The Agent Orange Widows Club

After their husbands died of an aggressive brain cancer, the widows of Vietnam veterans have found one another as they fight the VA for benefits.

See also: Vietnam Veterans with Glioblastoma Multiforme Stage 4 Brain Cancer

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Targeting NF-κB in glioblastoma: A therapeutic approach

This is the level of complexity that the VA needs to understand and link to the treatment of this aggressive cancer, which is obviously caused by virus-driven energy theft. When the VA understands that, the treatment will open the floodgates of litigation for all the pathology in every veteran who ever served overseas and failed to adapt to the viruses encountered during the stressful conditions of war.

“…we used the NBD peptide, a peptide corresponding to the NEMO binding domain that specifically inhibits the induction of NF-κB activity (15). The NBD peptide has been used previously to inhibit inflammation in animal models such as acute inflammation in carrageenan-induced mouse paw edema and collagen-induced arthritis (31) or Duchenne muscular dystrophy (13). One of our main reasons for choosing the NBD peptide to treat GBM is the reported ability of NBD to enter into the CNS and exert an effect on NF-κB activation in a mouse model of Parkinson’s disease (14). Indeed, our results show that NBD treatment of mice with GBM significantly extended their survival, probably as a result of the specific inhibition of NF-κB not only in the tumor cells but also in the tumor microenvironment.”

My conclusion: Even if the VA understands what all serious scientists have learned about energy-dependent biophysically constrained biologically-based cause and effect, liberal academics will continue to try to prevent dissemination of accurate information. The facts about virus-driven energy theft compared to nutrient energy-dependent ecological adaptation refute every aspect of neo-Darwinian nonsense that is still being taught to your children and grandchildren if they are attending public schools.

Grady was the first person to get the treatment dripped through a tube into a space in the brain where spinal fluid is made, sending it down the path the cancer traveled to his spine.

This makes me wonder how Jimmy Carter’s brain cancer was cured. So far as I know, the cure must link genetically engineered cell type differentiation from viral latency in the cells dripped into the brain to the natural information processing.

Natural information processing can then link natural selection for energy-dependent codon optimality from base pair changes to RNA-mediated amino acid substitutions that stabilize the supercoiled DNA of all living genera, and prevent the accumulation of virus-caused mutations.

See for instance: DNAM-1-based chimeric antigen receptors enhance T cell effector function and exhibit in vivo efficacy against melanoma.

CAR is the acronymn for chimeric antigen receptor. See for an example of how CAR-T cell treatment must link energy-dependent changes in the microRNA/messenger RNA balance of the mouse model organism to vial latency via the anti-EGFRvIII chimeric antigen receptor.

Expression of miR-17-92 enhances anti-tumor activity of T-cells transduced with the anti-EGFRvIII chimeric antigen receptor in mice bearing human GBM xenografts

CONCLUSION:
These results warrant the development of novel CAR-T-cell strategies that incorporate miR-17-92 to improve therapeutic potency, especially in patients with GBM [glioblastoma].

Targeting NF-κB in glioblastoma: A therapeutic approach (revisited)

We have established a lentivirus-induced mouse model of malignant gliomas, which faithfully captures the pathophysiology and molecular signature of mesenchymal human GBM.

See also: MicroRNA-based regulation of epithelial–hybrid–mesenchymal fate determination

Now that treatment is based on what was learned about virus-driven energy theft in the mouse model organism, how much longer will it be before viruses are linked to all pathology via changes in the microRNA/messenger RNA balance that clearly link virus-driven messenger RNA degradation to tissue-type specific pathology in all cells of all living genera?

See also: A Constitutive Intrinsic Inflammatory Signaling Circuit Composed of miR-196b, Meis2, PPP3CC, and p65 Drives Prostate Cancer Castration Resistance

Reported as: Scientists uncover new way to defeat therapy-resistant prostate cancer

In addition to IκBα/NF-κB, the signaling circuit includes the microRNA miR-196b-3p, Meis2 and PPP3CC. While miR-196b-3p promotes tumor development, Meis2, which is an essential developmental gene in mammals, can disrupt the circuit when overexpressed. The protein PPP3CC can inhibit NF-κB activity in prostate cancer cells.

The likelihood that all signaling circuits include either nutrient energy-dependent microRNAs, which are linked to healthy longevity or viral microRNAs that are linked from virus-driven energy theft to pathology peaked at the time that more than 50,000 published works had reported on differences in microRNAs that linked hydrogen-atom transfer in DNA base pairs in solution to healthy longevity or to all pathology. (May 2016)

See for comparison: microRNA. On December 29, 2016 there were more than 56,600 published works.

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