Studies on the pathogenesis of B cell malignancies

KHM-10B是由一名伯基特淋巴瘤患者建立的。常规细胞遗传学分析未发现8q24参与，Southern blot研究未检测到c-myc癌基因重排。然而，荧光原位杂交（FISH）检测发现，22q11部分的掩码t(8; 22)（q24; q11）被转移到8q24位点。用羟基脲和噻咪啶将kkm - 10b细胞阻滞在S期，同步细胞在无药培养基中进行细胞周期。c-myc和max在整个细胞周期内均有组成性表达；与另一种伯基特淋巴瘤细胞系Raji中发现的一样。KHM-11是由IgA-kappa型侵袭性骨髓瘤患者的胸腔积液建立的，该患者血清乳酸脱氢酶高，对长春新素、阿霉素和地塞米松联合治疗（VAD）极度耐药。除了正常的浆细胞抗原CD38和PCA-1的表达外，新鲜细胞和kkm -11上都发现了CD45。其他t细胞或b细胞抗原，如CD2、4、8、19和20均为阴性。在kkm -11的培养上清中发现IL-6，该上清刺激了该细胞系的生长，提示IL-6的自分泌机制。这些发现表明kkm -11是一种cd45阳性的未成熟浆细胞系。这两种细胞系kkm - 10b和kkm -11应该成为了解B细胞恶性肿瘤发病机制的有用工具。

KHM-10B was established from a patient with Burkitt's lymphoma. Conventional cytogenetic analysis revealed no detectable 8q24 involvement, and the rearrangement of c-myc oncogene could not detected by Southern blot study. However, fluorecence in situ hybridization (FISH) assay identified masked t(8 ; 22)(q24 ; q11) which is the 22q11 portion was translocated to the 8q24 locus. Using hydroxyurea and thimidine, the KHM-10B cells were arrested at S phase, and the syncronized cells progressed the cell cycle in drug free medium. The constitutive expressions of c-myc and max were observed throughout the cell cycle ; as was found in another Burkitt's lymphoma cell line, Raji.KHM-11 was established from the pleural effusion of a patient with IgA-kappa type aggresive myeloma with high serum lactate dehydrogenase who was extermely resistant to vincristin, adriamycin and dexamethasone combination therapy (VAD). In addition to the expression of regular plasma cell antigens, CD38 and PCA-1, CD45 was found on both fresh cells and KHM-11. Other T-or B-cell antigens, such as CD2,4,8,19 and 20 were negative. IL-6 was found in the culture supernatant of KHM-11, and this supernatant stimulated the growth of this cell lines, indicating an IL-6 autocrine mechanism. These findings indicate that KHM-11 is a CD45-positive immature plasma cell line.Both cell lines, KHM-10B and KHM-11 should be a useful tool for understanding the pathogenesis of B cell maliganancies.