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Taking over the Atlas
Dear Colleagues,
The Atlas, once more, is in great danger, and I will have to proceed to a collective economic lay-off of all the team involved in the Atlas before the begining of April 2015 (a foundation having suddenly withdrawn its commitment to support the Atlas). I ask you herein if any Scientific Society (a Society of Cytogenetics, of Clinical Genetics, of Hematology, or a Cancer Society, or any other...), any University and/or Hospital, any Charity, or any database would be interested in taking over the Atlas, in whole or in part. If taking charge of the whole lot is too big, a consortium of various actors could be the solution (I am myself trying to find partners). Could you please spread the information, contact the relevant authorities, and find partners.
Survival of the Atlas will be critically dependant upon your ability to find solutions (and urgently!).
Kind regards.
Jean-Loup Huret jlhuret@AtlasGeneticsOncology.org
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Trisomy 19

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.

Translocations implicated (Data extracted from papers in the Atlas)

 +19 or trisomy 19

Bibliography

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, Billstrˆm R, Mauritzson N, Mitelman F
Cancer genetics and cytogenetics. 1994 ; 74 (1) : 62-65.
PMID 8194050
 
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
 
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
 
REVIEW articlesautomatic search in PubMed
Last year articlesautomatic search in PubMed

Contributor(s)

Written06-2003Edmond S.K. Ma, Thomas S.K. Wan

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 ]
URL : http://AtlasGeneticsOncology.org/Anomalies/tri19ID1039.html

© Atlas of Genetics and Cytogenetics in Oncology and Haematology
indexed on : Tue Feb 17 19:07:58 CET 2015


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