Tandem duplication of the FLT3 gene is found in acute lymphoblastic leukaemia as well as acute myeloid leukaemia but not in myelodysplastic syndrome or juvenile chronic myelogenous leukaemia in children

@article{Xu1999TandemDO,
  title={Tandem duplication of the FLT3 gene is found in acute lymphoblastic leukaemia as well as acute myeloid leukaemia but not in myelodysplastic syndrome or juvenile chronic myelogenous leukaemia in children},
  author={F Xu and Tomohiko Taki and H. W. Yang and Ryoji Hanada and Teruaki Hongo and Hiroaki Ohnishi and M Kobayashi and Fumio Bessho and Masayoshi Yanagisawa and Yasuhide Hayashi},
  journal={British Journal of Haematology},
  year={1999},
  volume={105}
}
We examined mRNA expression and internal tandem duplication of the Fms‐like tyrosine kinase 3 (FLT3) gene in haematological malignancies by reverse transcriptase‐polymerase chain reaction (RT‐PCR) and genomic PCR followed by sequencing. By RT‐PCR, expression of FLT3 was detected in 45/74 (61%) leukaemia cell lines and the frequency of expression of FLT3 was significantly higher in undifferentiated type (B‐precursor acute lymphoblastic leukaemia; ALL) than in differentiated type cell lines (B… 

FLT3 internal tandem duplication mutations in adult acute myeloid leukaemia define a high‐risk group

TLDR
It is demonstrated that the FLT3 ITD mutation occurs in a significant percentage of adult AML cases and is an important adverse prognostic factor that appears independent of conventional karyotypic findings.

FLT3 internal tandem duplication mutations in adult acute myeloid leukaemia define a high-risk group.

TLDR
It is demonstrated that the FLT3 ITD mutation occurs in a significant percentage of adult AML cases and is an important adverse prognostic factor that appears independent of conventional karyotypic findings.

FLT3 mutation and expression did not adversely affect clinical outcome of childhood acute leukaemia—a study of 531 Southeast Asian children by the Ma‐Spore study group

TLDR
FMS‐like tyrosine kinase 3 (FLT3) is critical for normal haematopoiesis and have been reported to be expressed in the majority of acute myeloid and lymphoid malignancies, but does not appear to be involved in the pathogenesis of AMKL, both in Down's and non‐Down's.

FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model.

TLDR
It is demonstrated that FLT3-ITD mutant proteins are sufficient to induce a myeloproliferative disorder, but are insufficient to recapitulate the AML phenotype observed in humans.

Prognostic significance of foetal‐like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia

The foetal like tyrosine kinase 3 mutation (Flt3) gene encodes a tyrosine kinase receptor that regulates proliferation and differentiation of haematopoietic stem cells. In children with acute

FLT3 mutations in a 10 year consecutive series of 177 childhood acute leukemias and their impact on global gene expression patterns

During 1995–2004, 209 children/adolescents were diagnosed with acute lymphoblastic or myeloid leukemia (ALL, AML) in Southern Sweden, of which 177 (85%), comprising 128 B‐lineage ALL, 34 AML, and 15

AML1 mutation and FLT3-internal tandem duplication in leukemia transformed from myelodysplastic syndrome.

TLDR
A 6-year-old girl with leukocytosis who developed acute mixed-lineage leukemia carrying trisomy 21 after 4 years from the initial diagnosis died after allogeneic stem cell transplantation, suggesting both AML1 mutation and FLT3-ITD may have a role in disease progression.

FLT3 internal tandem duplication in 234 children with acute myeloid leukemia: prognostic significance and relation to cellular drug resistance.

TLDR
It is concluded that FLT3/ITD is less common in pediatric than in adult AML and is a strong and independent adverse prognostic factor, and high ratios between mutant and WT-FLT3 further compromise prognosis.

Analysis of FLT 3 length mutations in 1003 patients with acute myeloid leukemia : correlation to cytogenetics , FAB subtype , and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease

TLDR
Besides the importance of FLT3-LM for biologic and clinical characterization of AML, its value as a marker for disease monitoring based on 120 follow-up samples of 34 patients is shown.

Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease.

TLDR
Besides the importance of FLT3-LM for biologic and clinical characterization of AML, its value as a marker for disease monitoring based on 120 follow-up samples of 34 patients is shown.
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Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic syndrome among various hematological malignancies. A study on a large series of patients and cell lines

TLDR
In the various cell lines examined, this abnormality was determined in only one derived from AML and never found in other hematological malignancies, emphasizing that the length mutation of FLT3 at JM/TK-I domains were restricted to AMl and MDS.

Internal tandem duplication of FLT3 associated with leukocytosis in acute promyelocytic leukemia

TLDR
Clinically, the presence of FLT3/ITD was related to high peripheral white blood cell counts as well as peripheral leukemia cell counts, and high ldh level, and low fibrinogen concentration, suggesting that FLT 3/ ITD plays a significant role in progression of APL.

Internal tandem duplication of the flt3 gene found in acute myeloid leukemia.

TLDR
The results suggest that an internal tandem duplication at the JM/TK1 domains of the flt3 gene is a somatic change detected preferentially in AML, possibly containing a monocytic component.

Tandem duplications of the FLT3 receptor gene are associated with leukemic transformation of myelodysplasia

TLDR
The fact that the accumulation of genetic events, including FLT3 duplication, correlates with leukemic transformation from antecedent myelodysplasia and with subsequent disease progression is uncovered.

Consistent detection of TLS/FUS-ERG chimeric transcripts in acute myeloid leukemia with t(16;21)(p11;q22) and identification of a novel transcript.

TLDR
It is found that the patients with t(16;21) are characterized by a relatively younger age, involvement of various subtypes of French-American-British classification and a poor prognosis, suggesting that t( 16;21)-AML is resistant to conventional chemotherapy.

Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages.

TLDR
The pattern of expression of FLT3 contrasts with the expression of FMS and KIT restricted to myeloid leukemias, and suggests that the FLT 3 product could play a role in the expansion of the leukemic blasts of both the myeloids and lymphoid lineages.

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TLDR
A form of acute myeloid leukaemia (AML), designated AML‐MO, with minimalMyeloid differentiation, not included previously in the FAB classification is described and its clinical and biological significance is not yet apparent.

Homozygous deletions of p16/MTS1 gene are frequent but mutations are infrequent in childhood T-cell acute lymphoblastic leukemia.

TLDR
The results suggest that p 16 gene alterations are involved in the development of T-ALLs and that the inactivation of the p16 gene occurs mainly through homozygous deletions rather than mutations.

Expression of the FLT3 gene in human leukemia-lymphoma cell lines.

TLDR
The pattern of expression ofFLT3 contrasts with the transcription of FMS and KIT and suggests that the FLT3 product may play a role primary in immature lymphoid cells.

Expression of the hematopoietic growth factor receptor FLT3 (STK-1/Flk2) in human leukemias.

TLDR
The possibility that overexpression of FLT3 could play a role in the survival and/or proliferation of malignant clones in acute myeloid and lymphoid leukemias is suggested.