Effect of a p210 multipeptide vaccine associated with imatinib or interferon in patients with chronic myeloid leukaemia and persistent residual disease: a multicentre observational trial

Do we have to kill the last CML cell?

“…58 Leukaemia-specific autologous CTLs can be elicited by peptide vaccination using the aminoacid sequence of the BCR-ABL junction, 59,60 and there is preliminary evidence that an immunological response to vaccination might result in a clinically significant reduction in the level of MRD. 60,61 Another interesting observation from allograft patients is the response to imatinib when used to treat relapse post-allograft: with or without donor lymphocyte infusion a stable CMR is typically achieved very quickly. 62,63 This suggests that, after allografting, the suppression of MRD by imatinib might help to restore effective immunological control.…”

Does our Current Understanding of Immune Tolerance, Autoimmunity, and Immunosuppressive Mechanisms Facilitate the Design of Efficient Cancer Vaccines?

“…The data obtained with dual siRNAs is encouraging and provide a new opportunity to successfully translate novel basic knowledge from the bench to the clinic. Despite the encouraging data discussed in this review, immunotherapeutic approaches, especially in the case of malignancies, are most likely to have effect when administered early in the course of disease or when the disease burden is low, for example following stem cell transplantation or other therapies such as chemotherapy [91].…”

“…With regard to rheumatoid arthritis, epitopes derived from different pathogens such as Mycobacterium tuberculosis activated synovial T cells [28]. Also, bacterial peptide mimics of the myelin basic protein epitope 85-99 (MBP [85][86][87][88][89][90][91][92][93][94][95][96][97][98][99] ) derived from different pathogens, such as M. tuberculosis, Bacillus subtillis and Staphylococcus aureus, induce demyelinating disease in mice that transgenically express a human MBP 85-99 -specific TCR and an HLA class II molecule that can present the peptide [29]. Depending on the experimental model or disease, CD8+ T cells can be the effector cells that can cause cell destruction, whereas CD4+ T cells can also be the effector cells, but usually the CD4+ T cells contribute to damage by a bystander mechanism such as the activation of macrophages resulting in proinflammatory cytokine production [30].…”

A pilot vaccination trial of synthetic analog peptides derived from the BCR-ABL breakpoints in CML patients with minimal disease

“…[1][2][3][4] Antileukemic effects were suggested in two of these trials. 3,4 Both trials involved patients with the b3a2 breakpoint.…”

“…[1][2][3][4] Antileukemic effects were suggested in two of these trials. 3,4 Both trials involved patients with the b3a2 breakpoint. Native peptides from either b3a2 or b2a2 breakpoints demonstrating strong binding to human leukocyte antigen (HLA)-A0201 have not been identified, and CD8 responses to HLA-A0201-restricted peptides have also not been observed in vaccinated patients.…”