From the Peanut Gallery...

I have always been interested in sports medicine and studying how certain conditions would affect an athlete on the molecular level. I am particularly attracted to any research on muscles and any other soft tissue in the body. This is why I found the blog on soft tissue sarcoma interesting titled, “Stopping the Spread of Soft Tissue Sarcoma: Is It Possible?”. In the study it was found that there was elevated STAT3 phosphorylation in rhabdomyosarcoma and this novel finding might just be the key to stopping it. The blog and the primary article both hint to a way to slow the spread of soft tissue sarcoma through the regulation of the STAT3 transcription factor (which allows for the producing of a protein) in cells. But is there a deeper cause? In actuality the STAT3 factor is supposed to be regulated by the SH2 domain, protein inhibitors of activated STATs and cytosine signaling protein suppressors. Through an imbalance in the pathway stems the problem. If researchers could find a way to return balance to the pathway then the sarcoma would cease or at the very least be slowed.

This similar imbalance also occurs in Neuroblastoma. In the blog titled: “Stopping Neuroblastoma Before It Kills!!!” based on the primary article by A. Gupta and others, we find that another protein is always activated in these cells. We find that an acid binding protein called CRABP II is always left activated due to the MycN transcription factor which is directly responsible for the proliferation of a neuroblastoma tumor. The common theme amongst both of these cancers is the signaling pathway. There is always an imbalance that leads to the over expression of something which then eventually leads to the formation of diseased cells. Soft tissue sarcoma and neuroblastoma do not involve the exact same pathway or even the same genes but they do exhibit a similar mechanism of onset. Something is always left on. This correlates with what we have learned so far because one of the main themes of cancer is its longevity and ability to leave something permanently “on” or “off”. Also, in order to determine what proteins were involved both studies examined either the tissue being affected or specifically the protein and its transduction ability. Both methods were able to tell researchers which proteins were responsible for the proliferation of the cancers. However, in the sarcoma study researchers used the western blot analysis to discover which protein was affecting the diseased tissue while the neuroblastoma study used a two dimensional gel to find out how CRABP II was communicating with other proteins to determine the frequency of attachment to it. From this they determined that CRABP II expression was elevated.

Based on the two blogs results, I only have two questions. The first is how many cell pathways are present in a cell and are the same pathways present in every cell? The second question is, is neuroblastoma a common childhood cancer for the same reason that retinoblastoma is a common childhood cancer?

“Stopping the Spread of Soft Tissue Sarcoma: Is It Possible?”: Primary Article
Chen, C., Cen, L., Chan, C., Hsieh, F., Chen, G., et al. (2007 June 28). Signal transducer and activator of transcription factor 3 is involved in cell growth and survival of human rhabdomyosarcoma and osteosarcoma cells. BMC Cancer, (7) 111.

“Stopping Neuroblastoma Before It Kills!!!”: Primary Article
Gupta A., Williams B.R., Hannash S.M., and Rawwas J. (2006, August 15). Cellular Retinoic Acid-Binding Protein II Is a Direct Transcriptional Target of MycN in Neuroblastoma. Cancer research, 66, 8100-8108.