Kruzelock R P, Murphy E C, Strong L C, Naylor S L, Hansen M F
Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
Cancer Res. 1997 Jan 1;57(1):106-9.
Mitotic recombination org nondysjunction are common mechanism for tumor-specific loss of constitutional heterozyosity (LOH) and tumor suppressor allelic inactivation and can be useful in localizing new putative tumor suppressor genes. In osteosarcoma, the highest frequencies of LOH have been reported for chromosomes 3q, 13q, 17p, and 18q. The high incidence of LOH on chromosome 3q suggests the presence of a novel tumor suppressor gene. To localize this putative tumor suppressor gene, we have used polymorphic markers on chromosome 3q to define the minimal region in which mitotic recombination or deletion results in LOH, which should contain the tumor suppressor gene. This putative tumor suppressor has been localized to a region between 3q26.2-3q26.3 of less that 1 cM between the polymorphic loci D3S1212 and D3S1246.
有丝分裂重组或染色体不分离是肿瘤特异性丧失结构杂合性(LOH)和肿瘤抑制等位基因失活的常见机制,可用于定位新的假定肿瘤抑制基因。在骨肉瘤中,已报道3q、13q、17p和18q染色体上的LOH频率最高。3q染色体上LOH的高发生率提示存在一个新的肿瘤抑制基因。为了定位这个假定的肿瘤抑制基因,我们使用了3q染色体上的多态性标记来定义有丝分裂重组或缺失导致LOH的最小区域,该区域应包含肿瘤抑制基因。这个假定的肿瘤抑制基因已定位到多态性位点D3S1212和D3S1246之间小于1 cM的3q26.2-3q26.3区域。