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Chronic Myeloid Leukemia With Rare Variant b2a3 (e13a3) BCR-ABL1 Fusion

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참고문헌 (10)

  1. Liu LG, "Chronic myelogenous leukemia with e13a3 (b2a3) type of BCR-ABL transcript having a DNA breakpoint between ABL exons a2 and a3", Am J Hematol, 74, pp.268~272 (2003)
  2. Moravcová J, "CML patient with rare b 2 a 3 (e 13 a 3) variant of BCR-ABL transcript: complete molecular response to imatinib", Leuk Res, 29, pp.1365~1366 (2005)
  3. Pienkowska-Grela B, "Complete cytogenetic and molecular response after imatinib treatment for chronic myeloid leukemia in a patient with atypical karyotype and BCR-ABL b2a3 transcript", Cancer Genet Cytogenet, 174, pp.111~115 (2007)
  4. Masuko M, "A chronic myeloid leukemia patient with atypical karyotype and BCR-ABL e13a3 transcript caused by complex chromosome rearrangement", Int J Hematol, 90, pp.230~234 (2009)
  5. Achkar WA, "A rare chronic myeloid leukemia case with Philadelphia chromosome, BCR-ABL e13a3 transcript and complex translocation involving four different chromosomes", Oncol Lett, 1, pp.797~800 (2010)
  6. McCarron SL, "Molecular response to imatinib in chronic myeloid leukaemia with a variant e13a3 BCR-ABL1 fusion", Med Oncol, 32, pp.452~ (2015)
  7. Franz WM, "Deletion of an N-terminal regulatory domain of the c-abl tyrosine kinase activates its oncogenic potential", EMBO J, 8, pp.137~147 (1989)
  8. Kato JY, "Amino acid substitutions sufficient to convert the nontransforming p60c-src protein to a transforming protein", Mol Cell Biol, 6, pp.4155~4160 (1986)
  9. Skorski T, "The SH3 domain contributes to BCR", ABL-dependent leukemogenesis in vivo: role in adhesion, invasion, and homing, 1998, pp.91, 406~418
  10. Gross AW, "Bcr-Abl with an SH3 deletion retains the ability to induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy", Mol Cell Biol, 19, pp.6918~6928 (1999)

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