Aaaaaand They’re Off: The 2013 World Cell Race Results
Dec10

Aaaaaand They’re Off: The 2013 World Cell Race Results

Today's post is by Nader Heidari, an associate editor at C&EN who loves watching cells race and paint dry. On Nov. 22, cells raced down ultrathin channels, vying for the position of fastest cell in the 2013 World Cell Race. At speeds of up to 300 micrometers/hour, cells blew down the maze-like track, running into dead ends and occasionally getting confused and turning around. Many cell lines didn't finish, but glory came to those who did. This year's victor (shown in the race video above) was MDA MB 231 s1, a human breast cancer cell line from Alexis Gautreau of the Laboratory of Enzymology & Structural Biochemistry, in France. Gautreau will receive a €400 voucher (that’s about $650) from Ibidi, one of the event's sponsors. The winning cells weren't the fastest, nor were they the smartest, but they prevailed because of their persistence and because they got a good head-start by entering the maze of channels more quickly than their competitors. Slow and steady wins the race! In second place was MFH 152, a sarcoma cell line from Mohamed Jemaà in Ariane Abrieu’s lab at the Research Center for Macromolecular Biochemistry, in France. Although they were fast and accurate, these cells took too long to actually start the race, falling behind MDA MB 231, according to the race organizers. Cell-racing fans don't have to wait until late next year for another dose of mitochondria-pumping action: The organizers are looking to start the first "Dicty World Race," tentatively scheduled for March 21, 2014. The stars of this show would be Dictyostelium, a type of slime mold. So keep an eye out for some pedal-to-the-flagella protist action! Related Stories: Cellular...

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Novartis’s Afinitor helps Pfizer’s Aromasin to Delay Breast Cancer
Sep27

Novartis’s Afinitor helps Pfizer’s Aromasin to Delay Breast Cancer

Looks like Afinitor (everolimus), a drug marketed by Novartis for various cancers, may soon have a new indication. Already approved for a variety of diseases – kidney cancer, pancreatic tumors, and organ rejection prevention – Afinitor shows new promise for breast cancer patients. Clinical data released Monday demonstrate marked improvement for hormone-resistant breast cancer patients when Afinitor, an mTOR inhibitor, is used in combination with the aromatase inhibitor Aromasin (exemestane). Patients receiving both drugs delayed disease progression an average of 7 months, versus 3 months for Aromasin alone. Standard therapy for breast cancer includes treatment with estrogen receptor antagonists, such as Aromasin and tamoxifen, which bind in the estrogen receptor pocket of cancer cells, slowing proliferation (see the excellent NCI website for more information on breast cancer treatment). Aromasin itself has a very similar structure to estrone (a natural body hormone that binds to estrogen receptors) except that it irreversibly modifies the receptor pocket upon binding, making Aromasin a so-called “covalent” or “suicide” inhibitor (see Lila Guterman’s article from Sept. 5, 2011 issue of C&EN for more on drugs that bind for keeps). Like Aromasin, Afinitor follows the trend of being structurally related to a natural binder of a key cancer target protein. mTOR (mammalian target of rapamycin), the protein target of Afinitor and related macrolides, was first discovered through binding studies using rapamycin, a polyketide natural product found in a soil bacterium from Easter Island (its Polynesian name is Rapa Nui, hence, rapamycin). Rapamycin also goes by the generic name sirolimus, of which so many analogues have been prepared that all go by the catch-all “limus drugs.” The attachment of a hydroxyethyl (CH2CH2OH) tail to rapamycin produces everolimus, which compared to sirolimus demonstrates better pharmacokinetic properties, including higher bioavailability (greater proportion of drug reaching target sites) and a shorter plasma half-life (meaning the drug doesn’t stick around as long, which can help curb toxicity or other side effects). Note: Please see Sally Church’s post on Pharma Strategy Blog for more info on mTOR pathway biology and coverage of ECCO 2011 conference information regarding...

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