Osteosarcoma development and stem cell differentiation

被引:311
作者
Tang, Ni [1 ,2 ,3 ]
Song, Wen-Xin [1 ]
Luo, Jinyong [1 ,2 ,3 ]
Haydon, Rex C. [1 ]
He, Tong-Chuan [1 ,2 ,3 ]
机构
[1] Univ Chicago, Med Ctr, Dept Surg, Mol Oncol Lab, Chicago, IL 60637 USA
[2] Chongqing Med Univ, Affiliated Hosp 2, Chongqing, Peoples R China
[3] Chongqing Med Univ, Key Lab Diagnost Med, Chinese Minist Educ, Chongqing, Peoples R China
关键词
D O I
10.1007/s11999-008-0335-z
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
Osteosarcoma is the most common nonhematologic malignancy of bone in children and adults. The peak incidence occurs in the second decade of life, with a smaller peak after age 50. Osteosarcoma typically arises around the growth plate of long bones. Most osteosarcoma tumors are of high grade and tend to develop pulmonary metastases. Despite clinical improvements, patients with metastatic or recurrent diseases have a poor prognosis. Here, we reviewed the current understanding of human osteosarcoma, with an emphasis on potential links between defective osteogenic differentiation and bone tumorigenesis. Existing data indicate osteosarcoma tumors display a broad range of genetic and molecular alterations, including the gains, losses, or arrangements of chromosomal regions, inactivation of tumor suppressor genes, and the deregulation of major signaling pathways. However, except for p53 and/or RB mutations, most alterations are not constantly detected in the majority of osteosarcoma tumors. With a rapid expansion of our knowledge about stem cell biology, emerging evidence suggests osteosarcoma should be regarded as a differentiation disease caused by genetic and epigenetic changes that interrupt osteoblast differentiation from mesenchymal stem cells. Understanding the molecular pathogenesis of human osteosarcoma could ultimately lead to the development of diagnostic and prognostic markers, as well as targeted therapeutics for osteosarcoma patients.
引用
收藏
页码:2114 / 2130
页数:17
相关论文
共 300 条
[1]  
ABRAMSON DH, 1984, OPHTHALMOLOGY, V91, P1351
[2]   A microsatellite fluorescent method for linkage analysis in familial retinoblastoma and deletion detection at the RBI locus in retinoblastoma and osteosarcoma [J].
Alonso, J ;
García-Miguel, P ;
Abelairas, J ;
Mendiola, M ;
Pestaña, A .
DIAGNOSTIC MOLECULAR PATHOLOGY, 2001, 10 (01) :9-14
[3]  
ANDREASSEN A, 1993, CANCER RES, V53, P468
[4]  
ARAKI N, 1991, CLIN ORTHOP RELAT R, P271
[5]   Telomerase activity in skeletal sarcomas [J].
Aue, G ;
Muralidhar, B ;
Schwartz, HS ;
Butler, MG .
ANNALS OF SURGICAL ONCOLOGY, 1998, 5 (07) :627-634
[6]   Molecular cloning and characterization of the human budding uninhibited by benomyl (BUB3) promoter [J].
Baek, WK ;
Park, JW ;
Lim, JH ;
Suh, SI ;
Suh, MH ;
Gabrielson, E ;
Kwon, TK .
GENE, 2002, 295 (01) :117-123
[7]   Annexins II and V inhibit cell migration [J].
Balch, C ;
Dedman, JR .
EXPERIMENTAL CELL RESEARCH, 1997, 237 (02) :259-263
[8]  
Barker N, 2000, BIOESSAYS, V22, P961
[9]   AMPLIFICATION OF C-MYC ONCOGENE AND ABSENCE OF C-HA-RAS POINT MUTATION IN HUMAN BONE SARCOMA [J].
BARRIOS, C ;
CASTRESANA, JS ;
RUIZ, J ;
KREICBERGS, A .
JOURNAL OF ORTHOPAEDIC RESEARCH, 1993, 11 (04) :556-563
[10]   CLINICOPATHOLOGICAL CORRELATIONS AND SHORT-TERM PROGNOSIS IN MUSCULOSKELETAL SARCOMA WITH C-MYC ONCOGENE AMPLIFICATION [J].
BARRIOS, C ;
CASTRESANA, JS ;
KREICBERGS, A .
AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS, 1994, 17 (03) :273-276