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Conference Paper: Pim1 is upregulated by hypoxia in hepatocellular carcinoma and promotes tumor progression
Title | Pim1 is upregulated by hypoxia in hepatocellular carcinoma and promotes tumor progression |
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Authors | |
Issue Date | 2014 |
Publisher | International Liver Cancer Association. |
Citation | The 8th Annual Conference of the International Liver Cancer Association (ILCA 2014), Kyoto, Japan, 5-7 September 2014. In Book of Abstracts, 2014, p. 38, abstract P-022 How to Cite? |
Abstract | INTRODUCTION: Hepatocellular carcinoma (HCC) is the second/third most common fatal cancer in Hong Kong and Southeast Asia associated with frequent tumor recurrence and metastasis. Apart from surgical intervention, tumor control at cellular and molecular levels can possibly improve clinical outcome. HCC is characteristically one of the most rapidly proliferating tumors which often outpace functional blood supply, leading to a regional oxygen deprivation. Therefore, molecular changes induced by hypoxia are attractive therapeutic targets. Overexpression of PIM1, a serine/threonine kinase, has been identified in recent years in solid cancers such as prostate cancer, gastric cancer, and pancreatic cancer. In the latter, PIM1 was upregulated by hypoxia. In this study, we aim at investigating the expression, functional role, and regulatory mechanism of PIM1 in HCC, which have … |
Description | Poster Session - Molecular pathogenesis, molecular pathology, cell biology and translational research: no. P-022 |
Persistent Identifier | http://hdl.handle.net/10722/211332 |
DC Field | Value | Language |
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dc.contributor.author | Lo, R | - |
dc.contributor.author | Leung, CON | - |
dc.contributor.author | Kai, AKL | - |
dc.contributor.author | Wong, C | - |
dc.contributor.author | Ng, I | - |
dc.date.accessioned | 2015-07-08T04:33:51Z | - |
dc.date.available | 2015-07-08T04:33:51Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | The 8th Annual Conference of the International Liver Cancer Association (ILCA 2014), Kyoto, Japan, 5-7 September 2014. In Book of Abstracts, 2014, p. 38, abstract P-022 | - |
dc.identifier.uri | http://hdl.handle.net/10722/211332 | - |
dc.description | Poster Session - Molecular pathogenesis, molecular pathology, cell biology and translational research: no. P-022 | - |
dc.description.abstract | INTRODUCTION: Hepatocellular carcinoma (HCC) is the second/third most common fatal cancer in Hong Kong and Southeast Asia associated with frequent tumor recurrence and metastasis. Apart from surgical intervention, tumor control at cellular and molecular levels can possibly improve clinical outcome. HCC is characteristically one of the most rapidly proliferating tumors which often outpace functional blood supply, leading to a regional oxygen deprivation. Therefore, molecular changes induced by hypoxia are attractive therapeutic targets. Overexpression of PIM1, a serine/threonine kinase, has been identified in recent years in solid cancers such as prostate cancer, gastric cancer, and pancreatic cancer. In the latter, PIM1 was upregulated by hypoxia. In this study, we aim at investigating the expression, functional role, and regulatory mechanism of PIM1 in HCC, which have … | - |
dc.language | eng | - |
dc.publisher | International Liver Cancer Association. | - |
dc.relation.ispartof | Annual Conference of the International Liver Cancer Association, ILCA 2014 | - |
dc.title | Pim1 is upregulated by hypoxia in hepatocellular carcinoma and promotes tumor progression | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Lo, R: loregina@hku.hk | - |
dc.identifier.email | Leung, CON: conleung@hku.hk | - |
dc.identifier.email | Kai, AKL: klakai@hku.hk | - |
dc.identifier.email | Wong, C: carmencl@pathology.hku.hk | - |
dc.identifier.email | Ng, I: iolng@hku.hk | - |
dc.identifier.authority | Lo, R=rp01359 | - |
dc.identifier.authority | Wong, C=rp01602 | - |
dc.identifier.authority | Ng, I=rp00335 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.hkuros | 244281 | - |
dc.identifier.spage | 38, abstract P-022 | - |
dc.identifier.epage | 38, abstract P-022 | - |