Resistance to CDK2 inhibitors is associated with selection of polyploid cells in CCNE1-amplified ovarian cancer.

Purpose: Amplification of cyclin E1 (CCNE1) is associated with poor outcome in breast, lung, and other solid cancers, and is the most prominent structural variant associated with primary treatment failure in high-grade serous ovarian cancer (HGSC). We have previously shown that CCNE1-amplified tumors show amplicon-dependent sensitivity to CCNE1 suppression. Here, we explore targeting CDK2 as a novel therapeutic strategy in CCNE1-amplified cancers and mechanisms of resistance.

Deletion(20q) as the sole abnormality in plasma cell myeloma is not associated with plasma cells as identified by cIg FISH.

Deletion of 20q is a common finding in myeloid disorders but it is also observed in plasma cell myeloma (PCM). As a del(20q) in a patient receiving treatment for myeloma may indicate therapy-related myelodysplastic syndrome (t-MDS), it is important to differentiate chromosome abnormalities associated with myeloma from those reflecting t-MDS. We performed fluorescence in situ hybridization (FISH) using a 20q12 probe (D20S108) in conjunction with cytoplasmic immunoglobulin (cIg) staining in 20 PCM cases with a del(20q) in order to confirm the cell type involved.

Secondary clonal cytogenetic abnormalities following successful treatment of acute promyelocytic leukemia.

To identify patients who developed secondary clonal cytogenetic aberrations (CCA) following therapy for acute promyelocytic leukemia (APL), we retrospectively analyzed cytogenetic results from 123 patients diagnosed with APL between 1995 and 2007, who had ongoing cytogenetic analysis undertaken in our laboratory. During follow-up for APL we identified 12 patients (9.8%) who developed CCA, not detected at diagnosis of APL and unrelated to their original APL karyotype.