Sporting Life 10k For Kids with Cancer
The Sporting Life 10k is scheduled for May 2, 2010 and is supporting Camp Oochigeas, a camp for children with cancer. With no government funding, Camp Oochigeas relies on the generosity of volunteers, donors, community participants and the Hospital for Sick Children to provide year-round programs for children affected by childhood cancer at their campsite in Muskoka and at no cost to their families. I am personally raising at least $250 (update: at least $500) for this charity — please support me in my fundraising efforts.

Gearing-up: Nike + iPod
To get in-gear for the 10k, I joined Nikeplus.com (my profile page) and consulted their “coach”. Unfortunately, Nikeplus only offers a 12-week program — not 42 days (as at yesterday) — so I figure I’ll follow the first 5.5 weeks of the program to get in-shape for the big run. Yesterday, I was assigned my first run from coach — I had to run 4.82km! Talk about being thrown into the deep-end. So, I ventured to the University of Toronto gym to run the indoor track with my Nike + iPod sensor and iPhone to track my progress.

Although I had to walk for a few periods of time, here are my net results for run #1:

• Distance: 4.82km
• Duration: 30:42
• Pace: 6′22″ /km
• Fastest Kilometer: 5′42″
• Calories Burned: 371

If you join Nikeplus, add me as a friend (username: jsookman).

More Details on the 10k Race
It is Canada’s easiest and one of the fastest downhill 10k’s (a good starter, I think…), and it runs right down the middle of Canada’s most famous street—Yonge Street! The start line is four blocks south of Sporting Life (at Yonge & Roselawn). From there, the course heads south on Yonge Street all the way to Richmond Street. It then turns west on Richmond, south on Peter/Blue Jays Way past Gretzky’s to Front St. The course then goes west along Front, south on Bathurst, west on Fort York Blvd. to finish! See the map below.

Course Map/Overview

Once again, please consider contributing to Camp Oochigeas. It is performing miracles for these children.

Researchers at USC mentioned that you could then take these “immune signatures” generated by the immune response against a tumour — and target them with whichever drugs or therapy is best suited. This builds on personalized medicine, here’s why: lets say two tumours exist, A + B, where A is a breast tumour and B is a prostate tumour. Generally tumours A + B will have different biochemistry for reasons including: (1) different cell of origin; and (2) different prepotency for specific mutations thus causing cancers in the different cells. Traditionally, drugs have either tries to poison these cells, or hijack an intracellular process associated with a specific mutation found in one cancer. By looking at the immune response signature, you could generate immune-specific drugs that could target tumour illiciting similar immune signatures. Therefore, it could be found for one drug commonly used for tumour A to work perfectly in tumour B if the immune response signatures are in alignment.

In the article, the researchers generated signatures using real-time PCR on 14 pro-immunity genes, and 11 anti-immunity genes from 5 different mouse tumour models. This is merely a start to what seems to be the tip of the iceburg here. It will be excited to see future developments.

In any case, these EDVs have been shown to target tumorigenic tissue, being fed by blood vessels; 30% of an IV dosage reached the cancerous region within 2 hours. It has so far been proven safe in dogs with advanced non-Hodgkin’s lymphoma, as well as in pigs and monkeys.

The study also suggests that these EDVs can carry RNAi or siRNA-based products to their destination, as delivery of these nucleic acids has been proven difficult due to nuclease/enzymatic degredation before reaching its target.

Adapted from [NewScientist] from [Cancer Cell (vol 11, p431) "Bacterially Derived 400 nm Particles for Encapsulation and Cancer Cell Targeting of Chemotherapeutics"]

EnGeneIC, bacteria, EDV, delivery vehicles, cancer, cell division, chromosome, tumorigenic, blood vessels, non-Hodgkin’s, RNAi, siRNA, nucleic acid, nuclease, enzyme

Another biomarker might be coming! Pharmacogenomics companies: ready … go!

Full story at Geneticsandhealth.com.

• Cancer patients increased their qualities of life with exposure to Mycobacterium vaccae
• M. vaccae activated a group of neurons to produce more serotonin mitigating depression

Full article at Getting Dirty May Lift Your Mood.

probiotic, bacteria, brain, chemical, serotonin, cancer, neurons, depression

Apparently McDonald’s Chicken McNuggets are composed of 38 ingredients, and are 56% corn! The book goes into each in detail, but I want to concentrate on the genetics aspect of this. Here is a list of chemical additives that are harmful to your DNA:

dimethylpolysiloxene: suspected carcinogen, established mutagen, tumorigen, and reproductive effector. It is also flammable.

tertiary butylhydroquinone (TBHQ): antioxidant derived from petroleum. TBHQ is a form of butane (lighter fluid). FDA limits addition of TBHQ to less than 0.02% percent of the oil per nugget [Suggestion: choose hotdogs over chicken mcnuggets in a spur of the moment eating contest.]

So, what are you eating next time you go out to McDonald’s?

antioxidant, carcinogen, chicken, DNA, mcdonalds, mutagen, mutation, tumorigenic

So, what do scientists propose that 14-3-3 sigma does? It plays a role in cell division. Specifically, it helps cells finish cytokinesis and separate into two distinct cells, right at the end of cell division. Michael Yaffe, an associate professor of biology and biological engineering and leader of the research team said “The cells try to divide and try to divide, and they just give up. They can’t finish cytokinesis.” This results in a single cell with two nuclei.

Key information not to be missed from the article:

• Fused, or binucleate, cells have recently been shown to be precursors to cancer cells. They are often found in so-called “dysplastic” tissue, which consists of cells that are not fully normal but are not cancerous. Comparing tumors to weeds, Yaffe explained that those tissues act as fertile “soil” for tumor development. “Tumors grow in epithelial tissues that are already deranged for some reason, and something about that soil makes it better able to grow weeds.”
• Loss of 14-3-3 sigma in dysplastic tissue could serve as a marker to help doctors predict whether tumors will develop. “Our hope is that it will be possible to monitor 14-3-3 expression in these ‘benign’ conditions, a subset of which may not be so benign,” said Yaffe.
• The researchers were initially intrigued by the fact that 14-3-3 sigma is missing in normal tissue that surrounds tumors, which suggested that its function is lost very early in tumor development. Once the researchers started investigating the protein, they eventually unraveled a complex signaling pathway whose disruption leads to the failure of cell division.
• They discovered that 14-3-3 sigma is most active during mitosis, when it helps control production of proteins necessary for division.
• 14-3-3 sigma interacts with a translation factor known as eIF4B, whichforms part of an enzyme that allows mRNA to unwind so the ribosome can read its sequence.
• When 14-3-3 sigma is knocked out, eIF4B is not produced, and mRNA for the protein p58 cannot be translated. p58 plays a critical role in the final splitting of one cell into two during mitosis, so when it is missing, the cells cannot fully divide.
• When p58 function is restored, the cells resume normal division.

  The story was orginally issued by MIT, and covered by ScienceDaily under the title: MIT Identifies Role Of Key Protein In Tumor Growth