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posted by oldcookie48
My husband is 77 yr old. He was diagnosed 2013 w/GBM 4. Full Resection & Radiation. Took TMZ for 12 mos, then CCNU for 6 mos. Optune for 15 mos/stopped due to skin issues-skin cancer. Recurrence in 2018. Full resection/radiation. Now on 10th round of TMZ. Taking Ben Wms' Supplement cocktail since 2013. Only RX: Valproic Acid (never had seizures), Celebrex, Bactrim. Only issues are cognitive, motivation, fatigue. He is MGMT meth. Seattle NO says go to 12 mos (that 2 left). UCSF NO suggesting he stop TMZ due to fatigue since no validation it helps past 6 mos. Blood runs are good.
Stephen, do you think we should finish the last two rds to make 12 or stop at 10?? NO's leaving it up to us. Any other recommendations based on his gene testing below? I have been ill so difficult for me to focus very well. My husband can't focus at all so leaving it up to me.
Appreciate your thoughts. Thank you kindly.
INTERPRETATION:
Tumor-only sequencing of this recurrent glioblastoma demonstrates a hotspot mutation in the promoter region of the TERT gene, focal deep deletion of the CDKN2A and CDKN2B tumor suppressor genes on chromosome 9p21, focal amplification of the MDM4 oncogene on chromosome 1q32, focal amplification of the PDGFRA oncogene on chromosome 4q12, a nonsense mutation in the PTEN tumor suppressor gene with loss of the remaining wildtype allele, a frameshift mutation in the BCOR tumor suppressor gene, and focal amplification of the EGFR oncogene on chromosome 7p11. This EGFR amplification is accompanied by a missense mutation that localizes within the extracellular ligand-binding domain and has been recurrently found in glioblastomas, often in conjunction with gene amplification as seen in this tumor [refs. 1-2]. This EGFR mutation is present on a majority of the amplified EGFR alleles given its allele frequency of 74%. Extracellular domain mutations in EGFR have been shown to correlate with resistance to type I EGFR inhibitors such as erlotinib but sensitivity to type II EGFR inhibitors [ref. 3].
The quantity of somatic mutations and mutational signature of this recurrent tumor is not suggestive of the hypermutation that is known to occur in a subset of gliomas following treatment with alkylating agents such as temozolomide [ref. 4].
Chromosomal copy number changes in the tumor include gain of 7 and losses of distal 2p, interstitial 3q, 8p, 9p, 10, portions of 11q, 13q, distal 14q, and distal
Only 11 of the 1,068 microsatellites assessed in the tumor (<2%) demonstrate instability, consistent with a microsatellite stable tumor.
Together, the genetic profile is consistent with the diagnosis of recurrent glioblastoma, IDH-wildtype, WHO grade IV. The cytogenetic alterations (trisomy 7, monosomy 10) and genetic alterations (CDKN2A deletion, TERT promoter and PTEN mutations, amplifications of EGFR, PDGFRA, and MDM4) are some of the most common seen in IDH-wildtype glioblastomas arising within the cerebral hemispheres in adults [ref. 1]. Additionally, this glioblastoma demonstrates a truncating mutation in BCOR, which encodes a transcriptional co-repressor protein that is commonly inactivated in pediatric high-grade gliomas but is not known to be a recurrently mutated or deleted gene in adult IDH-wildtype glioblastoma [refs. 5-6].
Genetic features of a diffuse lower-grade glioma (e.g. chromosomes 1p/19q co-deletion or mutations involving IDH1, IDH2, TP53, ATRX, CIC, and FUBP1) are not identified.
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