Archives For Cancer

“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

Brain metastases caused by solid tumors in others parts of the body and cause many cancer related deaths.  Human cytomegalovirus (HCMV or CMV) is recently been detected consistently using the latest methods reviewing brain metastases tumors from primary breast and colorectal cancers.

This report shows for the first time a very high prevalence of CMV infection in brain metastasis from both breast and colorectal cancers.  CMV proteins now being proven to drive cancers were detected in 99% (n = 78) brain metastasis samples and also in 92% to 100% (n = 25) of corresponding breast and colorectal cancer specimens.

Patients who had low-grade CMV infections in the primary tumor or the brain metastasis had a longer time to tumor progression and overall longer survival (13.5 months Overall Survivial with low-grade infection compared to 6.9 months with high grade infections).  Time to tumor progression was also longer with low-grade CMV infections at 65.1 months average versus 30 months with high-grade infection.  Importantly, the presence of CMV in brain metastasis may open new treatment options as recently tests with Glioblastoma brain tumors have shown significant increases in survival by treating these highly prevalent CMV infected tumors with anti-virals like Valcyte.

Research also shows 94% of lymph node metastasis of breast cancer and 99% of brain metastasis of colorectal and breast cancers are CMV protein positive, but virus positivity is nearly absent in healthy surrounding tissues implying a viral presence in metastasis initiating cells.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4311044/

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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Vitamin D

Starting off, Vitamin D is not a Vitamin, long time ago mis-namer. It’s actually a Pro-Hormone – a precursor building block to hormones and it’s unbelievably important. It acts as a molecular switch activating at least 200 target genes in our bodies, thereby regulating gene expression. And many of these are the ON switches for our immune system! I only wish I knew then, what I know now.

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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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HCMV is found is 99%+ of Glioblastoma Brain Tumors.  Researchers are now beginning to measure the level of CMV infection in the tumors as a prognostic marker for expected survival.  The research shows that Low Levels of CMV in a Glioblastoma tumor correlates to survival beyond 18 months.  Actively treating CMV in Glioblastoma has a direct and positive improvement in patients survival length.  This issue needs further research and the same research applied to other cancers to improve their survival rates.

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P53 Tumor Suppressor Gene – P53 gene (chromosome 17p13.1) is mutated in some Medulloblastomas. Besides Medulloblastoma, P53 down regulation is also known to contribute to Osteosarcoma, Basal Cell Sarcoma (skin cancer) and Gorlin Syndrome (includes issues like sternum bone deformation).  For those new to this topic, P53 is a gene in every cell in the human body that polices your cells for DNA damage and try’s to stop / repair it. So often if not always in cancer, one or multiple oncogenes will be over expressed driving cancer ( for my son it’s MYC) and anti oncogenes or Tumor Suppressor genes are being suppressed like P53, Since there are dietary supplements that have shown some capability to help turn P53 back up, it seems very worthy to evaluate this avenue if you believe you have P53 being down regulated, particularly if you have the added complications I mentioned that are also specifically linked to P53 chromosome damage.  And since this blog is primarily focused on Viral drivers of cancer, it should be noted that several viruses including CMV are known causes of P53 suppression as well.

http://www.cell.com/abstract/S0092-8674(11)01516-9

http://p53.free.fr/Database/p53_cancer/p53_germline.html

http://www.nature.com/onc/journal/v20/n53/full/1204946a.html

I’ve tried looking into ways to upregulate P53 genes.  Some that I researched include: Silymarin, aka Milk Thistle, as well as Melatonin.
http://mct.aacrjournals.org/content/4/2/207.long

http://www.ncbi.nlm.nih.gov/m/pubmed/22002314/

Another Anti-Oncogene suppressed in Medulloblastoma is PCDH10 located at chromosome 4q28.3 down-regulated in 73% of sampled Medulloblastoma tumor samples.

PCDH10 is a candidate tumor suppressor gene in medulloblastoma.
Hospital for Sick Children, Toronto

The aim of this study was to investigate the genetic and epigenetic mechanisms contributing to PCDH10 down-regulation in medulloblastoma. We examined the role of PCDH10 as a mediator of medulloblastoma cell proliferation, cell cycle progression, and cell migration.

METHODS:
We identified a focal homozygous deletion of PCDH10 in medulloblastoma by surveying a cohort of 212 tumors by Affymetrix SNP array analysis. PCDH10 expression was assessed by quantitative reverse transcriptase PCR in a series of 26 tumors. The promoter methylation status of PCDH10 was determined using methylation specific PCR and Sequenom MassCLEAVE analysis. Functional studies examining the role of PCDH10 in medulloblastoma development were performed by re-expression of PCDH10 in the DAOY medulloblastoma cell line, and then, cell proliferation, cell cycle distribution, and cell migration assays were performed.

RESULTS:
We report a very focal homozygous deletion on chromosome 4q28.3 harbouring the PCDH10 gene. We demonstrate that PCDH10 transcription is down-regulated in 19/26 (73%) of medulloblastomas suggesting that other mechanisms also could be involved in gene repression. We found that DNA hypermethylation contributed to the deregulation of PCDH10 in 11/44 (25%) of medulloblastoma cell lines and primary tumours. Using a stable cell line (DAOY) re-expressing PCDH10, we observed that cell migration was impaired upon restoration of PCDH10 expression.

CONCLUSIONS:
Our findings suggest that genetic and epigenetic deregulation of PCDH10 occurs in a significant portion of medulloblastoma patients. Failure to express PCDH10 may result in loss of inhibition of cell migration, thereby contributing to medulloblastoma progression.

http://www.ncbi.nlm.nih.gov/pubmed/21597995

Silencing of PCDH10 is also a known cause Epileptic seizures and other cancers.

http://www.ihop-net.org/UniPub/iHOP/bng/101549.html