PCS, a gene related to the immunoglobulin super family of axonal glycoproteins is expressed in murine plasma cell tumors.
PCS, a gene related to the immunoglobulin super family of axonal glycoproteins is expressed in murine plasma cell tumors.
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PCS 是一种与轴突糖蛋白免疫球蛋白超家族相关的基因，在小鼠浆细胞肿瘤中表达。
DOI：
10.1007/978-3-642-77633-5_28
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发表时间：
1992
影响因子：
--
通讯作者：
Marcu,KB
中科院分区：
文献类型：
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作者：
Connelly,MA;Grady,RC;Mushinski,JF;Marcu,KB
Pristane(四甲基十五烷)是一种支链烷基石蜡油，在BALB/CAN和其他敏感的小鼠品系中诱导腹膜内浆细胞肿瘤(PCT)，潜伏期分别为最短到平均120至210天(Potter，1972)。PCT有两个相互易位的染色体之一，总是涉及15号染色体上的D2/3带，以及12号染色体上的免疫球蛋白重链(IGH)基因座或6号染色体上的Kappa轻链基因座(IgK)(Ohno等人，1979)。D2/3带后来被发现是c-mycgene基因座，这种染色体重排激活的原癌基因被证明是浆细胞瘤发生的一个促成因素(Mushinski，1988；Marcu等人，1992)。与Pristane一起注射含有癌基因的逆转录病毒(v-abl、myc和raf或myc和ras)和Pristane(Potter等人，1973；Ohno等人，1984；Potter等人，1987；Clynes等人，1988；Troppmair等人，1989)和含有激活的myc癌基因的病毒诱导的PCT而不与c-myc相关的染色体易位时，浆细胞分化迅速加速(50-120天平均潜伏期)(Potter等人，1987；Clynes等人，1988；Tromair等人，1989)。最近，含有v-abl和c-myc的逆转录病毒被发现是最有效的癌基因组合，无论有或没有野生型Moloney辅助病毒，以及在没有Pristane的情况下，100%的成年BALB/c小鼠都能诱导PCT(WeisSinger等人，1991年)。这些观察结果共同认为，除了c-myc激活外，恶性浆细胞肿瘤的形成还需要多种基因事件。事实上，至少有三个隐性遗传位点被认为在不敏感的小鼠品系中对PCT的形成具有抗性，但除了myc之外，这些基因和其他显性作用基因的身份尚不清楚。
Intraperitoneal plasma cell tumors (PCTs) are induced by pristane (tetramethylpentadecane), a branched-chain alkane paraffin oil, in BALB/cAn and other susceptible mouse strains with minimal to mean latencies of 120 to 210 days respectively (Potter, 1972). PCTs harbor one of two reciprocal chromosome translocations always involving band D2/3 on chromosome 15 and either the Immunoglobulin heavy chain (IgH) locus on 12 or the kappa light chain locus (IgK) on 6 (Ohno et al., 1979). Band D2/3 was subsequently found to be thec-mycgene locus and the activation of this proto-oncogene by such chromosomal rearrangements has been shown to be a contributing factor for plasmacytomagenesis (reviewed by Mushinski, 1988; Marcu et al., 1992). Plasmacytomagenesis was rapidly accelerated (50–120 day mean latencies) upon injection of oncogene-containing retroviruses (v-abl, myc and raf or myc and ras) along with pristane (Potter et al., 1973; Ohno et al., 1984; Potter et al., 1987; Clynes et al., 1988; Troppmair et al., 1989) and viruses-containing an activated myc oncogene induced PCTs without c-myc associated chromosome translocations (Potter et al., 1987; Clynes et al., 1988; Troppmair et al., 1989). Recently, a retrovirus harboring v-abl and c-myc was found to be the most potent oncogene combination inducing PCTs in 100% of adult BALB/c mice with or without a wild type Moloney helper virus and also in the absence of pristane (Weissinger et al., 1991). These observations would collectively argue that multiple genetic events in addition to c-myc activation are required for malignant plasma cell tumor formation. Indeed, at least three recessive genetic loci are believed to confer resistance to PCT formation in non-sensitive mouse strains but the identities of these genes and other dominant acting ones in addition to myc remain unknown.