Biomedical Engineering Reference
In-Depth Information
Can Stem Cell Therapy Work in Neurological Tumors?
In their recent work, the Cedars-Sinai researchers documented that several genes
that speed up and control the proliferation process could be used to rapidly expand
the supply of marrow-derived neural stem cells, writing in the article that “this novel
method of expansion may prove to be useful in the design of novel therapeutics for
the treatment of brain disorders, including tumors” [
27
] .
What Regulates Cancer Stem Cells?
Based on our previous large-scale gene expression study by cDNA microarray,
upregulation of one gene, called Maternal Embryonic Leucine-zipper Kinase
(MELK), was found both in normal neural stem cell (NSC) and in malignant BT [
28,
29
]. Therefore, it was likely that MELK plays a role in the similar subset of cells
existing in both NSC and BT, which is the “stem cell” in normal brains and in malig-
nant tumors. So far, by using gene knockdown technique, called RNA interference,
scientists identified that MELK is a critical regulator of normal NSC proliferation.
They have initiated treatment of MELK RNA interference of BT cells [
29
] .
Role of Stem Cells in Brain Cancer
Ontogeny (development of an organism) and oncology (cancer development) share
many common features. From the 1870s the connection between development and
cancer has been reported for various types of cancers. Existence of “cancer stem
cells” with aberrant cell division has also been reported more recently. The connec-
tion between cancer and development is clearly evident in teratocarcinomas. The
teratocarcinomas are able to differentiate into normal mature cells when trans-
planted into another animal [
30,
31
]. This alternation between developmental and
tumor cells status demonstrates how closely development and cancer are related.
McCulloch explored the connection between normal development of blood cells
and leukemia [
32
]. According to him, normal hematopoietic development requires
the interaction of stem cell factor with its receptor, c-kit [
32
] . A hierarchy of stem
and progenitor cells differentiates and produces different sublineages of cells result-
ing from response to varied growth factors. Malignancies of the hematopoietic sys-
tem originate from two sources: those with an increased growth in an early stem cell
produce acute leukemia, while those that arise from a decreased response to death
or differentiation in a stem cell produce chronic leukemia.
The present-day challenge is to decode the common molecular mechanism and
genes involved in self-renewal for cancer cells and stem cells.
The notion that antiangiogenic therapy targets cancer stem cells has important
implications for evaluating and optimizing the use of antiangiogenic drugs in cancer.
