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本文引用的文献

1
FISH mapping of Philadelphia negative BCR/ABL1 positive CML.费城阴性BCR/ABL1阳性慢性粒细胞白血病的荧光原位杂交定位
Mol Cytogenet. 2008 Jul 18;1:14. doi: 10.1186/1755-8166-1-14.
2
A complex translocation t(5;9;22) in Philadelphia cells involving the short arm of chromosome 5 in a case of chronic myelogenous leukemia.在一例慢性髓性白血病患者的费城细胞中发现涉及5号染色体短臂的复杂易位t(5;9;22) 。
J Exp Clin Cancer Res. 2007 Sep;26(3):411-5.
3
Chronic myeloid leukaemia as a model of disease evolution in human cancer.慢性髓性白血病作为人类癌症疾病演变的模型。
Nat Rev Cancer. 2007 Jun;7(6):441-53. doi: 10.1038/nrc2147.
4
Location of the BCR/ABL fusion genes on both chromosomes 9q34 in Ph negative chronic myeloid leukemia.Ph阴性慢性髓性白血病中BCR/ABL融合基因在两条9号染色体q34上的定位。
Leuk Lymphoma. 2002 Aug;43(8):1695-700. doi: 10.1080/1042819021000003063.
5
The ABL/BCR fusion gene on chromosome 9 in Ph-negative chronic myelogenous leukemia: a case for vigilance in fluorescence in situ hybridization interpretation.Ph阴性慢性髓性白血病中9号染色体上的ABL/BCR融合基因：荧光原位杂交解读中需警惕的一个案例
Cancer Genet Cytogenet. 1998 Jul 1;104(1):57-60. doi: 10.1016/s0165-4608(97)00430-5.
6
Location of the BCR-ABL fusion gene on the 9q34 band in two cases of Ph-positive chronic myeloid leukemia.两例Ph阳性慢性髓性白血病中BCR-ABL融合基因在9q34染色体带上的定位
Genes Chromosomes Cancer. 1997 Oct;20(2):148-54.
7
Duplication of chromosome 9 carrying a BCR/ABL chimeric gene in Philadelphia chromosome negative chronic myeloid leukemia.9号染色体重复，在费城染色体阴性慢性髓性白血病中携带BCR/ABL嵌合基因。
Cancer Genet Cytogenet. 1996 Jul 15;89(2):166-9. doi: 10.1016/0165-4608(96)00039-8.
8
Translocation of BCR to chromosome 9 in a Philadelphia-negative chronic myeloid leukemia.费城阴性慢性髓性白血病中BCR向9号染色体的易位。
Cancer Genet Cytogenet. 1995 Nov;85(1):82-4. doi: 10.1016/0165-4608(95)00140-9.
9
Philadelphia-negative chronic myeloid leukaemia: detection by FISH of BCR-ABL fusion gene localized either to chromosome 9 or chromosome 22.
Br J Haematol. 1994 Jun;87(2):409-12. doi: 10.1111/j.1365-2141.1994.tb04933.x.
10
Translocation of BCR to chromosome 9: a new cytogenetic variant detected by FISH in two Ph-negative, BCR-positive patients with chronic myeloid leukemia.BCR基因易位至9号染色体：在两名Ph阴性、BCR阳性的慢性髓性白血病患者中通过荧光原位杂交检测到的一种新的细胞遗传学变异。
Genes Chromosomes Cancer. 1993 Dec;8(4):237-45. doi: 10.1002/gcc.2870080406.

在一例费城染色体阴性的慢性髓性白血病病例中，3' ABL区域插入到1号染色体长臂。

Insertion of the 3' ABL region into the long arm of chromosome 1 in a Philadelphia chromosome-negative chronic myeloid leukemia case.

作者信息

Al-Achkar Walid, Liehr Thomas, Wafa Abdulsamad

机构信息

Molecular Biology and Biotechnology Department, Human Genetics Division, Atomic Energy Commission of Syria, Damascus, Syria.

出版信息

Oncol Lett. 2010 Nov;1(6):951-954. doi: 10.3892/ol.2010.180. Epub 2010 Sep 23.

DOI:10.3892/ol.2010.180
PMID:22870093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3412448/
Abstract

Chronic myeloid leukemia (CML) is a pluripotent hematopoietic stem cell disorder almost always characterized by the presence of the Philadelphia chromosome (Ph), usually due to t(9;22)(q34;q11). The presence of Ph results in the formation of the BCR/ABL fusion gene, which is a constitutively activated tyrosine kinase. Approximately 1% of CML patients appear to have a Ph-negative karyotype but carry a cryptic BCR/ABL fusion that can be located by fluorescence in situ hybridization (FISH) at chromosome 22q11, 9q34 or a third chromosome. This study investigated a rare Ph-negative CML case with insertion of the 3' ABL region into the long arm of derivative chromosome 1 but lacking the 5' BCR region on der(22).

摘要

慢性髓性白血病（CML）是一种多能造血干细胞疾病，几乎总是以费城染色体（Ph）的存在为特征，通常是由于t(9;22)(q34;q11)。Ph的存在导致BCR/ABL融合基因的形成，这是一种组成型激活的酪氨酸激酶。大约1%的CML患者似乎具有Ph阴性核型，但携带一种隐匿性BCR/ABL融合，可通过荧光原位杂交（FISH）定位在22q11、9q34或第三条染色体上。本研究调查了一例罕见的Ph阴性CML病例，其3' ABL区域插入衍生染色体1的长臂，但在der(22)上缺乏5' BCR区域。