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Olli Kallioniemi

Researcher at University of Helsinki

Publications -  376
Citations -  44711

Olli Kallioniemi is an academic researcher from University of Helsinki. The author has contributed to research in topics: Cancer & Prostate cancer. The author has an hindex of 90, co-authored 353 publications receiving 42021 citations. Previous affiliations of Olli Kallioniemi include European Bioinformatics Institute & Åbo Akademi University.

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Integrative functional genomics analysis of sustained polyploidy phenotypes in breast cancer cells identifies an oncogenic profile for GINS2.

TL;DR: Bioinformatic analysis of published gene expression and DNA copy number studies of clinical breast tumors suggested GINS2 to be associated with the aggressive characteristics of a subgroup of breast cancers in vivo suggesting potential use of G INS2 staining as a biomarker of cell proliferation as well as a potential therapeutic target.
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Flow cytometric analysis of DNA ploidy and S-phase fraction from prostatic carcinomas: implications for prognosis and response to endocrine therapy.

TL;DR: In this article, the ploidy and S-phase fraction (SPF) from 78 paraffin-embedded primary prostatic carcinomas were analyzed by DNA flow cytometry and it was shown that SPF was associated with high tumour grade, large size of prostate and presence of distant metastases.
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The miR-15a-miR-16-1 locus is homozygously deleted in a subset of prostate cancers.

TL;DR: The data indicate that putative tumor suppressors, miR‐15a and miR-16‐1, are homozygously deleted in a subset of prostate cancers, further suggesting that these miRNAs could be important in the development of prostate cancer.
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Detection of retinoblastoma gene copy number in metaphase chromosomes and interphase nuclei by fluorescence in situ hybridization.

TL;DR: Analysis of clinical breast cancer samples showed that most of the cells contained two copies of the RB1 gene, even when restriction fragment length polymorphism analysis showed loss of heterozygosity (LOH) at theRB1 locus, which indicates that LOH at the RB 1 locus in breast cancer cells probably involves mechanisms other than physical deletion.