Ben Williams' treatment summary as it appears on astrocytomaoptions.com.
Ben's tumor was recently determined to be positive for the IDH1 mutation, and positive for MGMT promoter methylation.
Information compiled from Ben’s book Surviving Terminal Cancer, and from the summary of his story at virtualtrials.com.
March 31, 1995. At the age of 50, Ben underwent a subtotal resection of a large (180 cubic centimetre) glioma of the right parietal cortex, and was given an initial diagnosis of anaplastic astrocytoma, which was later upgraded to glioblastoma after a more thorough inspection of the resected tumour tissue. Extensive residual tumour remained post-surgery.
Radiation therapy consisted of the standard 55-60 Gy to the tumour area plus 2 cm beyond the tumour boundary.
The first MRI post-radiation showed neither shrinkage nor growth of the tumour.
June 1995. Two weeks prior to his first round of chemotherapy Ben began taking oral high-dose tamoxifen at a dose of 220mg daily. Tamoxifen treatment was continued until March 1998. Side effects of tamoxifen included blood clots which he treated with Aspirin and long walks.
July 1995. First round of intravenous BCNU (carmustine) chemotherapy combined with 600mg per day of verapamil taken during the week surrounding BCNU chemo. The verapamil was intended to block the drug extrusion pump mechanism at the blood-brain barrier, and therefore increase the penetration of BCNU past this barrier.
The first post-chemotherapy MRI showed a moderate degree of tumour shrinkage.
Between the first and second round of chemotherapy, Ben began taking oral Accutane (13-cis retinoic acid) at a dose of 160 mg per day on a two week on/ one week off schedule (he later reduced the dose to 120 mg per day). Accutane was not taken on the days of chemotherapy. Accutane treatment continued until December 1995.
Also around this time he added melatonin at 15mg per evening and the immune-boosting mushroom supplement polysaccharide Krestin (PSK) at a dose of 3 grams per day. He continues taking 10mg of melatonin to this day (2014).
August 1995. Second chemotherapy cycle, this time consisting of oral procarbazine, oral lomustine (CCNU) and intravenous vincristine. This regimen is known as PCV. Verapamil was again taken to improve the brain uptake of the chemotherapy during the week surrounding oral lomustine treatment.
Second post-chemotherapy MRI showed an “enormous” reduction in the residual tumour.
Third chemotherapy cycle, PCV.
Added oral gamma linolenic acid (GLA) at a dose of 2-2.5 gram GLA daily, consisting of 10 capsules of borage seed oil.
Late November. Third post-chemotherapy MRI again showed substantial shrinkage of the residual tumour.
Early December. Fourth cycle of chemotherapy consisting of BCNU. Ben decided to switch back to BCNU due to stomach pain caused by procarbazine and neuropathy caused by vincristine.
January 1996. Fourth post-chemotherapy MRI. No evidence of residual tumour, first “clean” MRI.
Fifth cycle of chemotherapy again consisted of BCNU, followed by another clean MRI.
The sixth and last cycle of chemotherapy consisted of PCV with a half-dose of vincristine to increase its tolerability. This was again followed by another clean MRI.
Many clean MRIs followed, though Ben continued daily high-dose tamoxifen treatment until March 1998.