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Trisomy 19

Written2003-06Edmond S.K. Ma, Thomas S.K. Wan
Hematology Division, Department of Pathology, The University of Hong Kong, Queen Mary Hospital, Hong Kong, P.R. China

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Identity

ICD-Topo C420,C421,C424 BLOOD, BONE MARROW, & HEMATOPOIETIC SYS
ICD-Morpho 9861/3 AML with mutated NPM1; AML with mutated CEBPA; Acute myeloid leukaemia, NOS
ICD-Morpho 9989/3 Myelodysplastic syndrome, unclassifiable
Atlas_Id 1039

Clinics and Pathology

Disease Trisomy 19 (+19) as a sole karyotypic aberration is strongly associated with myeloid disorder. In a previously published literature review, among 31 patients with isolated +19, 25 were diagnosed with myeloid malignancy, including acute myeloid leukaemia (AML) in 14 cases and myelodysplastic syndrome (MDS) in 11 cases. Four out of the 14 AML patients had a preceding MDS phase, with +19 appearing at the time of leukaemic transformation. None of the MDS or AML cases, however, had a history of exposure to radiotherapy and chemotherapy. Hence isolated +19 is associated with a subgroup of de novo myeloid disorder, in which the clinical characteristics and prognostic impact require further delineation.

As a secondary or additional abnormality, +19 is frequently encountered in chronic myeloid leukaemia (CML). Though not as common as trisomy 8, i(17q) and extra Ph chromosome, +19 is nevertheless seen in up to 15% of CML patients with additional abnormalities.

Frequent gain of chromosome 19 or 19q was recently detected by comparative genomic hybridization in 4 out of 12 (33.3%) patients samples of acute megakaryoblastic leukaemia (AML-M7) and 9 out of 11 (81.8%) megakaryoblastic cell lines. In none of the primary patient samples was the abnormality detected by G-banding analysis. In another study on childhood and adult AML-M7, +19 was detected in 7 out of 53 patients, although as an additional abnormality in all cases. It appears +19 may play a role in the pathogenesis of megakaryoblastic leukaemia.

Etiology Isolated +19 is probably associated with de novo myeloid disorders, as none of the AML and MDS cases with this abnormality reported had a history of prior radiotherapy or chemotherapy exposure.
Prognosis Although isolated +19 is strongly associated with myeloid disorders, most probably de novo disease, its prognostic significance requires further elucidation.

Bibliography

Frequent gain of chromosome 19 in megakaryoblastic leukemias detected by comparative genomic hybridization.
Alvarez S, MacGrogan D, Calasanz MJ, Nimer SD, Jhanwar SC
Genes, chromosomes & cancer. 2001 ; 32 (3) : 285-293.
PMID 11579469
 
Trisomy 19 in a patient with myelodysplastic syndrome and thrombocytosis.
Humphries JE, Wheby MS
Cancer genetics and cytogenetics. 1990 ; 44 (2) : 187-191.
PMID 2297677
 
Trisomy 19 as the sole chromosomal anomaly in hematologic neoplasms.
Johansson B, Billströ R, Mauritzson N, Mitelman F
Cancer genetics and cytogenetics. 1994 ; 74 (1) : 62-65.
PMID 8194050
 
Chromosome 19 abnormalities are commonly seen in AML, M7.
Nimer SD, MacGrogan D, Jhanwar S, Alvarez S
Blood. 2002 ; 100 (10) : 3838-3839.
PMID 12411327
 

Citation

This paper should be referenced as such :
Ma, ESK ; Wan, TSK
+19 or trisomy 19
Atlas Genet Cytogenet Oncol Haematol. 2003;7(3):185-185.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Anomalies/tri19ID1039.html


Other genes implicated (Data extracted from papers in the Atlas) [ 2 ]

Genes ABL1 BCR

Translocations implicated (Data extracted from papers in the Atlas)

 +19 or trisomy 19

External links

Mitelman database+19 [Case List]    +19 [Association List] Mitelman database (CGAP - NCBI)
arrayMapTopo ( C42) Morph ( 9861/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]
arrayMapTopo ( C42) Morph ( 9989/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]
 
 
Disease databaseTrisomy 19
REVIEW articlesautomatic search in PubMed
Last year articlesautomatic search in PubMed
All articlesautomatic search in PubMed


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indexed on : Sat Sep 10 10:33:22 CEST 2016


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