Cancer Carnival #36

Once again, it's the first Friday of the month, which means it's time for the Cancer Research Blog Carnival. The Carnival relies on posts and hosts, so be sure to submit your posts for next month, and if you're tired of seeing it here on the Bayblab, drop us a line to sign up as a host. On to the posts...

First up, we have a post from Byte Size Bio that arrived just after the last carnival went live. In it, he looks at a paper investigating a role of pseudogene mRNA in regulating tumour biology. By interacting with miRNA, some of these pseudogene mRNAs may act as tumour supressors or oncogenes!

PTEN1 is a pseudogene which shares a very recent common ancestor with PTEN. A mutation in PTEN1 prevents it from being translated into a protein product, but it can still be transcribed to PTEN1 mRNA. Laura Poliseno and her colleagues have shown that PTEN1 mRNA, being very similar in sequence to PTEN mRNA attracts miRNA molecules that target PTEN mRNA. In other words, PTEN1 mRNA lures PTEN-specific miRNA molecules away from PTEN mRNA, lowering the number of inactivated PTEN mRNAs.

This is a pretty cool finding, and the post was an Editor's Selection from Researchblogging.org, so be sure to check it out.

Here at the Bayblab, Rob points to recent research about fructose metabolism in pancreatic cancer. Orac, at Respectful Insolence, also writes about this study.

So how was fructose metabolized in pancreatic cancer cells? For the most part, it was used to generate nucleic acid synthesis. Compared to glucose, fructose induces is preferentially metabolized via the nonoxidative pentose phosphate pathway to synthesize nucleic acids and increase uric acid production. What this means is that fructose provides the raw materials for cancer cells to make more DNA, which cells must do in order to divide and proliferate.

At the Spittoon, 23andMe's blog, their SNPwatch feature highlights mutations associated with liver cancer in Hep-B infected patients.

Rs12136376 is near several genes: KIF1B, UBE4B and PGD. Multiple lines of evidence suggest that one or more of these genes are plausible candidates for HCC susceptibility. Changes in the region of the genome where they are found are commonly seen in many different cancers, including HCC.

Details of the SNP, the analysis and outcomes are all explained in the post.

Keith Robison at Omics! Omics! discusses a project undertaken by Genentech and Affymetrix to scan over 400 tumour genomes for mutations. Keith has a really good explanation of the methodology while MassGenomics has a broader overview of the study findings.

Finally, in another piece of research blogging, Michelle at C6-H12-O6 looks at a paper invesigating the effects of caloric restriction on glioblastoma multiforme, a malignant and invasive brain cancer.

As I said, CR-induced ketosis has been known to reduce non-invasive brain tumors. It appears that cancer cells are highly dependent on glycolysis for energy and for some reason (unknown to me, although I'm sure there's literature out there on it) seem incapable of mitochondrial respiration. As such, they cannot use ketones for energy like healthy cells can. Up until now, this hasn't been tested in more invasive cancers, where the tradeoff in neurological impairment might be worth it to stop or delay the spread of the cancer.

This is a nice write up with a good description of the background metabolism. And I don't just say that because of my own interest in CR.

That's it for this month's Cancer Research Blog Carnival. For older editions, visit the Carnival Homepage. Don't forget, the CRBC has subscription options; you can follow by email or RSS feed. An aggregated feed of credible, rotating health and medicine blog carnivals is also available. For a broader collection of science-related blog carnivals, sign up for the Science, Medicine, Environment and Nature Blog Carnival Twitter Feed.