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首页> 外文期刊>Genomics >Genetic mapping of a Ptch1-associated rhabdomyosarcoma susceptibility locus on mouse chromosome 2.
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Genetic mapping of a Ptch1-associated rhabdomyosarcoma susceptibility locus on mouse chromosome 2.

机译：小鼠2号染色体上与Ptch1相关的横纹肌肉瘤易感基因座的遗传图谱。

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摘要

Mutations in the Patched (Ptch1) gene are responsible for various familial and sporadic cancers. Ptch1(neo67/+) mice, in which exons 6 and 7 are deleted, show genetic background-dependent susceptibility to the development of muscle tumors resembling human rhabdomyosarcoma (RMS); BALB/c (BALB) is a susceptible strain whereas C57BL/6 (B6) shows resistance. A genome-wide linkage analysis was carried out using Ptch1(neo67/+)mice produced from B6 x (BALB x B6) backcrosses to identify loci involved in the control of RMS susceptibility. Quantitative trait locus mapping with the censored tumor latency time as the quantitative parameter was used to detect a significant RMS susceptibility modifier locus, Parms1 (Patched-Associated RMS 1), on chromosome 2 between D2Mit37 and D2Mit102 (LRS = 10). A Kaplan-Meier survival curve revealed that mice with the B6/BALB genotype develop tumors more frequently and much faster as compared to mice homozygous for the B6 allele (P = 0.02). Additional loci not reaching linkage significance were also detected for medulloblastoma resistance.
机译：Patched（Ptch1）基因中的突变是导致各种家族性和散发性癌症的原因。 Ptch1（neo67 / +）小鼠，其中外显子6和7被删除，表现出遗传背景依赖敏感性发展为类似于人类横纹肌肉瘤（RMS）的肌肉肿瘤。 BALB / c（BALB）是易感菌株，而C57BL / 6（B6）显示出抗性。使用从B6 x（BALB x B6）回交产生的Ptch1（neo67 / +）小鼠进行了全基因组连锁分析，以鉴定参与RMS敏感性控制的基因座。以被检查的肿瘤潜伏期为定量参数的定量性状基因座作图被用于检测D2Mit37和D2Mit102（LRS = 10）之间的2号染色体上的重要RMS磁化率修饰位点Parms1（Patched-Associated RMS 1）。 Kaplan-Meier生存曲线显示，与纯合B6等位基因的小鼠相比，具有B6 / BALB基因型的小鼠更容易发生肿瘤，且肿瘤发生速度更快（P = 0.02）。还检测到其他未达到连锁意义的基因座对髓母细胞瘤的抵抗力。

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