Orthomolecularism for prostate cancer-1

The development of a malignant prostate cancer cell from a normal prostatic glandular cell requires multiple transformation events. Normal human prostate epithelial cells or even primary prostate cancer cells undergo ~30 population doublings before becoming senescent. Prostate cancer cells arise from luminal rather than basal cells. Stimulation and inhibition of prostate cancer cell growth by PGFs and cellular regulators may depend on the presence of the androgen receptor (AR) in an androgen-depleted environment. During prostate cancer progression, bones are most frequently affected by metastases, assumed that bone cells support the growth of prostate cancer cells by producing paracrine stimulators such as growth factors. EGF-related peptides appear to function as growth-promoting factors for prostate cancer cells. The evidence linking endogenous serum androgen levels with risk of carcinoma of prostate (CaP) is not conclusive. In human, a higher expression of the c-Met protooncogene on the prostate cancer cells is associated with a higher degree of invasiveness. When initially diagnosed, the majority of prostate cancers respond to androgen deprivation; however, over time they lose their dependency on androgens and the tumour recurs. Prostate cancer cells that escape androgen ablation maintain the capacity to undergo apoptosis.

Prostate cancer patients develop a number of pronounced circadian endocrine changes affecting mainly central hormone namely prolactin, growth hormone and TSH. The epidemiology of prostate cancer is profound. Carcinoma of prostate (CaP) is unlike many other cancers in that it grows very slowly. Familial prostate cancer has 2 important factors: 1- early age at onset, and 2- the number of multiple affected family members. Oxidative pathways are important in prostate cancer progression. The hereditary prostate cancer gene (HPC1) is localised to the long arm of chromosome 1. Melatonin inhibits prostate cancer cells. Prostate cancer cells have much less zinc than normal prostate cells. Cyclooxygenase (COX) disturbs the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in prostate cancer cells. The small cell prostate cancer is not hormonally sensitive. Prostate cancer cells have robust telomerase activity (high telomerase activity and short telomeres).

Prostate cancer cells may escape the protective role of androgens mechanism by mutations in the AR. Progression of prostate cancer (Pca) is associated with the development of an adequate blood supply by means of angiogenesis and metastases to regional lymph nodes or other structures and organs, such as bone, liver or lung, etc. For a prostate cancer cell to become highly metastatic, metastatic suppressor gene(s) must be inactivated by mutation, allelic loss, or epigenetic inactivation (hypermethylation). Inflammation plays a role in the pathobiogenesis of prostate cancer. Tumour cells appear to adapt to hypoxia by secreting angiogenetic factors. In CaP, androgen stimulation may enhance EGFR activation with EGF in prostate cancer cells.

ORTHOMOLECULARISM FOR PROSTATE CANCER-1

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