Lakhani S R, Collins N, Stratton M R, Sloane J P
Department of Histopathology, Royal Marsden NHS Trust, Sutton, Surrey.
J Clin Pathol. 1995 Jul;48(7):611-5. doi: 10.1136/jcp.48.7.611.
To determine if allelic loss on chromosomes 16q and 17p, commonly encountered in in situ and invasive ductal carcinomas, is present in atypical ductal hyperplasia (ADH); to determine whether ADH is a neoplastic (clonal) or hyperplastic (polyclonal) proliferation.
Fourteen cases of ADH were examined for allele loss at loci on chromosome 16q and 17p using a microdissection technique, polymorphic DNA markers and the polymerase chain reaction (PCR).
Loss of heterozygosity (LOH) was detected in five of nine informative cases on chromosome 16q at the microsatellite D16S413 and two of eight informative cases on chromosome 17p at D17S796.
The incidence of LOH at these loci is similar to that previously observed in ductal carcinoma in situ and in invasive ductal carcinoma. Because of the nature of the technique used, our findings also demonstrate that ADH is a monoclonal, and hence, neoplastic proliferation rather than a hyperplastic (polyclonal) condition as its name suggests. There is thus a case for including ADH, as presently defined, within the spectrum of ductal carcinoma in situ.
确定原位和浸润性导管癌中常见的16号染色体长臂和17号染色体短臂上等位基因缺失是否存在于非典型导管增生(ADH)中;确定ADH是肿瘤性(克隆性)还是增生性(多克隆性)增殖。
采用显微切割技术、多态性DNA标记和聚合酶链反应(PCR),对14例ADH病例进行16号染色体长臂和17号染色体短臂上基因座的等位基因缺失检测。
在9例信息充分的病例中,有5例在16号染色体长臂的微卫星D16S413处检测到杂合性缺失(LOH);在8例信息充分的病例中,有2例在17号染色体短臂的D17S796处检测到LOH。
这些基因座处的LOH发生率与先前在原位导管癌和浸润性导管癌中观察到的相似。由于所用技术的性质,我们的研究结果还表明,ADH是一种单克隆性的,因此是肿瘤性增殖,而不是如其名称所暗示的增生性(多克隆性)病变。因此,有理由将目前定义的ADH纳入原位导管癌的范畴。