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“During the last years increasing evidence implies that human cytomegalovirus (CMV) can be attributed to human malignancies arising from numerous tissues. In this perspective, we will review and discuss the potential mechanisms through which CMV infection may contribute to brain tumors by affecting tumor cell initiation, progression and metastasis formation. Recent evidence also suggests that anti-CMV treatment results in impaired tumor growth of CMV positive xenografts in animal models and potentially increased survival in CMV positive glioblastoma patients. Based on these observations and the high tumor promoting capacity of this virus, the classical and novel antiviral therapies against CMV should be revisited as they may represent a great promise for halting tumor progression and lower cancer deaths.”

CMV In Human Brain Tumors – World Journal Experimental Medicine

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iStock_000006391407XSmallMany factors contribute to Cancer, but the key catalyst (even the underlying engine) is one of many Viruses, particularly CMV, but also VZV, Epstein Barr as well as other Viruses SV-40, BK, JCV and HPV. Each cancer in our body has one to many viruses associated with it. Some key ones are HPV – Human Papilloma Virus causes Cervical, Anal, Mouth, Throat, Lung, Vaginal and Penile Cancers. Epstein Barr causes Lymphoma, JC Polyoma Virus causes Colon Cancer. Epstein Barr, HPV & CMV have all been associated with Breast Cancer, thus one reason for it’s prevalence. Now down to kids Cancer, Medulloblastoma Neuroblastoma and it’s 99% terminal twin cancer Glioblastoma. For these cancers its mainly CMV (Human Cytomegalovirus), though other viruses like SV-40, JC and BK are also capable and have been found in these tumors.

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The human cytomegalovirus (HCMV) and glioma sym- posium was convened on April 17, 2011 in Washington, DC, and was attended by oncologists and virologists involved in studying the relationship between HCMV and gliomas. The purpose of the meeting was to reach a consensus on the role of HCMV in the pathology of gliomas and to clarify directions for future research. First, the group summarized data that describe how HCMV biology overlaps with the key pathways of cancer. Then, on the basis of published data and ongoing research, a consensus was reached that there is sufficient evidence to conclude that HCMV sequences and viral gene expression exist in most, if not all, malig- nant gliomas, that HCMV could modulate the malig- nant phenotype in glioblastomas by interacting with key signaling pathways; and that HCMV could serve as a novel target for a variety of therapeutic strategies. In summary, existing evidence supports an oncomodula- tory role for HCMV in malignant gliomas, but future studies need to focus on determining the role of HCMV as a glioma-initiating event.

HallmarksOfCancerList

https://www.dropbox.com/s/u0f80r60kc8qkh5/%28H%29%20Neuro%20Oncol-2012-Dziurzynski-246-55.pdf

“HCMV can also do every one of the things that¬†generally considered the 10 hallmarks ofcancer,” says Kalejta, a member of the McArdle Laboratory for Cancer Research, Carbone Cancer Center, Stem Cell and Regenerative Medicine Center and Institute for Molecular Virology at UW-Madison.

http://www.med.wisc.edu/news-events/new-evidence-links-virus-to-brain-cancer/32922

“We have confirmed the presence of active CMV infection in 99% of malignant Glioblastoma tumors and in 90% of Medulloblastoma and Neuroblastoma tumors.”

“Will Anti-Viral drugs give new hope for malignant Glioblastoma patients?”

http://www.cmm.ki.se/en/Research/Cardiovascular-and-Metabolic-Diseases/Cell-and-Molecular-Immunology/Cia/Our-research/CMV-infection-in-cancer/

Significant Association of Multiple Human Cytomegalovirus Genomic Loci with Glioblastoma Multiforme Samples

Not surprisingly, human cancer viruses can produce within cells one or more of the molecular hallmarks of cancer (10) that promote cellular plasticity (through genomic instability, inflammation, deregulation of cellular energetics, and induction of angiogenic and metastatic processes), proliferation (by sustaining proliferative signaling, evading growth suppressors, and enabling replicative immortality), and survival (avoidance of immune detection and inhibition of apoptosis).

“HCMV is the most common infection of human fetal brain, and HCMV was known to be able to persistently infect glioma cells and become reactivated in a chronic inflammatory state”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214144/pdf/2042-4280-2-10.pdf