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Depleted in ER− tumors were the cytobands 4p16, 5q11 13, 5q22, 5q31, 14q22 23 which show more frequent loss in basal tumors, and 16p11 p13 which shows more frequent gain in luminal tumors [30].

However, some differences were visually apparent, such as the more frequent gain of 1q, 8q and 17q regions in IBCs, or the more frequent loss of 4p, 8p, 11q, and 16q regions in nIBCs.

The cases with loss of E2 also showed more frequent gain on 3q (P<0.05).

However, a few discordances exist, mainly corresponding to more frequent gain of 16p and less frequent aberrations on chromosome 7 in the current study.

Cases of HPV16-positive HG-SIL in which the E2 gene was disrupted showed significantly more CNIs and significantly more frequent gain on 3q than cases in which the E2 gene was intact.

Similar(55)

Luminal cell lines were characterized by more frequent gains on 1q, 8q, 11q, 12q, 14q, 17q and 20q, and losses on 8p, 9p, 11q, 13q, and 18p.

The non-GCB group was genomically characterized by more frequent gains at 11q24.1 and 3q (P < 0.05).

The non-GCB subtype was genomically characterized by more frequent gains at 11q24.3 and 3q13.2 (P < 0.05).

We propose that this shift is not due to better EV but rather an effect resulting from more frequent gains than losses.

The GCB group was genomically characterized by more frequent gains at 7q (7q22.1, P < 0.05), and losses at 16q (P < 0.05) (Figs 2and 3a–c, Table 3).

Surprisingly, the location of more frequent gains and losses in the cell lines very closely mirrored those in the primary tumors (Fig. 1).

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