate cancer. [1] It is approved at a dosage of 50 mg/day as a combination therapy with a gonadotropin-releasing hormone analogue (GnRH analogue) or orchiectomy (that is, surgical or medical castration) in the treatment of stage D2 metastatic prostate cancer (mPC), [2] [3] and as a monotherapy at a dosage of 150 mg/day ...
[citation needed] Radiotherapy uses ionizing radiation to kill prostate cancer cells. When absorbed in tissue, ionizing radiation such as gamma and x-rays damage the DNA in cancer cells, which increases the probability of apoptosis (cell death). Normal cells are able to repair radiation damage, while cancer cells are not.
In prostate cancer, removal of testicular T through castration (surgical or chemical removal or inactivation of testicles) helps eliminate the growth-promoting effects of androgens. [79] However, in some cases, metastatic tumors can develop into castration-resistant prostate cancer (CRPC). [ 80 ]
The LNCaP (Lymph Node Carcinoma of the Prostate) cell line was established from a metastatic lesion of human prostatic adenocarcinoma.The LNCaP cells grow readily in vitro (up to 8 x 10 5 cells/sq cm; doubling time, 60 hr), form clones and are highly resistant to human fibroblast interferon. [1]