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Invasive micropapillary carcinoma (IMPC) is a rare (up to 2%) and aggressive form of breast cancer.1 ,2 IMPC shows high intratumoral morphological diversity, which represents the degree of cell differentiation, as well as the architectural and invasive growth patterns of tumour cells. Morphologically, these tumours are characterised by the presence of hollow-like (tubular) and morula-like (alveolar) structures of cuboidal-to-columnar neoplastic cells, which are surrounded by empty spaces (retraction clefts) and display an inversion of cell polarity, detected by aberrant localisation of glycoprotein MUC-1 at the stromal–basal surface.1 ,3 In addition, micropapillary tumour clusters can be represented by tumour cells arranged in solid patterns (structures), trabecular structures and discrete (small) groups.3–6 It has been suggested that morphological diversity of IMPC is related to chemotherapy resistance,7 whereas the presence of retraction clefts around tumour clusters is associated with increased lymphangiogenesis and lymph node metastasis.8
Considerable intratumour morphological heterogeneity in breast cancer most likely results from genetic and epigenetic instability of the tumour cells.9 ,10 Previously, the relationships between morphologically distinct components and specific chromosome aberrations have been found in metaplastic and invasive ductal breast carcinomas,11 ,12 the latter is now classified as invasive carcinoma of no special type (IC NST), and is the most common histological type of breast cancer.1
IMPC demonstrates a heterogeneous pattern of chromosome aberrations, and tends to be genetically a more complex disease than IC NST.11 ,12 IMPC more often harboured gains of chromosomes 1q, 8q, 17q and 20q, and losses of 1p, 8p, 13q, 16q and 22q,13 ,14 which were emphasised by Marchio and coauthors13 as previously associated with breast tumours of high histological grade. In contrast, concurrent gain of 1q and 16p and deletion of 16q, related to low …
Contributors EVD and NAS designed the study. MVZ and VMP collected the tumour samples. EVD and TSG performed laser microdissection and whole genome amplification. NAS and SAV performed array comparative genomic hybridisation and analysed data. EVD, NAS and SAV wrote the paper. INL, NVC and VMP assisted in critiquing, editing and refining the paper. All authors reviewed the manuscript.
Funding The study was supported by the Russian Scientific Foundation (grant #14-15-00318). The study was done using equipment under support of Human Proteome Project of Russian Academy of Sciences. EVD was supported by Tomsk State University Competitiveness Improvement Programme.
Competing interests None declared.
Patient consent Obtained.
Ethics approval The procedures followed in this study were in accordance with the Declaration of Helsinki (1964, amended in 1975 and 1983). This study was approved by the institutional (Cancer Research Institute, SB RAMS) review board, the patient signed an informed consent for voluntary participation, and the number of ethical approval was 10 (29 September 2011).
Provenance and peer review Not commissioned; externally peer reviewed.
EVD and NAS contributed equally.
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