Thalidomide and lenalidomide: Mechanism-based potential drug combinations

被引：84

作者：

Vallet, Sonia ^{[1
,2
]}

Palumbo, Antonio ^{[3
]}

Raje, Noopur ^{[1
,2
]}

Boccadoro, Mario ^{[3
]}

Anderson, Kenneth C. ^{[2
]}

机构：

[1] Massachusetts Gen Hosp, Ctr Canc, Div Hematol Oncol, Boston, MA USA

[2] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA

[3] Univ Turin, Dipartimento Med & Oncol Sperimentale, Cattedra Ematol, Turin, Italy

来源：

LEUKEMIA & LYMPHOMA | 2008年 / 49卷 / 07期

关键词：

lenalidomide; thalidomide; multiple myeloma; bone marrow microenvironment; combination therapies;

D O I：

10.1080/10428190802005191

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Thalidomide and its analogue lenalidomide are potent anti-inflammatory, anti-angiogenic and immunomodulatory drugs, successfully used for the treatment of hematological cancers, in particular multiple myeloma (MM). Both drugs reveal a dual mechanism of action: they target tumour cells by direct cytotoxicity and, indirectly, by interfering with several components of the bone marrow microenvironment. Lenalidomide and thalidomide are versatile drugs with a broad range of activities that potentiate the anti-MM effects of conventional and novel agents. Here, we review the mechanism of action of these drugs, providing a rationale for combination studies in order to improve patient outcome and reduce side effects.

引用

页码：1238 / 1245

页数：8

共 78 条

[1] Osteoclasts enhance myeloma cell growth and survival via cell-cell contact: a vicious cycle between bone destruction and myeloma expansion [J].

Abe, M ;

Hiura, K ;

Wilde, J ;

Shioyasono, A ;

Moriyama, K ;

Hashimoto, T ;

Kido, S ;

Oshima, T ;

Shibata, H ;

Ozaki, S ;

Inoue, D ;

Matsumoto, T .

BLOOD, 2004, 104 (08) :2484-2491

[2] Role for macrophage inflammatory protein (MIP)-1α and MIP-1β in the development of osteolytic lesions in multiple myeloma [J].

Abe, M ;

Hiura, K ;

Wilde, J ;

Moriyama, K ;

Hashimoto, T ;

Ozaki, S ;

Wakatsuki, S ;

Kosaka, M ;

Kido, S ;

Inoue, D ;

Matsumoto, T .

BLOOD, 2002, 100 (06) :2195-2202

[3] Angiogenesis in acute and chronic leukemias and myelodysplastic syndromes [J].

Aguayo, A ;

Kantarjian, H ;

Manshouri, T ;

Gidel, C ;

Estey, E ;

Thomas, D ;

Koller, C ;

Estrov, Z ;

O'Brien, S ;

Keating, M ;

Freireich, E ;

Albitar, M .

BLOOD, 2000, 96 (06) :2240-2245

[4] Thalidomide derivative CC-4047 inhibits osteoclast formation by down-regulation of PU.1 [J].

Anderson, G ;

Gries, M ;

Kurihara, N ;

Honjo, T ;

Anderson, J ;

Donnenberg, V ;

Donnenberg, A ;

Ghobrial, I ;

Mapara, MY ;

Stirling, D ;

Roodman, D ;

Lentzsch, S .

BLOOD, 2006, 107 (08) :3098-3105

[5]

ATRA E, 1993, CLIN EXP RHEUMATOL, V11, P487

[6] Timeline - The evolution of thalidomide and its IMiD derivatives as anticancer agents [J].

Bartlett, JB ;

Dredge, K ;

Dalgleish, AG .

NATURE REVIEWS CANCER, 2004, 4 (04) :314-322

[7] Thalidomide in newly diagnosed multiple myeloma: influence of thalidomide treatment on peripheral blood stem cell collection yield [J].

Breitkreutz, I. ;

Lokhorst, H. M. ;

Raab, M. S. ;

van der Holt, B. ;

Cremer, F. W. ;

Herrmann, D. ;

Glasmacher, A. ;

Schmidt-Wolf, I. G. H. ;

Blau, I. W. ;

Martin, H. ;

Salwender, H. ;

Haenel, A. ;

Sonneveld, P. ;

Goldschmidt, H. .

LEUKEMIA, 2007, 21 (06) :1294-1299

[8]

BREITKREUTZ SVI, 2006, BLOOD, V108, P3485

[9] Identification of genes downstream of Pax6 in the mouse lens using cDNA microarrays [J].

Chauhan, BK ;

Reed, NA ;

Zhang, WJ ;

Duncan, MK ;

Kilimann, MW ;

Cvekl, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (13) :11539-11548

[10] Apaf-1/cytochrome c-independent and Smac-dependent induction of apoptosis in multiple myeloma (MM) cells [J].

Chauhan, D ;

Hideshima, T ;

Rosen, S ;

Reed, JC ;

Kharbanda, S ;

Anderson, KC .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (27) :24453-24456

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