Ductal breast carcinoma develops through different patterns of chromosomal evolution

Abstract

In a previous study that used comparative genomic hybridization (CGH) to analyze 43 ductal breast carcinomas selected for hyperdiploidy, we proposed the existence of two distinct pathways of chromosomal evolution. In the present study, in which we reassessed our cytogenetic findings on 158 ductal breast carcinomas selected for having a modal number of chromosomes of fewer than 60, we confirmed the existence of two subtypes of tumors. Along with the great majority of tumors (142 of 158) that evolved through structural rearrangements with no or very few whole-chromosome gains, we found that a minor subset (16 of 158) evolved through progressive gains of whole chromosomes with no or only a few associated rearrangements. In this article, we describe the karyotypes of these 16 tumors together with data from CGH, which was performed for 10 of them. Chromosomes 5, 7, 8, and 20 were the most frequently gained. Our findings support the evidence of a new pathway of chromosomal evolution in a small subset of ductal breast carcinomas characterized by numerical chromosome aberrations.

Comparative expressed sequence hybridization reveals differential gene expression in morphological breast cancer subtypes

“…Using ERBB2 status as a major discriminating factor for poorly differentiated IDC‐NOS, we made an interesting observation: CESH yielded more expression variation between poorly differentiated ERBB2 ‐positive and grade‐matched ERBB2 ‐negative IDC‐NOS than between ductal and lobular carcinoma (5 versus 3 at 95% CL/4 versus 2 at 99% CL). These findings strengthen the hypothesis that IDC‐NOS, even within‐grade, is a heterogeneous group of diseases exhibiting various genetically discernible subgroups 35. We could further establish an ERBB2 expression signature comprising four chromosomal regions that were up‐regulated in node‐negative, ERBB2 ‐positive IDC‐NOS: 3q24–q26.3, 14q24–q31, 17q12, and 20q12–q13.1 (95% CL).…”

Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromes

“…For example, close to 50 cases of acute lymphoblastic leukemias (ALL), many of which of T-cell lineage, with +8 as the single anomaly have been published, and some solid tumor types/lesions, in particular desmoid tumors and Dupuytren's contracture, are also characterized by this abnormality [16][17][18]. Trisomy 8 is also common together with other chromosomal aberrations in a large number of tumor types, such as colon, breast, and head and neck cancer [19][20][21], Wilms tumor [22], and hepatoblastoma [23].…”