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+9 or trisomy 9

Written2006-09Ulrike Bacher, Claudia Haferlach
Department for Internal Medicine III, Klinikum Grosshadern, Ludwig-Maximilians-University, Marchioninistr. 15, D-81377 Munich, Germany

(Note : for Links provided by Atlas : click)

Identity

ICD-Topo C420,C421,C424 BLOOD, BONE MARROW, & HEMATOPOIETIC SYS
ICD-Morpho 9811/3 B lymphoblastic leukaemia/lymphoma, NOS
ICD-Morpho 9837/3 T lymphoblastic leukaemia/lymphoma
ICD-Morpho 9861/3 AML with mutated NPM1; AML with mutated CEBPA; Acute myeloid leukaemia, NOS
ICD-Morpho 9975/3 Chronic myelogenous leukaemia, BCR-ABL1 positive; Myeloproliferative neoplasm, unclassifiable; Myelodysplastic/myeloproliferative neoplasm, unclassifiable
ICD-Morpho 9989/3 Myelodysplastic syndrome, unclassifiable
Atlas_Id 1020
Note Occurs in a large spectrum of myeloid and lymphatic malignancies - chronic myeloproliferative disorders (CMPD), acute myeloid leukemias (AML), myelodysplastic syndromes (MDS), acute lymphoblastic leukemias (ALL) of B-lineage and of T-lineage. Strong association to the CMPD and especially to polycythemia vera (PV).
 
  +9 (G-banding)

Clinics and Pathology

Disease Chronic myeloproliferative disorders
Epidemiology All CMPD: approx. 2% of all cases, approx. 10% of all chromosomal aberrant cases. PV: around 7% of all cases, around 16% of all chromosomal aberrant cases.
Cytogenetics One of the most frequent anomalies (with del(20q), +8, and del(13q)) in BCR- ABL negative CMPD, especially in PV and in chronic idiopathic myelofibrosis (CIMF).
Additional anomalies: PV: in 50% as sole abnormality, in 50% of all cases most frequently in combination with numerical gain of chromosome 8.
Genes +9 is assumed to represent a gain-of-function mechanism with respect to the JAK2 gene on 9p24 coding for the JAK2 kinase. Additionally, a cooperation of +9 with the V617F mutation of the JAK2 gene is hypothesized.
Prognosis No prognostic impact according to follow-up studies of limited sample sizes.

Disease Acute myeloid leukemia
Phenotype / cell stem origin FAB subtypes M2, M4, M5.
Epidemiology Frequent in combination with other chromosomal changes. Extremely rare as sole abnormality (around 0.1% of all cases).
Cytogenetics Additional anomalies: In combination with other numerical gains (mainly +8) in simple karyotypes or in complex aberrant karyotypes (at least 3 chromosomal abnormalities).
Genes Not known.
Prognosis Intermediate prognosis as sole aberration or as +8,+9 in simple karyotypes. Complex aberrant karyotypes have an inferior prognosis.

Disease Myelodysplastic syndrome
Epidemiology Rare.
Cytogenetics Additional anomalies: Occurrence as sole abnormality or within complex aberrant karyotype.
Genes Not known
Prognosis Intermediate prognosis as sole aberration. Complex aberrant karyotypes have an inferior prognosis.

Disease B-lineage acute lymphoblastic leukemia
Epidemiology Rare in Philadelphia-positive and in Philadelphia-negative B-lineage.
Cytogenetics Additional anomalies: Philadelphia-negative ALL: Occurrence in hyperdiploid karyotypes (equal or more than 47 chromosomes) mostly in combination with other numerical gains. Philadelphia-positive ALL: Rare additional change.
Genes Not known.
Prognosis Philadelphia-negative ALL with high hyperdiploid karyotype (equal or more than 51 chromosomes) shows a good prognosis, gain of chromosome 9 is not typical and prognostic impact of trisomy 9 in this setting unknown. In Philadelphia-positive ALL additional chromosomal anomalies probably enhance the inferior prognosis.

