A progressive increase in the degree of allelic imbalance (calculated as the number of SNP markers with allelic imbalance/total SNP markers examined) of chromosomes 1p, 5q, 8p, 18q, 22q, and Xp was noted when comparing atypical proliferative tumors with noninvasive MPSCs and low-grade serous carcinomas (invasive MPSCs).4 In particular, allelic imbalance of chromosome 5q was more frequently observed in noninvasive MPSCs compared with atypical proliferative tumors. Moreover, allelic imbalance of chromosome 1p, which harbors tumor suppressor genes, including MYCL1 and NOERY/ARH1, was more frequently found in low-grade serous carcinoma (invasive MPSC) compared with noninvasive MPSCs. The allelic imbalance patterns in atypical proliferative tumors were also found in noninvasive MPSCs containing adjacent atypical proliferative tumor components, further supporting the view that atypical proliferative tumors are the precursors of MPSCs. On the contrary, all high-grade serous carcinomas including the very earliest tumors (less than 8 mm confined to one ovary) showed high levels of allelic imbalance. Since allelic imbalance reflects chromosomal instability (changes in DNA copy number), the previous findings suggest a stepwise increase in chromosomal instability in the progression to low-grade serous carcinoma in contrast to a high level of chromosomal instability in high-grade serous carcinoma, even in their earliest stage of development. Microsatellite instability also reflects the genetic instability in tumor cells. Microsatellite instability has been studied in serous borderline tumors using 69 microsatellite markers.39
Similar to high-grade serous carcinoma in which frequency of microsatellite instability is rare,40 serous borderline tumors showed no evidence of microsatellite instability. Thus, microsatellite instability is not a likely hallmark of ovarian carcinoma.
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