Impact of p53 status to response of temozolomide in low MGMT expression glioblastomas: preliminary results.

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As you all may of surmised , Joshua’s doctors prescribed Temador as a chemo to aid in the brain tumor eradication.
We’ve had a total of 5 brain mets over Joshua’s 5 1/2 years of fighting ASPS. Our last bout in April of 2016.

We discovered 2 tumors ..a year to date from our previous 3 treated in 2015.

We treated the 3mm leftside optically located with SRS and once again took Temador for 5 days at 250mg.

Josh had had his primary tumor tested and Temador was one of the meds recommended to be a good candidate for treatment.

In reading of the markers that have been determined to give good results while using Temador for brain tumors, and reading of bio markers in a study that included ASPS patients , this could explain our success.

This was a study of bio markers and ASPS was mentioned.

Multi-platform profiling of over 2000 sarcomas: Identification of biomarkers and novel therapeutic targets

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494935
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“Low MGMT expression, a temozolomide associated biomarker, was noted in a variety of sarcomas including alveolar soft part sarcoma (21 ASPS), desmoid, EHE, perivascular epithelioid cell tumor (PEComa), endometrial stromal sarcoma (ESS), giant cell tumor, liposarcoma, LMS, malignant peripheral nerve sheath tumor (MPNST), osteosarcoma and UPS. There was low expression of MGMT in 65.3% of the sarcomas overall.”

Also ASPS has been marked as having the p53 oncogene -
Correction protien/gene, in which if I understand it correctly , to respond and regulate cell cycles . After the Temador interferes and creates damage on the MGMT marked cells then the mutated P53 protien is allowed t to go about it’s normal function and aids with the Temador to induce death. Apoptosis :)

P53 proteins are cancer mutations in people with the p53 gene, and reportedly are present in half of cancers .

https://www.ncbi.nlm.nih.gov/m/pubmed/9039259
Impact of p53 status to response of temozolomide in low MGMT expression glioblastomas: preliminary results.

METHODS: In this retrospective study, glioblastomas with low MGMT expression receiving surgical resection, radiotherapy and temozolomide capsule chemotherapy were divided into high and low mutant p53 expression groups. Patient age, gender, KPS score and extent of resection were analysed between the two groups by t-test and Fisher's exact test, respectively. Correlation between p53 status and control of tumor growth was analysed by survival analysis.


https://www.ncbi.nlm.nih.gov/pubmed/18647495/

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RESULTS: In total, 30 patients were included in the study. No statistically significant differences in age, gender, KPS score or extent of resection existed between the two groups. Patients with both low mutant p53 expression and low MGMT had much longer progression-free survival time to temozolomide capsule than those with high mutant p53 expression and low MGMT (p<0.05) Overall survival time did not reach statistical significance between the two groups.


CONCLUSION: p53 in addition to MGMT plays a role in chemotherapy resistance to temozolomide. Glioblastoma patients with both low MGMT and low mutant p53 expression have higher progression-free survival time and may have longer term prognosis compared with those patients with both low MGMT and high mutant p53 expression.