Reporter and Curator: Dr. Sudipta Saha, Ph.D.
Hepatocellular carcinoma is one of the most common malignancies worldwide, and it has a poor prognosis due to its rapid development and early metastasis. An understanding of tumor metabolism would be helpful for the clinical diagnosis and therapy of hepatocellular carcinoma. Chronic hepatitis B virus infection is the primary risk factor for hepatocellular carcinoma, and the majority of hepatocellular carcinoma cases develop from hepatitis infections and subsequent cirrhosis. Rapid development and early metastasis are the typical characteristics of hepatocellular carcinoma, which always results in a poor prognosis. Therefore, investigating the hepatocarcinogenesis mechanism is very important for decreasing the incidence and mortality of hepatocellular carcinoma. The abnormal metabolism of cancer has been considered an important characteristic of tumors, which could clarify the pathogenesis and provide potential therapeutic targets for clinical treatments. According to the Warburg effect, the deregulated energy metabolism of cancer cells may also modify many related metabolic pathways that influence various biological processes, such as cell proliferation and apoptosis. As a common characteristic of cancer cells, modified metabolism has been the focus of cancer research.
Because of its asymptomatic nature, hepatocellular carcinoma is usually diagnosed at late and advanced stages, for which there are no effective therapies. Thus, biomarkers for early detection and molecular targets for treating hepatocellular carcinoma are urgently needed. Emerging high-throughput metabolomics technologies have been widely applied, aiming at the discovery of candidate biomarkers for cancer staging, prediction of recurrence and prognosis, and treatment selection. Tissue metabolomics is a useful tool for studying the abnormal metabolisms of diseases, and it can provide information about the metabolic modifications and the upstream regulative mechanism in diseases. More importantly, the systemic metabolic characteristics of tissues could provide opportunities for exploring novel diagnostic markers or therapeutic targets for clinical applications. Tissue metabolomics is conducted using a pairwise comparison of different parts of tissue from each patient, which can remove individual differences, such as age, sex, region, etc. The differences between the tumor cells and their surrounding host cells may reflect the interactions of the tumor and the host, which are important clues for studying the invasion and metastasis of tumors. Metabolic profiles, which are affected by many physiological and pathological processes, may provide further insight into the metabolic consequences of this severe liver disease. Small-molecule metabolites have an important role in biological systems and represent attractive candidates to understand hepatocellular carcinoma phenotypes. The power of metabolomics allows an unparalleled opportunity to query the molecular mechanisms of hepatocellular carcinoma.
Source References:
http://www.ncbi.nlm.nih.gov/pubmed/23824744
http://www.ncbi.nlm.nih.gov/pubmed/23150189
http://onlinelibrary.wiley.com/doi/10.1002/hep.26350/abstract
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This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.