Ramiro Almudena, Reina San-Martin Bernardo, McBride Kevin, Jankovic Mila, Barreto Vasco, Nussenzweig André, Nussenzweig Michel C
DNA Hypermutation and Cancer Group, Spanish National Cancer Center (CNIO), Melchor Fernandez Almagro, 3, 28029 Madrid, Spain.
Adv Immunol. 2007;94:75-107. doi: 10.1016/S0065-2776(06)94003-6.
Although B and T lymphocytes are similar in many respects including diversification of their antigen receptor genes by V(D)J recombination, 95% of all lymphomas diagnosed in the western world are of B-cell origin. Many of these are derived from mature B cells [Kuppers, R. (2005). Mechanisms of B-cell lymphoma pathogenesis. Nat. Rev. Cancer 5, 251-262] and display hallmark chromosome translocations involving immunoglobulin genes and a proto-oncogene partner whose expression becomes deregulated as a result of the translocation reaction [Kuppers, R. (2005). Mechanisms of B-cell lymphoma pathogenesis. Nat. Rev. Cancer 5, 251-262; Kuppers, R., and Dalla-Favera, R. (2001). Mechanisms of chromosomal translocations in B cell lymphomas. Oncogene 20, 5580-5594]. These translocations are essential to the etiology of B-cell neoplasms. Here we will review how the B-cell specific molecular events required for immunoglobulin class switch recombination are initiated and how they contribute to chromosome translocations in vivo.
尽管B淋巴细胞和T淋巴细胞在许多方面相似，包括通过V(D)J重排使其抗原受体基因多样化，但在西方世界诊断出的所有淋巴瘤中，95%起源于B细胞。其中许多源自成熟B细胞[库珀斯，R.（2005年）。B细胞淋巴瘤发病机制。《自然评论：癌症》5，251 - 262]，并表现出涉及免疫球蛋白基因和原癌基因伙伴的标志性染色体易位，由于易位反应，其表达变得失调[库珀斯，R.（2005年）。B细胞淋巴瘤发病机制。《自然评论：癌症》5，251 - 262；库珀斯，R.，和达拉 - 法韦拉，R.（2001年）。B细胞淋巴瘤中染色体易位的机制。《癌基因》20，5580 - 5594]。这些易位对于B细胞肿瘤的病因至关重要。在这里，我们将综述免疫球蛋白类别转换重排所需的B细胞特异性分子事件是如何启动的，以及它们如何在体内促成染色体易位。
