ScienceDaily (Apr. 9, 2008) — A new study suggests that a genetic fingerprint associated with normal embryonic stem cells may be important for the development and function of cancer stem cells. The research, published by Cell Press in the April 10th issue of Cell Stem Cell, demonstrates that embryonic stem cells and multiple types of human cancer cells share a genetic expression pattern that is repressed in normal differentiated cells, a finding that may have significant clinical implications for cancer therapeutics.
"Self-renewal is a hallmark of stem cells and cancer, but existence of a shared stemness program remains controversial," explains study co-author, Dr. Howard Y. Chang from Stanford University. Dr. Chang, Dr. Eran Segal from the Weizmann Institute in Israel and their colleagues constructed a gene module map to systematically relate transcriptional programs in embryonic stem cells (ESCs), adult tissue stem cells and human cancers.
The researchers identified two predominant gene modules that distinguish ESCs and adult tissue stem cells. "Importantly, the ESC-like transcriptional program was activated in diverse human epithelial cancers and strongly predicted metastasis and death," says Dr. Segal. Conversely, the adult tissue stem gene module had an opposite pattern, activated in normal tissues relative to cancer and repressed in various human cancers when compared to normal tissues.
The researchers went on to demonstrate that c-Myc, but not other oncogenes, was sufficient to reactivate the ESC-like program in normal and cancer cells. In primary cells transformed by tumor-inducing genes Ras and I B, c-Myc increased the number of tumor-initiating cells that exhibited key properties associated with cancer stem cells and dramatically increased the frequency of tumor formation in mice.
These findings suggest that activation of an ESC-like transcriptional program in differentiated adult cells may induce pathologic self-renewal characteristics of cancer stem cells. Further, the map of gene modules may prove to be a valuable tool for establishing improved standards for classifying and defining stem cells by using the expression signature modules as "fingerprints" rather than reliance on just a few molecular markers.
The researchers include David J. Wong, Stanford University, Stanford, CA; Helen Liu, Stanford University, Stanford, CA; Todd W. Ridky, Stanford University, Stanford, CA; David Cassarino, Stanford University, Stanford, CA; Eran Segal, Weizmann Institute, Rehovot, Israel; and Howard Y. Chang, Stanford University, Stanford, CA.
Again, there are only three sources of stem cells: 1) allo (one species to same species), autologous (your own cells) and xeno (animal cells). All embryonic cells have potential for causing cancer because they are non-differentiating cells. Progenitor stem cells do not cause cancer; PROVIDED they are properly “manufactured/cultured”.
Progenitor stem cells are the most prolific (greatest efficacy) of all stem cells, while autologous cells have the least efficacy (65 year old stem cells are not as potent as eight week old stem cells!). Assuming fetal cells are manufactured properly, they will be FREE of all known antigens, thus NO NEED to take immune-suppression drugs for the rest of one’s life. Regrettably, organ transplant recipients do not have the luxury.
Lastly, progenitor cells “home”! Which quite simply means once injected into the recipient body they immediately migrate to the diseased or damaged organ or tissue from where they came in the donor’s body, e.g. liver-to-liver, retina to retina, etc. If upon arriving at the presumed damaged organ and find no damage, then they are just eventually absorbed into the body harmlessly!
This is really a very simple process that science tries to make difficult.