Retinoids in combination therapies for the treatment of cancer: mechanisms and perspectives

被引：41
作者：
Ortiz, MA [1 ]
Bayon, Y [1 ]
Lopez-Hernandez, FJ [1 ]
Piedrafita, FJ [1 ]
机构：
[1] Sidney Kimmel Canc Ctr, San Diego, CA 92121 USA
来源：
DRUG RESISTANCE UPDATES | 2002年 / 5卷 / 3-4期
关键词：
retinoids; combination therapy; retinoid-related molecules; apoptosis;
D O I：
10.1016/S1368-7646(02)00050-X
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Retinoid derivatives have been of special interest in cancer research because of their antiproliferative and differentiation-inducing activities in premalignant and malignant cells. Some retinoids are clinically effective in cancer therapy and prevention, and all-trans-retinoic acid is being used for the treatment of acute promyelocytic leukemia. Unfortunately, classical retinoids are not effective against most advanced solid tumors and cause undesirable side effects, which have limited the full development of retinoids as chemopreventive and chemotherapeutic drugs. The recent identification of selective retinoid derivatives capable of inducing apoptosis and their combination with other anticancer therapies promises a more effective and less toxic manner to the successful use of retinoids in cancer therapy. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码：162 / 175
页数：14
相关论文
共 134 条
[1]   Retinoic acid-induced apoptosis in leukemia cells is mediated by paracrine action of tumor-selective death ligand TRAIL [J].
Altucci, L ;
Rossin, A ;
Raffelsberger, W ;
Reitmair, A ;
Chomienne, C ;
Gronemeyer, H .
NATURE MEDICINE, 2001, 7 (06) :680-686
[2]   Analysis of prognostic factors in newly diagnosed patients with acute promyelocytic leukemia: the APL92 study of the Japan Adult Leukemia Study Group (JALSG) [J].
Asou, N ;
Adachi, K ;
Tamura, J ;
Kanamaru, A ;
Kageyama, S ;
Hiraoka, A ;
Omoto, E ;
Akiyama, H ;
Tsubaki, K ;
Saito, K ;
Kuriyama, K ;
Oh, H ;
Kitano, K ;
Miyawaki, S ;
Takeyama, K ;
Yamada, O ;
Nishikawa, K ;
Takahashi, M ;
Matsuda, S ;
Ohtake, S ;
Ohno, R .
CANCER CHEMOTHERAPY AND PHARMACOLOGY, 2001, 48 (Suppl 1) :S65-S71
[3]  
BEARD RL, 1999, HANDB EXP PHARM, V139, P185
[4]   Adenine nucleotide translocator mediates the mitochondrial membrane permeabilization induced by lonidamine, arsenite and CD437 [J].
Belzacq, AS ;
El Hamel, C ;
Vieira, HLA ;
Cohen, I ;
Haouzi, D ;
Métivier, D ;
Marchetti, P ;
Brenner, C ;
Kroemer, G .
ONCOGENE, 2001, 20 (52) :7579-7587
[5]   13cis-and all-trans retinoic acid have antiproliferative effects on CML cells and render IFNα antiproliferative potency after combined treatment in vitro [J].
Benthin, M ;
Dallmann, I ;
Atzpodien, J .
CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS, 2001, 16 (04) :323-331
[6]   IDENTIFICATION OF SYNTHETIC RETINOIDS WITH SELECTIVITY FOR HUMAN NUCLEAR RETINOIC ACID RECEPTOR-GAMMA [J].
BERNARD, BA ;
BERNARDON, JM ;
DELESCLUSE, C ;
MARTIN, B ;
LENOIR, MC ;
MAIGNAN, J ;
CHARPENTIER, B ;
PILGRIM, WR ;
REICHERT, U ;
SHROOT, B .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 186 (02) :977-983
[7]  
Bischoff ED, 1998, CANCER RES, V58, P479
[8]   The nuclear factor kappa B (NF-κB):: A potential therapeutic target for estrogen receptor negative breast cancers [J].
Biswas, DK ;
Dai, SC ;
Cruz, A ;
Weiser, B ;
Graner, E ;
Pardee, AB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (18) :10386-10391
[9]   Apoptosis induction by arsenic: mechanisms of action and possible clinical applications for treating therapy-resistant cancers [J].
Bode, A ;
Dong, ZG .
DRUG RESISTANCE UPDATES, 2000, 3 (01) :21-29
[10]   Apoptosis: mediator or mode of cell killing by anticancer agents? [J].
Brown, JM ;
Wouters, BG .
DRUG RESISTANCE UPDATES, 2001, 4 (02) :135-136
12345678910