Cancer lutein

KHACHIK F, BEECHER G R and SMITH J c (1995) Lutein, lycopene, and their oxidative metabolites in chemoprevention of cancer , J Cell Biochem Supp, 22, 236-46. 

Carotenoids and prostate cancer — Numerous epidemiological studies including prospective cohort and case-control studies have demonstrated the protective roles of lycopene, tomatoes, and tomato-derived products on prostate cancer risk other carotenoids showed no effects. " In two studies based on correlations between plasma levels or dietary intake of various carotenoids and prostate cancer risk, lycopene appeared inversely associated with prostate cancer but no association was reported for a-carotene, P-carotene, lutein, zeaxanthin, or p-cryptoxanthin. - Nevertheless, a protective role of all these carotenoids (provided by tomatoes, pumpkin, spinach, watermelon, and citrus fruits) against prostate cancer was recently reported by Jian et al. ... 

Carotenoids and breast cancer — Among seven case-control studies investigating the correlation between different carotenoid plasma levels or dietary intakes and breast cancer risk, five showed significant inverse associations with some carotenoids. - In most cases, this protective effect was due to 3-carotene and lutein. However, one (the Canadian National Breast Screening Study ) showed no association for all studied carotenoids including (I-carotene and lutein. More recently, another study even demonstrated a positive correlation between breast cancer risk and tissue and serum levels of P-carotenes and total carotenes. Nevertheless, these observational results must be confirmed by intervention studies to prove consistent. 

Carotenoids and urino-digestive cancers — On the whole, findings from epidemiological studies did not demonstrate a protective role of carotenoids against colorectal, gastric, and bladder cancers. Indeed, most prospective and case-control studies of colorectal cancer showed no association with dietary intake or plasma level of most carotenoids. - Only lycopene and lutein were shown to be protective against colorectal cancer. Otherwise, findings from the ATBC study s showed no effect of P-carotene supplementation on colorectal cancer. 

Data concerning gastric cancer are scarce. The prospective Netherlands Cohort Study found no correlation between lutein dietary intake and gastric cancer risk, whereas findings from the Physicians Health Study and the ATBC study reported no effect of P-carotene on gastric cancer incidence. Two case-control studies and three intervention trials (ATBC, CARET, and the Physicians Health Study ) showed no association of P-carotene, lycopene, lutein, zeaxanthin, and P-cryptoxanthin. 

Lutein has some structural similarities to P-carotene, reported to enhance the development of lung cancer when given in supplement form to heavy smokers. The available data indicate that lutein in food would not be expected to have this effect. The committee was unable to assess whether lutein in the form of supplements would produce the reported effect in heavy smokers. 

Hormonal therapies that have been studied in the treatment of primary or early breast cancer include antiestrogens, oophorectomy, ovarian irradiation, luteinizing hormone-releasing hormone (LHRH) agonists, and aromatase inhibitors. 

Outline the role of luteinizing hormone-releasing hormone (LHRH) agonists in the treatment of prostate cancer. 

Androgen ablation with a luteinizing hormone-releasing hormone (LHRH) agonist plus an antiandrogen should be used prior to radiation therapy for patients with locally advanced prostate cancer to improve outcomes over radiation therapy alone. 

Marks LS. Luteinizing hormone-releasing hormone agonists in the treatment of men with prostate cancer Timing, alternatives, and the 1-year implant. Urology 2003 62(6 suppl 1) 36—42. 

Carotenoids can strongly modulate apoptotic pathways (Palozza et al., 2006). For example, it has been demonstrated that lutein and zeaxanthin modulate the expression of anti-and pro-apoptotic factors and can selectively induce apoptosis in cancer cells but not in normal cells (Chew et al., 2003 Maccarrone et al., 2005). 

Gunasekera, RS, Sewgobind, K, Desai, S, Dunn, L, Black, HS, McKeehan, WL, and Patil, B, 2007. Lycopene and lutein inhibit proliferation in rat prostate carcinoma cells. Nutr Cancer 58, 171-177. 

Sumantran, VN, Zhang, R, Lee, DS, and Wicha, MS, 2000. Differential regulation of apoptosis in normal versus transformed mammary epithelium by lutein and retinoic acid. Cancer Epidemiol Biomarkers Prev 9, 257-263. 

Carotenoids are a class of lipophilic compounds with a polyisoprenoid structure. Most carotenoids contain a series of conjugated double bonds, which are sensitive to oxidative modification and cis-trans isomerization. There are six major carotenoids (ji-carotenc, a-carotene, lycopene, P-cryptoxanthin, lutein, and zeaxanthin) that can be routinely found in human plasma and tissues. Among them, p-carotene has been the most extensively studied. More recently, lycopene has attracted considerable attention due to its association with a decreased risk of certain chronic diseases, including cancers. Considerable efforts have been expended in order to identify its biological and physiochemical properties. Relative to P-carotene, lycopene has the same molecular mass and chemical formula, yet lycopene is an open-polyene chain lacking the P-ionone ring structure. While the metabolism of P-carotene has been extensively studied, the metabolism of lycopene remains poorly understood. 

A study at the Harvard School of Public Health done on 48,000 men for 4 years reported that men who ate 10 or more servings of tomato products (such as tomatoes, tomato sauce, pizza sauce) per week had up to 34% less chance to develop prostate cancer (Giovannucci and others 1995). They showed that lycopene intake from tomato-based products is related to a low risk of prostate cancer, but consumption of other carotenoids ((3-carotene, a-carotene, lutein, (3-cryptoxanthin) or retinol was not associated with the risk of prostate cancer. 

The major initial treatment modality for advanced prostate cancer is androgen ablation (e.g., orchiectomy or luteinizing hormone-releasing hormone [LHRH] agonists with or without antiandrogens). After disease progression, secondary hormonal manipulations, cytotoxic chemotherapy, and supportive care are used. 

Several studies have linked lutein to a lower risk for eye, skin and other health disorders, probably through its antioxidant activity. Lutein is apparently metabolized to zeaxanthin, an isomer, and several other compounds which protect the macula from ultraviolet radiation. The suggestion is that lutein may play a positive role in reducing macular degeneration. Other reports have linked lutein to a reduction of risk of cancer.13 Regardless, lutein is currently being promoted as an important dietary supplement. 

Klijn JG, Blarney RW, Boccardo F, Tominaya T, Duchateau L, Sylvester R. Combined tamoxifen and luteinizing-hormone (LHRH) agonist versus LHRH agonist alone in premenopausal advanced breast cancer a meta-analysis of four randomized trials. J Clin Oncol 2001 19 343-53. 

Buserelin (Suprefact) and leuprolide (Lupron) are peptide analogues of the hypothalamic hormone LH-RH (luteinizing hormone-releasing hormone). Chronic exposure of the pituitary to these agents abolishes gonadotropin release and results in markedly decreased estrogen and testosterone production by the gonads. Their major clinical use is in the palliative hormonal therapy of cancer of the prostate. 

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