Archives For Viral Cancer

Viral Cancer I’ve written often about the fact that 99% of Glioblastoma and 92% of Medulloblastoma show active CMV infections  and show signs that CMV has hit and run certain tumor cells making genetic and epigenetic changes.  

Now researchers are testing Neuroblastoma for CMV and the latest research shows 100% of the tumors showed signs of CMV or cyclomegalovirus.  This continues to reinforce that brain cancers key consistent factor is the triggering of oncogenisis  is by a viral infection that over expresses oncogenes and disables key anti-oncogenes thus driving these devastating cancers and leads towards potential opportunities for new and less devastating treatment options including using anti-virals like Valcyte. 

https://www.dropbox.com/s/kz18ub4qbkjj2gy/ijc28265.pdf

Viral Cancer

Genes are biological chemical software routines that do specific tasks in our bodies. Oncogenes are genes that have been proven to contribute to the development and growth of cancer.  There are approx. 50 distinct Oncogenes known and some that are found often over expressed in Medulloblastoma are MYC , MYCN and TAG. MYC and MYCN alone cause many hallmarks of cancer. When these genes are ran, they accelerate DNA replication, they turn off programmed cell death in two ways, drives new blood vessels to the cell / tumor and more (footnote ***).

Anti-Oncogenes are genes with the ability to police Oncogenes and keep them from going out of control and causing cancer (The most common damaged Medulloblastoma Anti-oncogene is P53 also known as TP53. There are two copies of TP53 and both must be damaged for this gene to be silenced (footnotes * **). When cancer happens, a couple basic things happen:

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New England Journal of Medicine

http://www.nejm.org/doi/full/10.1056/NEJMc1302145

Cytomegalovirus (CMV) DNA and proteins are expressed in several types of human cancers and metastases1 but not in healthy surrounding tissues, suggesting a possible role for the virus in the cancer.2 The malignant brain tumor glioblastoma has a dismal prognosis, with a median overall survival of 12 to 14 months and a 2-year survival of 15 to 26%. We examined more than 250 cases of glioblastoma (Fig. S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). Of these patients, only 1 was CMV-negative. Of the 75 patients we evaluated, the median rate of overall survival was 33 months in those with low-grade CMV infection and 13 months in those with high-grade CMV infection (P=0.04); the median rates of 2-year survival were 63.6% and 17.2%, respectively (P=0.003),3 which suggests that CMV affects tumor progression.
In an animal model, anti-CMV treatment reduced the growth of medulloblastoma by 72%.4 In the Valcyte Treatment of Glioblastoma Patients in Sweden (VIGAS) study,5 a double-blind clinical trial of valganciclovir involving 42 patients with glioblastoma, we found that tumor growth (the primary end point) was not significantly reduced at 3 and 6 months after surgery. However, in exploratory analyses, 22 patients receiving at least 6 months of antiviral therapy, as compared with contemporary controls, had an increased rate of 2-year survival (50% vs. 20.6%, P<0.001) and increased median overall survival (24.1 vs. 13.7 months, P=0.003). The ethics committee approved the experimental treatment protocol for patients enrolled in the VIGAS study. Owing to the promising results of this study, 28 patients at our hospital have received anti-CMV therapy for compassionate use in addition to their standard therapy (Section S2 in the Supplementary Appendix). Patients in the VIGAS study and those who were treated for compassionate use provided written informed consent for analyses of biologic samples and outcomes. Approval by the institutional review board was not required.

Here we present current retrospective data on 50 patients with glioblastoma who received valganciclovir as an add-on to standard therapy at Karolinska University Hospital as adjuvant treatment (Section S2 in the Supplementary Appendix). The rate of survival of treated patients was remarkably high: at 2 years, 62% were alive, as compared with 18% of contemporary controls with a similar disease stage, surgical-resection grade, and baseline treatment (P<0.001) (Figure 1AFIGURE 1
Kaplan–Meier Estimates of Overall Survival in Patients with Glioblastoma Receiving Antiviral Therapy against Cytomegalovirus (CMV).
, and Table S1 in the Supplementary Appendix). The median overall survival was 25.0 months, as compared with 13.5 months in the controls (P<0.001). The median survival was higher among 40 patients who received at least 6 months of valganciclovir; their 2-year rate of survival was 70%, and their median overall survival was 30.1 months (P<0.001) (Figure 1B). The survival rate was highest among 25 patients who received continuous valganciclovir treatment after the first 6 months, with a 2-year survival rate of 90% and median overall survival of 56.4 months (P<0.001) (Figure 1C). It is unlikely that any bias in patient selection could have resulted in these high rates of survival. Our results highlight the need for a randomized trial targeting CMV in patients with glioblastomas.

This is my latest research of my hypothesis that viruses cause cancer. This is in presentation form and I’ve also included the link to my key research backup for all that I can back-up from medical and scientific research. Appreciate your thoughts and considerations.

Gary Elsasser “Ayden’s Dad”

Viral Cancer Hypothesis Presentation

Research PDF

Viral Cancer Hypothesis Backup Research

https://www.dropbox.com/sh/6cgwg7cw1irxsui/2vBB71XDkL

Cancer CellHit & Run – An active viral infection, rewrites Stem, Progenitor Cells, etc, with Cancer programming then disappears. Eventually the right micro-environment happens and the infected repgrogrammed cells  wake up and begin tumors.  So often researchers look for viral traces, do not find them, then discard the consideration of viruses causing cancer.  This single flawed research conclusion misdirects science off target.  Once we understand and accept that this Hit, Reprogram & Run ability of the Virus to cause cancer, then it disappears with little or no trace, then this leads us to focus more on Anti-viral therapeutic treatments and especially anti-viral vaccinations to stop cancer at it’s root cause.  It’s an very important point that focus on eliminating active cancer tumors is treating the symptom, not the cause.  Until we focus on the cause, we are destined to repeat failure and be surprised by that fact.

http://vir.sgmjournals.org/content/91/9/2176.full.pdf+html

http://www.livescience.com/10023-viruses-cancer-previously-thought.html

“Sufficient evidence has emerged to suggest that HCMV could modulate the malignant phenotype in Glioblastomas , and elements of it’s biology overlap those considered to be the hallmarks of cancer.”

http://kalejta.virology.wisc.edu/sites/kalejta.virology.wisc.edu/files/Dziurzynski_et_al.pdf