Acute leukemia: A pediatric perspective

被引：56

作者：

Downing, JR

Shannon, KM

机构：

[1] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA

[2] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Ctr Comprehens Canc, San Francisco, CA 94143 USA

来源：

CANCER CELL | 2002年 / 2卷 / 06期

关键词：

D O I：

10.1016/S1535-6108(02)00211-8

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The spectrum of hematological malignancies differs markedly between children and adults. Moreover, diseases such as acute lymphoblastic leukemia, acute myeloid leukemia, and myelodysplastic syndrome also demonstrate distinct biologic features and responses to treatment between these populations. In this review, we summarize our current understanding of the molecular pathology of acute leukemia and myelodysplastic syndrome, emphasizing areas in which studies in pediatric patients are providing unique insights into the hematopoietic malignancies of adults.

引用

收藏

页码：437 / 445

页数：9

相关论文

共 95 条

[1] THE C-MYC ONCOGENE DRIVEN BY IMMUNOGLOBULIN ENHANCERS INDUCES LYMPHOID MALIGNANCY IN TRANSGENIC MICE [J].

ADAMS, JM ;

HARRIS, AW ;

PINKERT, CA ;

CORCORAN, LM ;

ALEXANDER, WS ;

CORY, S ;

PALMITER, RD ;

BRINSTER, RL .

NATURE, 1985, 318 (6046) :533-538

[2] Mutations in the ELA2 gene encoding neutrophil elastase are present in most patients with sporadic severe congenital neutropenia but only in some patients with the familial form of the disease [J].

Ancliff, PJ ;

Gale, RE ;

Liesner, R ;

Hann, IM ;

Linch, DC .

BLOOD, 2001, 98 (09) :2645-2650

[3] The expression of ETV6/CBFA2 (TEL/AML1) is not sufficient for the transformation of hematopoietic cell lines in vitro or the induction of hematologic disease in vivo [J].

Andreasson, P ;

Schwaller, J ;

Anastasiadou, E ;

Aster, J ;

Gilliland, DG .

CANCER GENETICS AND CYTOGENETICS, 2001, 130 (02) :93-104

[4] Treatment of adult acute lymphoblastic leukemia (ALL): long-term follow-up of the GIMEMA ALL 0288 randomized study [J].

Annino, L ;

Vegna, ML ;

Camera, A ;

Specchia, G ;

Visani, G ;

Fioritoni, G ;

Ferrara, F ;

Peta, A ;

Ciolli, S ;

Deplano, W ;

Fabbiano, F ;

Sica, S ;

Di Raimondo, F ;

Cascavilla, N ;

Tabilio, A ;

Leoni, P ;

Invernizzi, R ;

Baccarani, M ;

Rotoli, B ;

Amadori, S ;

Mandelli, F .

BLOOD, 2002, 99 (03) :863-871

[5] Down syndrome, transient myeloproliferative syndrome, and leukemia: Bridging development and neoplasia [J].

Arceci, RJ .

JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY, 2002, 24 (01) :1-1

[6] Leukemic transformation in patients with severe congenital neutropenia [J].

Banerjee, A ;

Shannon, KM .

JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY, 2001, 23 (08) :487-495

[7] C-kit mutations in core binding factor leukemias [J].

Beghini, A ;

Peterlongo, P ;

Ripamonti, CB ;

Larizza, L ;

Cairoli, R ;

Morra, E ;

Mecucci, C .

BLOOD, 2000, 95 (02) :726-727

[8] Nf1 and Gmcsf interact in myeloid leukemogenesis [J].

Birnbaum, RA ;

O'Marcaigh, A ;

Wardak, Z ;

Zhang, YY ;

Dranoff, G ;

Jacks, T ;

Clapp, DW ;

Shannon, KM .

MOLECULAR CELL, 2000, 5 (01) :189-195

[9] PROTEINS REGULATING RAS AND ITS RELATIVES [J].

BOGUSKI, MS ;

MCCORMICK, F .

NATURE, 1993, 366 (6456) :643-654

[10] Loss of NF1 results in activation of the Ras signaling pathway and leads to aberrant growth in haematopoietic cells [J].

Bollag, G ;

Clapp, DW ;

Shih, S ;

Adler, F ;

Zhang, YY ;

Thompson, P ;

Lange, BJ ;

Freedman, MH ;

McCormick, F ;

Jacks, T ;

Shannon, K .

NATURE GENETICS, 1996, 12 (02) :144-148

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