TissueGnostics develops systems for automated identification and functional characterization of single cells in tissue sections, cultured and smeared cells as well as TMA. This includes automated image acquisition and image processing for immunohistochemistry and multi-chanel immunofluorescence.
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Aug 17, 2023
Register for an engaging webinar led by Naz Chaudary, Ph.D., and Research Technician, Alex Wang from the...
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RareCyte Orion’ platform has been used for collecting H&E and high-plex immunofluorescence images from the same cells...
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Using Cytek full spectrum flow cytometry, scientists at Hamad Medical Corporation, developed a 43 color panel to...
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Nature Article: The genomic landscape of pediatric acute lymphoblastic leukemia
Jun 29, 2023
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. Here, using whole-genome, exome and...
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This study evaluates the quantitative measurability of glial fibrillary acidic protein (GFAP), neurofilament light...
PET from Molecubes for imaging of neuroendocrine tumors
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HistoQuest software in cancer research
Mar 22, 2016
Prostate cancer (PCa) is the most prevalent cancer in men. Hyperactive STAT3 is thought to be oncogenic in PCa. However, targeting of the IL-6/STAT3 axis in PCa patients has failed to provide therapeutic benefit. Here we show that genetic inactivation of Stat3 or IL-6 signalling in a Pten-deficient PCa mouse model accelerates cancer progression leading to metastasis. Mechanistically, we identify p19ARF as a direct Stat3 target. Loss of Stat3 signalling disrupts the ARF–Mdm2–p53 tumour suppressor axis bypassing senescence. Strikingly, we also identify STAT3 and CDKN2A mutations in primary human PCa. STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases. In accordance, loss of STAT3 and p14ARF expression in patient tumours correlates with increased risk of disease recurrence and metastatic PCa. Thus, STAT3 and ARF may be prognostic markers to stratify high from low risk PCa patients. Our findings challenge the current discussion on therapeutic benefit or risk of IL-6/STAT3 inhibition.
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