Trop2 is considered to have an important function in tumor metastasis and the promotion of epithelial‑mesenchymal transition (EMT). E‑cadherin is a crucial factor in intercellular adhesion and EMT transformation. In the present study, we detected the expression of Trop2 and E‑cadherin in breast cancer (BC) to better define their prognostic value. The mRNA expression levels of these two genes in 20 cases of fresh BC tissues were detected by quantitative real‑time polymerase chain reaction (qRT‑PCR). We also detected the expression levels of these two genes by immunohistochemistry (IHC) in 312 BC tissues, and the correlations between the expression of these two genes and the clinicopathological characteristics in BC patients were analyzed. The mRNA and protein expression levels of the two genes in BC cell lines were studied by qRT‑PCR and western blotting. The results indicated that Trop2+/E‑cadherin‑ was expressed in BC tissues more than that in the matched adjacent tissues. The protein expression results obtained via IHC were similar to the mRNA expression results. Trop2+/E‑cadherin‑ that was expressed in BC was associated with lymph node status, metastasis, tumor‑node‑metastasis (TNM) stage, and ER‑/PR‑/HER2‑ expression. BC patients that expressed Trop2+/E‑cadherin‑ had poor overall survival rates. The results of Trop2 and E‑cadherin expression levels obtained in the BC cell lines were the same as those obtained in the BC tissues. Overall, Trop2 has a potential role in the promotion of EMT in BC and it could be considered as a therapeutic target in the future.

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Chromosomal instability (CIN) is an important hallmark of human cancer. CIN not only contributes to all stages of tumor development (initiation, promotion and progression) but also drives, in large measure, the acquisition of drug resistance by cancer cells. Although CIN is a cornerstone of the complex mutational architecture that underlies neoplastic cell development and tumor heterogeneity and has been tightly associated with treatment responses and survival of cancer patients, it may be one of the least understood features of the malignant phenotype in terms of genetic pathways and molecular mechanisms. Here we review new insights into the type of CIN seen in multiple myeloma (MM), a blood cancer of terminally differentiated, immunoglobulin-producing B-lymphocytes called plasma cells that remains incurable in the great majority of cases. We will consider bona fide myeloma CIN genes, methods for measuring CIN in myeloma cells, and novel approaches to CIN-targeted treatments of patients with myeloma. The new findings generate optimism that enhanced understanding of CIN will lead to the design and testing of new therapeutic strategies to overcome drug resistance in MM in the not-so-distant future.

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