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自从25年前发现费城染色体(Ph)以来,对人类白血病染色体的大量深入研究表明:Ph染色体通常是由第22号染色体与第9号染色体相互易位而变短了的第22号染色体,t(9;22)(q34;q11).绝大多数慢性粒细胞白血病(CML)患者都有这种起源于22号染色体的标记性Ph染色体;而在急性白血病(ALL)中则极为少见.作者在系列文章中首次报道CML中Ph染色体的一种新结构以及在ALL中发现的隐匿的Ph染色体;并对在CML中首次发现的起因于四个断裂点的复杂Ph易位加倒位的结构重排进行描述.但是关于Ph染色体的结构重排以及由此而引起的诸如c-abl,c-sis之类癌
Since the discovery of the Philadelphia chromosome (Ph) 25 years ago, extensive research on human leukemia chromosomes has shown that the Ph chromosome is usually chromosome 22, which is the result of a reciprocal translocation between chromosome 22 and chromosome 9, t (9; 22) (q34; q11). The vast majority of patients with chronic myelogenous leukemia (CML) have this type of marker Ph chromosome that originated on chromosome 22, and are extremely rare in acute leukemia (ALL). A new structure of the Ph chromosome in CML and the hidden Ph chromosome found in ALL were first reported in a series of articles; and the complex Ph translocations and inverted structures that were first discovered in CML due to four breakpoints were reported. Rearrangement is described. However, structural rearrangements of the Ph chromosome and resulting cancers such as c-abl, c-sis, etc.