Starting things off, our friends at the MolBio Hut (formerly MolBio Research Highlights) send us a post on adult stem cells and cancer relapse. This post is part of a blog feature that consists of posts on new research written by the authors of those papers. This is a great idea, and hopefully there will be many more in the series.
Given the fact that these “relapse-causing cells” are long lived and able to regenerate whole tumors, we sought out to find whether there was a relationship between cancer recurrence and intestinal stem cells. In this “Direct Connection”, I will describe our work entitled “The Intestinal Stem Cell Signature Identifies Colorectal Cancer Stem Cells and Predicts Disease Relapse”, published earlier this year on Cell Stem Cell.Genome Engineering sends us s couple of posts for the carnival. First is discussion of new research into a broad spectrum cancer vaccine.
Prostate cancer is the most common cancer in men. It is generally a slow growing form of cancer, though some men have a more aggressive form of the disease. Conventional management of prostate cancer includes ‘watch and wait’, surgery or radio-or chemotherapy. Animal studies of a prostate cancer DNA vaccine have suggested a new approach to cancer treatment that may have potential to stabilise or cure tumours.Of course this is still in very early stages and hasn't moved beyond animal models. Next is new research published in Nature on genes associated with estrogen-receptor negative breast cancer.
Breast cancer can be divided into two main types – oestrogen receptor-positive and oestrogen receptor-negative. Up to a third of breast cancers are oestrogen receptor-negative and are generally harder to treat because they are not responsive to treatments such as tamoxifen or other hormone-related treatments. There have been fewer advancements in therapeutics for this group. US researchers have linked a gene with this form of cancer and published the results in Nature.Sticking with cancer-related genes, also check out brief posts on leukemia genome sequencing to identify recurrent mutations and analysis of ovarian cancer genes in the Cancer Genome Atlas.
Over at Bionews, we have a post describing research into gene silencing that may have implications for cancer treatment.
Some cancer drugs already work through demethylation, but this process is non-specific, which can cause side effects and other problems, Dr Alfonso Bellacosa, an associate professor at Fox Chase, explained. Using a specific process it could be possible to turn on incorrectly silenced genes, leading to potential cancer therapeutics that target the mechanisms underlying cancer development.Finally, we have a two part piece on peer-reviewed research searching for new cancer drugs (part 1, part 2)
Metastasis—the spread of cancer from the place where it first started to another place in the body—is the most common reason that cancer treatments fail. To metastasize, some types of cancer cells rely on invadopodia, cellular membrane projections that act like feet, helping them “walk” away from the primary tumor and invade surrounding tissues. To determine how cells control invadopodia formation, Sanford-Burnham scientists screened a collection of pharmacologically active compounds to identify those that either promote or inhibit the process. They turned up several invadopodia inhibitors that target a family of enzymes called cyclin-dependent kinases (Cdks), revealing a previously unrecognized role for Cdks in invadopodia formation. These findings appeared online July 26 in Science Signaling.Keep an eye on that blog as the host of a future edition of the Cancer Carnival.
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.