The trial sounds interesting indeed. Although there is no study that shows this particular drug may have benefits for synovial sarcoma, there are studies that looked at the other similar drug mentioned, 5-aza-2’-deoxycytidine:
K Numoto, A Yoshida, S Sugihara, T Kunisada, Y Morimoto, Y Yoneda, Y Fujita, K Nishida, M Ouchida and T Ozaki,
Journal of cancer research and clinical oncology, Jan 2010
In this study, the methylation status of RASSF1A in synovial sarcomas and the effect of demethylation on synovial sarcoma were examined.The methylation status in 74 soft tissue sarcomas (STSs) including 21 synovial sarcomas was determined by methylation specific PCR. The effect of the de-methylating agent 5-aza-20-deoxycytidine (5-Aza-dC) on synovial sarcoma was examined using synovial sarcoma cell lines (SYO-1 and HS-SY-II).RASSF1A methylation was observed in 10 (47.6%) of 21 synovial sarcomas and in 10 (18.9%) of 53 the other STSs (P = 0.0295). De-methylation of the cells by treatment with 5-Aza-dC induced re-expression of RASSF1A and growth suppression of the cells. The calculated IC50 of 5-Aza-dC against the SYO-1 and the HS-SYII cells were 0.9 and 1.3 lM (96 h), respectively. With twice weekly administration of 1 or 10 mg/kg 5-Aza-dC, the growth of the mouse xenograft tumors of SYO-1 was significantly suppressed in comparison to the controls (P\0.01).This is the first report showing the anti-tumor effect of 5-Aza-dC on synovial sarcoma. 5-Aza-dC is suggested to have a good therapeutic potential against synovial sarcoma.
M Ayyoub, RN Taub, ML Keohan, M Hesdorffer, G Metthez, L Memeo, M Mansukhani, H Hibshoosh, CS Hesdorffer and D Valmori,
Cancer immunity, Aug 2004 09
Sarcomas are rare but aggressive malignant tumors associated with high mortality, for which the efficacy of standard therapies remains limited. In order to develop immunotherapeutic approaches for the treatment of sarcoma, we studied the relevance of cancer/testis antigens (CTAs), a group of antigens whose expression is developmentally regulated and that is specifically found in some tumor types, as sarcoma vaccine targets. CTA expression was assessed by PCR and/or immunohistochemistry (IHC) in sarcoma tumor samples that included different histological subtypes and sarcoma cell lines. Expression of HLA class I was assessed by IHC in tumor samples and by FACS analysis in cell lines. More than 70% of the tumor samples expressed at least one CTA. The majority of tumors and cell lines expressed normal levels of HLA class I. HLA class I expression in cell lines was enhanced upon treatment with IFN-gamma. CTA expression was enhanced or induced by treatment with the demethylating agent 5-aza-2'-deoxycytidine, resulting in recognition by specific CTLs. Interestingly, a spontaneous humoral and CD8+ T cellular response to the CTA NY-ESO-1 was detected in a synovial sarcoma patient. Together, these findings strongly support the implementation of CTA-based immunotherapy of sarcoma as a means to improve the efficacy of the standard therapy.
Was this trial suggested by NIH?
Did they check if you still have the engineered T-cells in your blood? What do they think about checkpoint inhibitors in your case?