Abstract:
:A 67-year-old female was referred to our hospital with a sternal fracture in March 2008. She received a diagnosis of multiple myeloma (MM) BJP-κ type (ISS stage III). G-banding karyotype revealed 46, XX, t(11;22)(q23.3;q11.2) (Hubacek, Gene 592:193-9, 2016), which was later confirmed to be congenital. After repeated rounds of chemotherapy with bortezomib and lenalidomide, she obtained a very good partial response in August 2014, and she was followed up with no treatment. However, she relapsed in February 2016. At that time, fluorescence in situ hybridization identified del(13q) and t(4;14)(p16;q32), which are associated with a poor prognosis. Furthermore, PCR analysis showed that the chromosome 11 breakpoint was at the APOA5/APOA4 locus at 11q23.3, which is associated with malignancy, and that the chromosome 22 breakpoint was at the SEPT5 intron 1 locus, which also plays a role in leukemogenesis through formation of a fusion gene with MLL. Although she was treated with three further lines of therapy, she died from disease progression in August 2017. Synergism between t(11;22) and t(4;14) may have induced the double-refractory phenotype to proteasome inhibitor and lenalidomide, at least during the chemorefractory phase. We present a biological analysis of this case and a review of the literature.
journal_name
Int J Hematoljournal_title
International journal of hematologyauthors
Suzuki R,Warita T,Nakamura Y,Kitamura Y,Aoyama Y,Ogawa Y,Kawada H,Ando Kdoi
10.1007/s12185-019-02603-3subject
Has Abstractpub_date
2019-06-01 00:00:00pages
731-736issue
6eissn
0925-5710issn
1865-3774pii
10.1007/s12185-019-02603-3journal_volume
109pub_type
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journal_title:International journal of hematology
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journal_title:International journal of hematology
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journal_title:International journal of hematology
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journal_title:International journal of hematology
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journal_title:International journal of hematology
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