Glioblastoma Brain cancer Sarcoma brain cancer treatment of $85000 [Video]

gofundme

https://gofund.me/f712e178

The $85,000.00 is to cover the costs of the therapy with 14 vaccines meant to give my body algorithmically predicted immunity to a possible relapse of brain Cancer. My form of brain cancer is Glioblastoma. My family recently found out from another family who have decided to go to Cegat clinic which will generate the treatment for Sarcoma, in their particular case. I will go for treatment for glioblastoma. I have been struggling with this problem since September 2022. My family found the clinic that will produce a personalized vaccine for my cancer. This Vaccine will be personalized for me based on genetic mapping and algorithmic predictions on the gene sequences they find in the tumor.

gofundme link is below.

https://gofund.me/f712e178
https://gofund.me/42ad60ec

Background: Fibroblast growth factor receptor FGFR inhibitors are currently used in clinical development. A subset of glioblastomas carries gene fusion of FGFR3 and transforming acidic coiled-coil protein 3. The prevalence of other FGFR3 alterations in glioma is currently unclear.

Methods: We performed RT-PCR in 101 glioblastoma samples to detect FGFR3-TACC3 fusions “RT-PCR cohort” and correlated results with FGFR3 immunohistochemistry IHC. Further, we applied FGFR3 IHC in 552 tissue microarray glioma samples (TMA cohort” and validated these results in two external cohorts with 319 patients. Gene panel sequencing was carried out in 88 samples “NGS cohort” to identify other possible FGFR3 alterations. Molecular modeling was performed on newly detected mutations.

Results: In the “RT-PCR cohort,” we identified FGFR3-TACC3 fusions in 2/101 glioblastomas. Positive IHC staining was observed in 73/1024 tumor samples of which 10 were strongly positive. In the “NGS cohort,” we identified FGFR3 fusions in 9/88 cases, FGFR3 amplification in 2/88 cases, and FGFR3 gene mutations in 7/88 cases in targeted sequencing. All FGFR3 fusions and amplifications and a novel FGFR3 K649R missense mutation were associated with FGFR3 overexpression (sensitivity and specificity of 93% and 95%, respectively, at cutoff IHC score greater than7. Modeling of these data indicated that Tyr647, a residue phosphorylated as a part of FGFR3 activation, is affected by the K649R mutation.

Conclusions: FGFR3 IHC is a useful screening tool for the detection of FGFR3 alterations and could be included in the workflow for isocitrate dehydrogenase (IDH) wild-type glioma diagnostics. Samples with positive FGFR3 staining could then be selected for NGS-based diagnostic tools.

Documentation Links from cegat.com

https://cegat.com/cancerfusionrx-with-extended-fusion-spectrum/