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Jennifer WongRSS Feed of this column.

My column covers the latest primary research discoveries in the life-science discipline. Much of what is reported here are considered discoveries that I think are the most significant and far-reaching... Read More »


McCormick Place- Chicago, IL, March 31st- April 4th 2012- was flocked with scientists across the world for the Annual American Association for Cancer Research (AACR) meeting. As with each year, the meeting featured endless plenary presentations, symposiums, as well as poster sessions and exhibitions that covered exciting advancements and technologies in the global effort to end cancer.

Induced pluripotent stem cell (iPSC) research in the last 2 years has faced many twists and turns. With scientists uncovering a number of disturbing genomic abnormalities in these cells, the future of iPSC technology looked like a sea of despair.

But lucky for those who persisted in this field of research, recent findings based on deep genome sequencing data revealed that these so-called "genomic abnormalities" simply reflect the normal genomic quirks of the original somatic cells from which iPSCs were derived. 

Cheng et al, 2012 (Cell Stem Cell 10, 337–344)Young et al 2012 (Cell Stem Cell 10, 1-13)
A major function of microRNAs is to inhibit messenger RNA (mRNA) translation by binding to a specific 3’ untranslated region (UTR) through sequence complementation. In a recent study published in the March 2012 issue of Cell Stem Cell, Boutet et al. discovered that Pax3 transcripts in muscle stem cells in vivo can have both long and short 3’UTRs, an effect controlled by differential poly-adenylation patterns during the course of development. While Pax3 transcripts with long 3’UTRs are susceptible to translational inhibition by miR-206, transcripts with short 3’UTR are profoundly resistant to miR-206. 
I have recently created a blog-site called Life-Dialogues that covers the latest topics in neuroscience, stem cell biology, cancer and molecular biology. 
So- if you were wondering where all my contents went- you can find my recent contents at To hear about my recent articles, you can also join the lifedialogues group on Facebook or follow me at twitter@lifedialogues.

Science2.0 is after-all the place where I published my earlier blogs, so I would still like to share my contents with the community here. I have decided to post a few of my most-read contents here for your reading pleasure. Stay tuned!

Cancer cells are, well, cancer cells; cells that grow uncontrollably in the host, and ignore all patterns and signals that govern the structural integrity of tissue and organs.

Much research in the last several decades have defined molecular features attributed to cancer cells, and more importantly what specifically can kill them. Decades of work goes by with the discovery of drugs that change the lives of many individuals and families touched by this disease. Yet despite the euphoria of success, scientists come face to face with a troubling problem of cancer cell resistance to treatment.

The same goes for rabbits thriving in Australia.

Cancer can be described as a cellular disease, which is thought to arise from misbehaving cells that divide uncontrollably in vivo. Our basic understanding of why this occurs is because these “cancer cells” have lost its ability to respond appropriately to endogenous stop signals that normally work to maintain the structural integrity of normal tissues. The resulting uncontrolled cell division results in the formation of a tumor.