ABL kinase mutation and relapse in 4 pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia cases

详细信息    查看全文

• 作者：Michinori Aoe (1)
  Akira Shimada (2)
  Michiko Muraoka (2)
  Kana Washio (2)
  Yoshimi Nakamura (1)
  Takahide Takahashi (1)
  Masahide Imada (1)
  Toshiyuki Watanabe (1)
  Ken Okada (1)
  Ritsuo Nishiuchi (3)
  Takako Miyamura (4)
  Kosuke Chayama (5)
  Misako Shibakura (6)
  Megumi Oda (2)
  Tsuneo Morishima (2)
  
• 关键词：ALL ; Ph ; BCR ; ABL ; Tyrosine kinase inhibitor
• 刊名：International Journal of Hematology
• 出版年：2014
• 出版时间：May 2014
• 年：2014
• 卷：99
• 期：5
• 页码：609-615
• 全文大小：
• 参考文献：1. Schlieben S, Borkhardt A, Reinisch I, Ritterbach J, Janssen JW, Ratei R, et al. Incidence and clinical outcome of children with BCR/ABL-positive acute lymphoblastic leukemia (ALL). A prospective RT-PCR study based on 673 patients enrolled in the German pediatric multicenter therapy trials ALL-BFM-90 and CoALL-05-92. Leukemia. 1996;10:957鈥?3.
  2. Aric貌 M, Valsecchi MG, Camitta B, Schrappe M, Chessells J, Baruchel A, et al. Outcome of treatment in children with Philadelphia chromosome-positive acute lymphoblastic leukemia. N Engl J Med. 2000;342:998鈥?006. CrossRef
  3. Schultz KR, Bowman WP, Aledo A, Slayton WB, Sather H, Devidas M, et al. Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a children鈥檚 oncology group study. J Clin Oncol. 2009;27:5175鈥?1. CrossRef
  4. Chang BH, Willis SG, Stork L, Hunger SP, Carroll WL, Camitta BM, et al. Imatinib resistant BCR-ABL1 mutations at relapse in children with Ph+ ALL: a Children鈥檚 Oncology Group (COG) study. Br J Haematol. 2012;157:507鈥?0. CrossRef
  5. Tamamyan G, Chao YH, Wang CH, Wu HP, Weng T, Peng CT, Wu KH. Dasatinib plus chemotherapy to achieve full donor chimerism and complete molecular remission in a child with relapsed philadelphia chromosome-positive acute lymphoblastic leukemia. Pediatr Blood Cancer. 2013;60:1727鈥?. CrossRef
  6. Kanda J. Effect of HLA mismatch on acute graft-versus-host disease. Int J Hematol. 2013;98:300鈥?. CrossRef
  7. Hochhaus A, Kreil S, Corbin AS, La Ros茅e P, M眉ller MC, Lahaye T, et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia. 2002;16:2190鈥?. CrossRef
  8. Pfeifer H, Wassmann B, Pavlova A, Wunderle L, Oldenburg J, Binckebanck A, et al. Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Blood. 2007;110:727鈥?4. CrossRef
  9. Lee S, Kim DW, Cho BS, Yoon JH, Shin SH, Yahng SA, et al. Impact of minimal residual disease kinetics during imatinib-based treatment on transplantation outcome in Philadelphia chromosome-positive acute lymphoblastic leukemia. Leukemia. 2012;26:2367鈥?4. CrossRef
  10. Schultz KR, Bowman WP, Aledo A, et al. Continuous dosing imatinib with intensive chemotherapy gives equivalent outcomes to allogeneic BMT for Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) with longer term follow up: updated results of Children鈥檚 Oncology Group (COG) AALL0031 [Abstract]. Pediatr Blood Cancer. 2010;54:788.
  11. Hochhaus A, La Ros茅e P, M眉ller MC, Ernst T, Cross NC. Impact of BCR-ABL mutations on patients with chronic myeloid leukemia. Cell Cycle. 2011;10(2):250鈥?0. CrossRef
  12. Soverini S, Colarossi S, Gnani A, Rosti G, Castagnetti F, Poerio A, et al. Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res. 2006;12(24):7374鈥?. CrossRef
  13. Jones D, Thomas D, Yin CC, O鈥橞rien S, Cortes JE, Jabbour E, et al. Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors. Cancer. 2008;113:985鈥?4. CrossRef
  14. Cortes JE, Kantarjian H, Shah NP, Bixby D, Mauro MJ, Flinn I, et al. Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med. 2012;367:2075鈥?8. CrossRef
  15. O鈥橦are T, Shakespeare WC, Zhu X, Eide CA, Rivera VM, Wang F, et al. AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell. 2009;16:401鈥?2. CrossRef
  
• 作者单位：Michinori Aoe (1)
  Akira Shimada (2)
  Michiko Muraoka (2)
  Kana Washio (2)
  Yoshimi Nakamura (1)
  Takahide Takahashi (1)
  Masahide Imada (1)
  Toshiyuki Watanabe (1)
  Ken Okada (1)
  Ritsuo Nishiuchi (3)
  Takako Miyamura (4)
  Kosuke Chayama (5)
  Misako Shibakura (6)
  Megumi Oda (2)
  Tsuneo Morishima (2)
  
  1. Division of Medical Support, Okayama University Hospital, Okayama, Japan
  2. Department of Pediatrics, Pediatric Hematology/Oncology, Okayama University Hospital, 2-5-1 Shikatacho, Kitaku, Okayama, 700-8558, Japan
  3. Department of Pediatrics, Kochi Health Sciences Center, Kochi, Japan
  4. Department of Pediatrics, Osaka University, Osaka, Japan
  5. Department of Pediatrics, Toyonaka Municipal Hospital, Osaka, Japan
  6. Field of Medical Technology, Okayama University Graduate School of Health Sciences, Okayama, Japan
  
• ISSN：1865-3774

文摘

The tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) revolutionized the treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph-ALL), which had showed poor prognosis before the dawn of IM treatment. However, if Ph-ALL patients showed IM resistance due to ABL kinase mutation, second-generation TKI, dasatinib or nilotinib, was recommended. We treated 4 pediatric Ph-ALL patients with both IM and bone marrow transplantation (BMT); however, 3 relapsed. We retrospectively examined the existence of ABL kinase mutation using PCR and direct sequencing methods, but there was no such mutation in all 4 diagnostic samples. Interestingly, two relapsed samples from patients who were not treated with IM before relapse did not show ABL kinase mutation and IM was still effective even after relapse. On the other hand, one patient who showed resistance to 3 TKI acquired dual ABL kinase mutations, F359C at the IM-resistant phase and F317I at the dasatinib-resistant phase, simultaneously. In summary, Ph-ALL patients relapsed with or without ABL kinase mutation. Furthermore, ABL kinase mutation was only found after IM treatment, so an IM-resistant clone might have been selected during the IM treatment and intensive chemotherapy. The appropriate combination of TKI and BMT must be discussed to cure Ph-ALL patients.