Statins and cholesterol lowering after a cancer diagnosis: Why not?

被引:12
作者
Moyad, MA
Merrick, GS
机构
[1] Univ Michigan, Med Ctr, Dept Urol, Ann Arbor, MI 48109 USA
[2] Schiffler Canc Ctr, Wheeling, WV 26003 USA
[3] Wheeling Jesuit Hosp, Wheeling Hosp, Wheeling, WV 26003 USA
关键词
statins; cancer; prostate cancer; cardiovascular disease;
D O I
10.1016/j.urolonc.2005.03.017
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
The pleiotropic effects of statins continue to garner attention. One area of interest that requires more attention is their potential, or that of another heart healthy agent, to impact favorably or inhibit the progression of numerous cancers, especially prostate cancer. Statins have accumulated a plethora of data in the area of general cancer cell line inhibition, and the potential to have a synergistic impact in patients receiving a variety of conventional treatments for a diversity of cancers is endorsed at least by laboratory and some preliminary small clinical studies. However, prostate cancer is unique compared to other cancers because, despite a high prevalence, some men choose watchful waiting or no treatment, especially if they are older and/or have a well-differentiated tumor. Thus, prostate cancer is a good candidate for the potential investigation of statins after diagnosis, with or without standard therapy. Regardless, because the number 1 or 2 cause of death in men with prostate cancer is cardiovascular disease than even in the worst-case scenario, these agents appear attractive for more immediate clinical study because they could impact a major cause of morbidity and mortality in these men. It is time to see the forest over the tree, and statins seem to have an argument as good as many other agents for allocating more money and time to test their ability as adjuvant therapy in a randomized trial or, in some cases, of nonaggressive disease as a potential monotherapy. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:49 / 55
页数:7
相关论文
共 60 条
[1]
Lovastatin augments sulindac-induced apoptosis in colon cancer cells and potentiates chemopreventive effects of sulindac [J].
Agarwal, B ;
Rao, CV ;
Bhendwal, S ;
Ramey, WR ;
Shirin, H ;
Reddy, BS ;
Holt, PR .
GASTROENTEROLOGY, 1999, 117 (04) :838-847
[2]
Agarwal B, 1999, CLIN CANCER RES, V5, P2223
[3]
Cyclin E deregulation alters the biologic properties of ovarian cancer cells [J].
Bedrosian, I ;
Lu, KH ;
Verschraegen, C ;
Keyomarsi, K .
ONCOGENE, 2004, 23 (15) :2648-2657
[4]
LOVASTATIN POTENTIATES THE PHOTOCYTOTOXIC EFFECT OF PHOTOFRIN-II DELIVERED TO HT29 HUMAN COLONIC ADENOCARCINOMA CELLS BY LOW-DENSITY-LIPOPROTEIN [J].
BIADE, S ;
MAZIERE, JC ;
MORA, L ;
SANTUS, R ;
MAZIERE, C ;
AUCLAIR, M ;
MORLIERE, P ;
DUBERTRET, L .
PHOTOCHEMISTRY AND PHOTOBIOLOGY, 1993, 57 (02) :371-375
[5]
Collisson EA, 2003, MOL CANCER THER, V2, P941
[6]
Dellavalle Robert P, 2003, Am J Ther, V10, P203, DOI 10.1097/00045391-200305000-00007
[7]
Dellavalle RP, 2001, J INVEST DERMATOL, V117, P761
[8]
Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: Exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features [J].
Demark-Wahnefried, W ;
Price, DT ;
Polascik, TJ ;
Robertson, CN ;
Anderson, EE ;
Paulson, DF ;
Walther, PJ ;
Gannon, M ;
Vollmer, RT .
UROLOGY, 2001, 58 (01) :47-52
[9]
Enhancement of paclitaxel activity against hormone-refractory prostate cancer cells in vitro and in vivo by quinacrine [J].
deSouza, PL ;
Castillo, M ;
Myers, CE .
BRITISH JOURNAL OF CANCER, 1997, 75 (11) :1593-1600
[10]
Co-administration of simvastatin and cytotoxic drugs is advantageous in myeloma cell lines [J].
Drucker, L ;
Afensiev, F ;
Radnay, J ;
Shapira, H ;
Lishner, M .
ANTI-CANCER DRUGS, 2004, 15 (01) :79-84