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DOI 10.1111/j.1600-0609.2010.01497.x

Медицинская библиотека · European journal of haematology · 2010

WT1 peptide vaccine induces reduction in minimal residual disease in an Imatinib-treated CML patient.

Oji Yusuke, Oka Yoshihiro, Nishida Sumiyuki, Tsuboi Akihiro, Kawakami Manabu, Shirakata Toshiaki, Takahashi Kazuko, Murao Ayako, Nakajima Hiroko, Narita Miwako, Takahashi Masuhiro, Morita Satoshi, Sakamoto Junichi, Tanaka Toshio, Kawase Ichiro, Hosen Naoki, Sugiyama Haruo

Клинический случайСтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

How to treat CML patients who are resistant to inhibitors of BCR-ABL tyrosine kinase such as Imatinib is a very important and urgent issue in clinical hematology. Here, we report a case of Imatinib-treated CML in which intradermally administered WT1 peptide vaccine elicited WT1-specific immune responses and the resultant reduction in the persistent residual disease in co-administration of Imatinib. BCR-ABL mRNA levels were being maintained under the detection limit for 8 months since week 77 of vaccination. No adverse effects except local erythema at the injection sites were observed. The tetramer assay revealed that the decrease in BCR-ABL mRNA levels was associated with the increase in frequency of WT1-specific cytotoxic T lymphocytes, notably effector-memory type of that, in the patient's peripheral blood. The case presented here indicates that WT1 peptide vaccine may become a safe and cure-oriented therapy for CML patients who have residual disease regardless of the treatment with Imatinib.

Для цитирования: Oji Yusuke, Oka Yoshihiro, Nishida Sumiyuki, Tsuboi Akihiro, Kawakami Manabu, Shirakata Toshiaki, Takahashi Kazuko, Murao Ayako, Nakajima Hiroko, Narita Miwako, Takahashi Masuhiro, Morita Satoshi, Sakamoto Junichi, Tanaka Toshio, Kawase Ichiro, Hosen Naoki, Sugiyama Haruo. WT1 peptide vaccine induces reduction in minimal residual disease in an Imatinib-treated CML patient.. European journal of haematology. 2010. DOI: 10.1111/j.1600-0609.2010.01497.x.

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