HOMOZYGOUS DELETION OF THE ALPHA-INTERFERON AND BETA-1-INTERFERON GENES IN HUMAN-LEUKEMIA AND DERIVED CELL-LINES
HOMOZYGOUS DELETION OF THE ALPHA-INTERFERON AND BETA-1-INTERFERON GENES IN HUMAN-LEUKEMIA AND DERIVED CELL-LINES
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DOI：
10.1073/pnas.85.14.5259
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发表时间：
1988-07-01
影响因子：
11.1
通讯作者：
ROWLEY, JD
中科院分区：
文献类型：
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作者：
DIAZ, MO;ZIEMIN, S;ROWLEY, JD
由于短臂缺失、不平衡易位或单体9的缺失，在淋巴样肿瘤患者的恶性细胞中，包括急性淋巴母细胞白血病和非霍奇金淋巴瘤患者，常可观察到一条9号染色体同源物的p21-22带的丢失。α-干扰素基因和β-干扰素基因被分配到这个染色体区域(9p21-22)。现在，我们提出了在肿瘤造血细胞系和原发白血病细胞中存在或不存在在光学显微镜水平上可检测到的染色体缺失的干扰素基因纯合缺失的证据。在这些细胞系中，干扰素基因的缺失伴随着嘌呤代谢酶5‘-甲基硫代腺苷磷酸化酶(EC2.4.2.28)的缺失。这些纯合子缺失可能与肿瘤抑制基因的丢失有关，该基因与这些肿瘤的发展有关。相关基因可能是干扰素基因本身，也可能是具有肿瘤抑制功能并与之密切相关的基因。
The loss of bands p21-22 from one chromosome 9 homologue as a consequence of a deletion of the short arm [del(9p], unbalanced translocation, or monosomy 9 is frequently observed in the malignant cells of patients with lymphoid neoplasias, including acute lymphoblastic leukemia and non-Hodgkin lymphoma. The .alpha.- and .beta.1-interferon genes have been assigned to this chromosome region (9p21-22). We now present evidence of the homozygous deletion of the interferon genes in neoplastic hematopoietic cell lines and primary leukemia cells in the presence or absence of chromosomal deletions that are detectable at the level of the light microscope. In these cell lines, the deletion of the interferon genes is accompanied by a deficiency of 5''-methylthioadenosine phosphorylase (EC 2.4.2.28), an enzyme of purine metabolism. These homozygous deletions may be associated with the loss of a tumor-suppressor gene that is involved in the development of these neoplasias. The relevant genes may be either the interferon genes themselves or gene that has a tumor-suppressor function and is closely linked to them.