Bachnou N, Laudet V, Jaffredo T, Quatannens B, Saule S, Dieterlen-Lièvre F
Institut d'Embryologie Cellulaire et Moléculaire du CNRS et du Collège de France, Nogent s/Marne.
Oncogene. 1991 Jun;6(6):1041-7.
We show that a construct designated as MAHEVA, which encodes oncogenes v-myc from MH2 virus and v-erbA from AEV under the control of the LTR of MH2, induces rapidly growing heart rhabdomyosarcomas, when it is injected in E3 but not E5 chick embryos. A similar pathology has previously been observed with MC29, within the same limited time frame. The tumors, which expressed P61-63myc, P75gag-erbA and Pr76gag proteins were detectable from E14 onwards. Compared with MC29, MAHEVA induced a secondary anomaly, not detectable prior to E17. This is the appearance of cartilage nodules within the heart rhabdomyosarcomas. The constant location of these nodules inside the rhabdomyosarcomas and their delayed appearance suggests that the chondrocytes originate from myoblasts prevented from differentiating by the expression of the v-myc product. This interpretation is supported by the appearance of chondrocytes in E3 heart muscle cells infected in vitro with MAHEVA.
我们发现，一种名为MAHEVA的构建体，在MH2的LTR控制下编码来自MH2病毒的癌基因v-myc和来自AEV的v-erbA，当将其注射到E3而非E5鸡胚中时，会诱导快速生长的心脏横纹肌肉瘤。此前在相同的有限时间范围内，用MC29也观察到了类似的病理情况。从E14起可检测到表达P61-63myc、P75gag-erbA和Pr76gag蛋白的肿瘤。与MC29相比，MAHEVA诱导了一种在E17之前无法检测到的继发性异常。这是心脏横纹肌肉瘤内软骨结节的出现。这些结节在横纹肌肉瘤内的恒定位置及其延迟出现表明，软骨细胞起源于因v-myc产物表达而无法分化的成肌细胞。体外感染MAHEVA的E3心肌细胞中软骨细胞的出现支持了这一解释。
