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Michael Michael

Researcher at Peter MacCallum Cancer Centre

Publications -  341
Citations -  13183

Michael Michael is an academic researcher from Peter MacCallum Cancer Centre. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 49, co-authored 299 publications receiving 11467 citations. Previous affiliations of Michael Michael include Flinders Medical Centre & University of Melbourne.

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Journal Article

Reduced accumulation of specific microRNAs in colorectal neoplasia.

TL;DR: A study was undertaken to investigate possible changes in microRNA levels during tumorigenesis, identifying a total of 28 different miRNA sequences, including 3 novel sequences and a further 7 that had previously been cloned only from mice.
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Hypoxic enhancement of exosome release by breast cancer cells

TL;DR: Evidence is provided that hypoxia promotes the release of exosomes by breast cancer cells, and that this hypoxic response may be mediated by HIF-1 α, and this has significant implications for understanding the hypoxic tumour phenotype.
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Quantitative evaluation of Escherichia coli host strains for tolerance to cytosine methylation in plasmid and phage recombinants

TL;DR: In this paper, the authors quantitatively evaluated a total of 39 E. coli strains for their tolerance to cytosine methylation in phage and plasmid cloning systems, and provided a rational basis for future construction of 'ideal' hosts combining optimal methylation tolerance with additional advantageous mutations.
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Safety and efficacy of first-line bevacizumab with FOLFOX, XELOX, FOLFIRI and fluoropyrimidines in metastatic colorectal cancer: the BEAT study

TL;DR: The BEAT study shows that the efficacy and safety profile of bevacizumab in routine clinical practice is consistent with results observed in prospective randomised clinical trials and another large observational study in the United States.
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MET Amplification Identifies a Small and Aggressive Subgroup of Esophagogastric Adenocarcinoma With Evidence of Responsiveness to Crizotinib

TL;DR: MET amplification defines a small and aggressive subset of GEC with indications of transient sensitivity to the targeted MET inhibitor crizotinib (PF-02341066), and survival analysis in patients with stages III and IV disease showed substantially shorter median survival in MET/EGFR-amplified groups.