Activation of the NF-κB pathway by the leukemogenic TEL-Jak2 and TEL-Abl fusion proteins leads to the accumulation of antiapoptotic IAP proteins and involves IKKα

Malinge, Sébastien; Monni, Richard; Bernard, Olivier A.; Penard-Lacronique, Virginie

doi:10.1038/sj.onc.1209390

Cited by 28 publications

(22 citation statements)

References 66 publications

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“…In vitro studies demonstrated that both aberrations lead to constitutive activation of the nonreceptor tyrosine kinase ABL1 with similar downstream effects associated to cellular growth, survival, growth factor independence and transforming capacity (Okuda et al, 1996;Malinge et al, 2006;Pecquet et al, 2007). However, differences between the two fusions have been described, for example, in the substrate preferences (Voss et al, 2000).…”

Section: Introductionmentioning

confidence: 95%

Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: Poor prognosis and prenatal origin

Zuna

Žaliová

Mužíková

et al. 2010

Genes Chromosomes & Cancer

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The ETV6/ABL1 (TEL/ABL) fusion gene is a rare aberration in malignant disorders. Only 19 cases of ETV6/ABL1-positive hematological malignancy have been published, diagnosed with chronic myeloid leukemia, other types of chronic myeloproliferative neoplasm, acute myeloid leukemia or acute lymphoblastic leukemia (ALL). This study reports three new cases (aged 8 months, 5 years, and 33 years) of ALL with the ETV6/ABL1 fusion found by screening 392 newly diagnosed ALL patients (335 children and 57 adults). A thorough review of the literature and an analysis of all published data, including the three new cases, suggest poor prognosis of ETV6/ABL1-positive acute leukemias. The course of the disease in the two pediatric patients is characterized by minimal residual disease monitoring, using quantification of both the ETV6/ABL1 transcript and immunoreceptor gene rearrangements. Eosinophilia could not be confirmed as a hallmark of the ETV6/ABL1-positive disease. Studies of neonatal blood spots demonstrated that, in the child diagnosed at five years, the ETV6/ABL1 fusion initiating the ALL originated prenatally.

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Section: Introductionmentioning

confidence: 95%

Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: Poor prognosis and prenatal origin

Zuna

Žaliová

Mužíková

et al. 2010

Genes Chromosomes & Cancer

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“…Transgenic mouse models have also illustrated the leukaemogenic properties of Tel-Jak2 in the B-and T-cell lineages (Carron et al, 2000;Dos Santos and Ghysdael, 2005). Expression of Tel-Abl and Tel-Jak2 in haematopoietic cells results in the constitutive activation of effectors and/or pathways associated to cellular growth and survival, in particular the two adapters Gab2 and Shc, the transcription factors Stat3 and Stat5 and effectors of the NF-kB, PI3-K/Akt and Ras/Erk1/2 pathways (Voss et al, 2000;Santos et al, 2001;Ho et al, 2002;Spiekermann et al, 2002;Malinge et al, 2006). Tel-Jak2 also activates effectors of the SAPK/JNK and p38 pathways (Ho et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation

et al. 2006

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“…Il a ainsi été montré que les protéines de fusion leucémogènes, TEL-Jak2 et TEL-Abl, stimulent l'activité de IKKα, activent de manière persistante NF-κB et induisent ainsi la production de molécules anti-apoptotiques importantes pour leurs propriétés leucémogènes. Toutefois, il semblerait que ce mécanisme n'induise pas la protéolyse de p100 [25]. …”

Section: Traf3unclassified

Voie alternative d’activation de NF-κB et cancer

Baud

Jacque

2008

Med Sci (Paris)

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Une vingtaine d'années après leur découverte, l'intérêt que suscitent les facteurs de transcription NF-κB (nuclear factor kB) émane de la multiplicité des réponses cellulaires auxquelles ces facteurs sont associés. Ils jouent en effet un rôle central dans la réponse inflammatoire, l'immunité innée et acquise, la balance survie/mort cellulaire, mais aussi la tumorigenèse [1][2][3][4][5]. Ainsi, une dérégulation de l'activité des facteurs NF-κB, via la production de formes anormales de NF-κB, ou un défaut de leurs activités transcriptionnelles, est retrouvée de manière récurrente dans des lymphomes et des leucémies, mais aussi dans des tumeurs solides [5, 37]. Plus récemment, il a été mis en évidence que les facteurs NF-κB participent également au dévelop-pement des tumeurs en activant des gènes de résistance à l'apoptose, rendant certaines tumeurs résistantes aux traitements chimiothéra-peutiques et radiothérapeutiques [6].

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Activation of the NF-κB pathway by the leukemogenic TEL-Jak2 and TEL-Abl fusion proteins leads to the accumulation of antiapoptotic IAP proteins and involves IKKα

Cited by 28 publications

References 66 publications

Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: Poor prognosis and prenatal origin

Acute leukemias with ETV6/ABL1 (TEL/ABL) fusion: Poor prognosis and prenatal origin

The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation

Voie alternative d’activation de NF-κB et cancer

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