03.09.2012 – GOLLYGEE!

Since I’m taking a trip to Philadelphia this weekend, I thought I’d share some science news from the city of brotherly love, andalso from my alma mater. Sarah Trice, a doctoral student in the University of Pennsylvania Department of Chemistry, and Professor Gary Molander have developed a new type of reagent to facilitate boronic acid synthesis. Boronic acids are one of the main ingredients of Suzuki-Miyaura cross-coupling reactions, which create carbon-carbon bonds in critical biaryl systems.

Paladium Catalyzed direct boronic acid synthesis from aryl chlorides. Image from JACS.

According to the write up, their new bis-boronic acid will replace the traditional bis(pinacolato)diboron, commonly referred to as BisPin, in the synthesis of pharmaceutical building blocks. It is more efficient, producing less waste and requiring less palladium catalyst. It also uses ethanol as a solvent instead of diethyl ether. Reactions with bis-boronic acids can also proceed at temperatures of 50-80 degrees Celsius compared to the 110 degrees required for reactions with BisPin.

They have decided not to patent their methodology, which they published in JACS, in December of 2010.

From ScienceNOW:

The big push in cancer treatment these days is to sample a person’s tumor, test it for mutations, and give the patient a drug tailored to a genetic weak spot in the tumor. A new study suggests one reason why this targeted drug strategy doesn’t always work. A solid tumor, it turns out, is not a mass of identical cancerous cells but a mosaic of genetically different cells that aren’t captured with a single biopsy. Some of these distinct cells may be resistant to the targeted drugs, allowing a tumor to persist or grow.

The classic view of how cancer develops is that a single, normal cell accumulates mutations that eventually allow or force it to divide uncontrollably. This “clone” then grows into a tumor of identical cells, which can also sow seed cells into the bloodstream that then take root somewhere else in the body, or metastasize. The assumption that tumors grow out from a single clone has spurred a rush to find drugs that block one of the clone’s genetic weak spots. But although the strategy has resulted in some very effective drugs—Iressa for lung cancer and a new melanoma drug called Zelboraf, for example—these drugs often stop working within a year or two. One reason could be that solid tumors already harbor a few cells, or clones, with “resistance” mutations that take over when the cells targeted by the drug are wiped out.

More here.

GOLLYGEE!

Date: 03.09.2012

from the city of brotherly love

how cancers become resistant