In a recent Mayo Clinic study, IFN-α induced a response rate that was 41% and more likely to occur in the absence of anemia or elevated erythrocyte sedimentation rate.
However, despite the significant activity of this compound in preclinical models, in Phase II clinical trial, it only induced a response rate of approximately 10% in a cohort of patients with non-small-cell lung cancer (NSCLC) (Magné et al, 2002; Dancey and Freidlin, 2003).
This standard regimen induces a response rate of 33%35%% and a median survival of 6 8 months, but a complete response is rare.
Despite its good tolerability, GO monotherapy only induces a response rate of 25 to 33%, similar to that previously reported in adults.
Even more recently, it was shown that an inhibitor of Bruton′s tyrosine kinase (BTK), ibrutinib, induces a response rate of >70% in relapsed and refractory MCL as a single agent (Wang et al, 2013).
Panitumumab induces a response rate of 10%, similar to that achieved with single-agent cetuximab in a similar patient population [ 4, 5], and demonstrates a modest but significant increase in median progression-free survival against best supportive care.
More recently, the resolution of the BRAF crystal structure has led to the development of better, more specific BRAF inhibitors such as the Plexxikon compound, PLX4032, which induced a dramatic response rate in phase I trials, validating BRAF as a clinically relevant target.
Interestingly, lenalidomide +/− DLI (n=8) induced a 61% response rate including 37% of CR.
NGR-hTNF induced a confirmed response rate of 7%, a DCR of 30%, and a median survival of 8.9 months.
Most reported results have shown that intraarterial chemotherapy induced a higher response rate and a lower level of toxicity than systemic chemotherapy in other genitourinary tumors [15], [16].
Looking at the association lenalidomide and DLIs, this particular option induced a 62% response rate in patients developing post allo-SCT EMR.