Disease T-lineage acute lymphoblastic leukemia.
Epidemiology Rare, up to 4% in childhood T-ALL.
Cytogenetics Additional anomalies: Occurs as sole or as combined anomaly.
Genes Not known.
Prognosis So far a prognostic impact could not be defined, which also might be due to the low analyzed case numbers.

Cytogenetics

 
  +9 (chromosome painting, WCP#9 (red))

Bibliography

Numerical chromosome aberrations in human neoplasia.
Heim S, Mitelman F
Cancer genetics and cytogenetics. 1986 ; 22 (2) : 99-108.
PMID 3708552
 
Karyotypic patterns in chronic myeloproliferative disorders: report on 74 cases and review of the literature.
Mertens F, Johansson B, Heim S, Kristoffersson U, Mitelman F
Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 1991 ; 5 (3) : 214-220.
PMID 2013980
 
Prognostic significance of additional chromosome abnormalities in adult patients with Philadelphia chromosome positive acute lymphoblastic leukaemia.
Rieder H, Ludwig WD, Gassmann W, Maurer J, Janssen JW, Gökbuget N, Schwartz S, Thiel E, Löffler H, Bartram CR, Hoelzer D, Fonatsch C
British journal of haematology. 1996 ; 95 (4) : 678-691.
PMID 8982045
 
New recurring cytogenetic abnormalities and association of blast cell karyotypes with prognosis in childhood T-cell acute lymphoblastic leukemia: a pediatric oncology group report of 343 cases.
Schneider NR, Carroll AJ, Shuster JJ, Pullen DJ, Link MP, Borowitz MJ, Camitta BM, Katz JA, Amylon MD
Blood. 2000 ; 96 (7) : 2543-2549.
PMID 11001909
 
Chromosome and molecular abnormalities in myelodysplastic syndromes.
Fenaux P
International journal of hematology. 2001 ; 73 (4) : 429-437.
PMID 11503956
 
Exploring polycythaemia vera with fluorescence in situ hybridization: additional cryptic 9p is the most frequent abnormality detected.
Najfeld V, Montella L, Scalise A, Fruchtman S
British journal of haematology. 2002 ; 119 (2) : 558-566.
PMID 12406101
 
Exploring polycythaemia vera with fluorescence in situ hybridization: additional cryptic 9p is the most frequent abnormality detected.
Najfeld V, Montella L, Scalise A, Fruchtman S
British journal of haematology. 2002 ; 119 (2) : 558-566.
PMID 12406101
 
Additional clonal abnormalities in Philadelphia-positive ALL and CML demonstrate a different cytogenetic pattern at diagnosis and follow different pathways at progression.
Bacher U, Haferlach T, Hiddemann W, Schnittger S, Kern W, Schoch C
Cancer genetics and cytogenetics. 2005 ; 157 (1) : 53-61.
PMID 15676148
 
Conventional cytogenetics of myeloproliferative diseases other than CML contribute valid information.
Bacher U, Haferlach T, Kern W, Hiddemann W, Schnittger S, Schoch C
Annals of hematology. 2005 ; 84 (4) : 250-257.
PMID 15692838
 
The role of the JAK2 mutations: A study in 1103 patients with CMPD and in 196 patients with AML.
Schnittger S, Bacher U, Petrides P, Kern W, Haferlach T, Schoch C
Leukemia, submitted. 2006.
 

Citation

This paper should be referenced as such :
Haferlach, C ; Bacher, U
+9 or trisomy 9
Atlas Genet Cytogenet Oncol Haematol. 2007;11(1):40-41.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Anomalies/tri9ID1020.html


Translocations implicated (Data extracted from papers in the Atlas)

 +9 or trisomy 9

External links

Mitelman database+9 [Case List]    +9 [Association List] Mitelman database (CGAP - NCBI)
arrayMapTopo ( C42) Morph ( 9811/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]
arrayMapTopo ( C42) Morph ( 9837/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]
arrayMapTopo ( C42) Morph ( 9861/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]
arrayMapTopo ( C42) Morph ( 9975/3) - 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 database+9 or trisomy 9
REVIEW articlesautomatic search in PubMed
Last year articlesautomatic search in PubMed
All articlesautomatic search in PubMed


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