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stanford scientific
SPOTLIGHTS
policy issue. Individuals and institutions that men, as well as a sidebar with this crucial Katz agrees that the complete ban
would like to lobby for change are urged note: “You can lobby for change without on donations was unnecessary and
to do so by contacting the FDA and their jeopardizing an adequate blood supply. If unwarranted: “I think they were wrong to
U.S. congressional representatives, not by eligible people decide not to donate, or if do this,” he says. Although SJSU officials
jeopardizing their community’s local blood deferred people encourage others not to reiterate that the decision is temporary,
supply and putting patients’ lives at risk.” donate in protest of this policy, the blood many students and other critics feel that
supply may be further jeopardized and any stoppage of life-saving donations is
The Stanford Blood Center’s website has patients may not receive life-saving blood counterproductive and unfair to the wrong
posted an explanation of the deferral products.” group of people.
regarding men who have had sex with
stanford scientific
SPOTLIGHTS
stanford scientific
SPOTLIGHTS
Truly defeating cancer, including preventing these maps are equivalent to “the genetic capable of setting off a signal cascade that
its return, will require a thorough ‘fingerprints’ of different types of stem cells.” could lead to the formation of cancer stem
understating of how the disease begins cell differentiation? To test this theory, the
and propagates. In a study published in the The researchers created a genome-wide group produced a squamous cell carcinoma,
April 2008 issue of Cell Stem Cell, Dr. Howard gene module map for both humans a model of human cancer in the epithelial
Chang, Assistant Professor of Dermatology and mice and compared the expression cells of mice. They then activated c-Myc in
at Stanford’s School of Medicine, and Dr. patterns between stem cells from normal the cancer cells and injected the cells into
David Wong, Instructor of Dermatology and or cancerous tissues. In this manner they immunodeficient mice to create model
a post-doctoral scholar in the Chang lab, identified several key gene groups involved tumors. In these c-Myc activated tumors, the
shed new light on the process by which in stem cell signaling as well as genes group found gene signatures characteristic
normal stem cells turn cancerous by creating specifically required for ESC and adult stem of both embryonic and cancer stem cells.
cancer stem cells. Targeting these stem cells, cell signaling.
which are responsible for the proliferation of From these observations, Wong concludes
tumors, is a key step towards preventing the In support of previous research, no single, that “reactivating the transcriptional
spread of the cancer and maximizing patient shared factor could be identified in all stem program characteristic of embryonic stem
survival. cell types. However, the group did identify cells is a key mechanism for converting
different modules that appeared to be a normal cell into a cancer stem cell.”
Gene Module Maps crucial for differentiation. These modules Moreover, this data supports the hypothesis
Like embryonic and adult stem cells, cancer could subsequently be divided into two that the expression of certain genes may
stem cells are able to differentiate into a distinct groups, one of which was associated affect the severity, prognosis, and chance of
variety of cell types. This suggests that specifically with embryonic stem cells, metastasis of different cancers.
different families of stem cells may each while the other was responsible for normal The Future of Cancer Research
be regulated by a common “stemness” differentiation and growth. Interestingly, The research in this field is groundbreaking
factor, an observation that led researchers it is the embryonic stem cell transcription and has many widespread implications that
to question whether all stem cells respond pathway that is frequently activated in could change the way cancer is treated or
to a single transcription pathway or if human cancers and allows tumors to diagnosed. According to Wong, “this ability
multiple pathways are involved. Previously, metastasize. to experimentally create cancer stem cells
researchers had had little success in isolating offers a new resource to investigate the
shared stemness genes. However, because c-Myc as the Cancer mechanism by which cancer stem cells
a number of potential candidates had been Stem Cell Trigger? arise from normal cells.” Likewise, the ability
identified, the Stanford group set out to Based on these findings, researchers in the to create cancer models in vitro will allow
determine the key players in this process. Chang lab were able to identify a key stem pharmaceutical companies to test their
cell transcription factor that was able to therapies in a more diverse sample of cancer
With the expectation that the proposed reprogram differentiated epithelial cells into models that nonetheless appropriately
“stemness” factor was present in all stem cancer stem cells. Specifically, they found represent real cancers.
cells, the Stanford researchers decided to that activation of the c-Myc gene had the
utilize a systems-level analysis approach that ability to induce the ESC program, causing Dr. Wong and his colleagues in the Chang
could identify common gene expression the cancerous transformation. This allowed lab are now working towards “further
patterns in embryonic stem cells (ESC), the group to first identify and then use other dissection of the genetic mechanism
adult stem cells, and cancerous stem cells. stem cell transcription factors to stimulate that turns a normal cell into a cancer
Using stem cell expression array profiles cancerous growth and proliferation in stem cell.” Looking beyond the arena
and a large collection of genes, they built a previously non-cancerous epithelial cells. of cancer research, he believes further
“gene module map” to catalog expression discoveries could be important “not only for
programs that are shared among the When asked about the goals of this research, understanding cancer but also for refining
different cell types. A “module” is a group Wong explained that he and his colleagues methods to reprogram somatic cells to
of genes that show concerted expression, “wanted to investigate the consequences of pluripotent stem cells for regenerative
suggesting they interact to regulate a activation of the ESC-like program by c-Myc medicine.”
common process. According to Wong, in a human cancer model.” Was c-Myc alone
stanford scientific