+13 or trisomy 13

Lee, Re; Dal, Cin P

doi:10.4267/2042/47494

Cited by 3 publications

(3 citation statements)

References 3 publications

(4 reference statements)

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“…Trisomy 13 has been described in AML M0 and M1 FAB, especially in men over 70 years of age (0.7%), MDS, PMF, and atypical chronic granulocytic leukemia (atypical CML). The prognosis of AML 13+ patients is unfavorable, with a median survival of 0.5-14.7 months [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient With Diffuse Large B Cell Non-Hodgkin Lymphoma and Acute Myeloid Leukemia Secondary to Primary Myelofibrosis

Bumbea¹,

Popov²,

Tomuleasa³

et al. 2022

Cureus

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Concomitant diagnosis of non-Hodgkin lymphoma (NHL) and acute myeloid leukemia secondary to chronic myeloproliferative neoplasms (MPNs) is rarely reported. Patients with MPNs may have a second neoplasm, and the risk of lymphoid line neoplasms is 2.5-3.5 times for lymphoid line neoplasms. The explanation for this association is the genetic instability of hematopoietic progenitors in MPNs. An 80-year-old Caucasian man, with many comorbidities, presents for physical asthenia, sweating. The right inguinal adenopathy was known one month before the examination. The patient was diagnosed concomitantly with diffuse large B cell lymphoma (DLBCL) and acute myeloid leukemia (AML) secondary to primary myelofibrosis (PMF) and presented trisomy 8, trisomy 13, and triple-negative PMF status. The patient initially received two well-tolerated R mini CHOP series. This type of treatment was selected to treat DLBCL for one unfit patient for intensive chemotherapy due to his age and comorbidities. R mini CHOP administration was followed by severe aplasia that lasted approximately two weeks followed by severe thrombocytosis that reached 4000 x109/L, and Thromboreductin recommendation was mandatory. The result of the treatment was a partial response but with severe adverse events like neutropenia G4, due to the delay of the treatment the patient lost the response. It was mandatory to select another treatment line and the chosen was venetoclax; it was selected for the simultaneous treatment of DLBCL and the underlying AML. It was obtained a significant reduction in the size of the inguinal lymph node block in two weeks of treatment. Severe neutropenia was diagnosed and complicated with sepsis. The evolution is unfavorable with the installation of multiple organ dysfunction. The presence of a complex karyotype (trisomy 8, trisomy 13) in a patient with myeloid metaplasia with triple-negative PMF was associated with blast transformation and severe thrombocytosis. The patient was diagnosed concomitantly with DLBCL, making the therapeutic decision difficult. Venetoclax has been shown to be useful in the treatment of DLBCL but has been associated with severe neutropenia, which has led to infectious complications.

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Section: Discussionmentioning

confidence: 99%

Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient With Diffuse Large B Cell Non-Hodgkin Lymphoma and Acute Myeloid Leukemia Secondary to Primary Myelofibrosis

Bumbea¹,

Popov²,

Tomuleasa³

et al. 2022

Cureus

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“…Trisomy 13 (+13), especially as solitary abnormality, is very rare, however it has been observed recurrently in myeloid neoplasia, mostly in AML, primary myelofibrosis, atypical CML and MDS. 40 Isolated +13 in a patient with MDS RAEB was first reported in 1989. 41 A second case report – also MDS RAEB - followed in 1990.…”

Section: Introductionmentioning

confidence: 98%

“… 1 This is contrasting the statement in the “Huret Atlas” saying that in the majority of cases +13 is the only cytogenetic abnormality. 40 In AML, trisomy 13 was shown to be closely associated with FLT3 overexpression and cooperating RUNX1 mutations. 45 , 46 …”

Section: Introductionmentioning

confidence: 99%

Rare Cytogenetic Abnormalities in Myelodysplastic Syndromes

Schanz¹,

Braulke²,

Haase

2015

Mediterr J Hematol Infect Dis

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The karyotype represents one of the main cornerstones for the International Prognostic Scoring System (IPSS) and the revised IPSS-R (IPSS-R) that are most widely used for prognostication in patients with myelodysplastic syndromes (MDS). The most frequent cytogenetic abnormalities in MDS, i.e. del(5q), -7/del(7q), +8, complex karyotypes, or −Y have been extensively explored for their prognostic impact. The IPSS-R also considers some less frequent abnormalities such as del(11q), isochromosome 17, +19, or 3q abnormalities. However, more than 600 different cytogenetic categories had been identified in a previous MDS study. This review aims to focus interest on selected rare cytogenetic abnormalities in patients with MDS. Examples are numerical gains of the chromosomes 11 (indicating rapid progression), of chromosome 14 or 14q (prognostically intermediate to favorable), -X (in females, with an intermediate prognosis), or numerical abnormalities of chromosome 21. Structural abnormalities are also considered, e.g. del(13q) that is associated with bone marrow failure syndromes and favorable response to immunosuppressive therapy. These and other rare cytogenetic abnormalities should be integrated into existing prognostication systems such as the IPSS-R. However, due to the very low number of cases, this is clearly dependent on international collaboration. Hopefully, this article will help to inaugurate this process.

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Recurrent Cytogenetic Abnormalities in Acute Myeloid Leukemia

Yang

Park

Wan

2016

Methods in Molecular Biology

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The spectrum of chromosomal abnormality associated with leukemogenesis of acute myeloid leukemia (AML) is broad and heterogeneous when compared to chronic myeloid leukemia and other myeloid neoplasms. Recurrent chromosomal translocations such as t(8;21), t(15;17), and inv(16) are frequently detected, but hundreds of other uncommon chromosomal aberrations from AML also exist. This chapter discusses 22 chromosomal abnormalities that are common structural, numerical aberrations, and other important but infrequent (less than 1 %) translocations emphasized in the WHO classification. Brief morphologic, cytogenetic, and clinical characteristics are summarized, so as to provide a concise reference to cancer cytogenetic laboratories. Morphology based on FAB classification is used together with the current WHO classification due to frequent mentioning in a vast number of reference literatures. Characteristic chromosomal aberrations of other myeloid neoplasms such as myelodysplastic syndrome and myeloproliferative neoplasm will be discussed in separate chapters-except for certain abnormalities such as t(9;22) in de novo AML. Gene mutations detected in normal karyotype AML by cutting edge next generation sequencing technology are also briefly mentioned.

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+13 or trisomy 13

Cited by 3 publications

References 3 publications

Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient With Diffuse Large B Cell Non-Hodgkin Lymphoma and Acute Myeloid Leukemia Secondary to Primary Myelofibrosis

Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient With Diffuse Large B Cell Non-Hodgkin Lymphoma and Acute Myeloid Leukemia Secondary to Primary Myelofibrosis

Rare Cytogenetic Abnormalities in Myelodysplastic Syndromes

Recurrent Cytogenetic Abnormalities in Acute Myeloid Leukemia

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