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Center point: IgH.TE'SLL mouse model can relifully reproduce the pathological characteristics of human CLL, Notch signal promotes the occurrence of CLL disease, promotes cell proliferation and CLL disease progression.
mutations in the NOTCH1 gene are common in chronic B lymphocytic leukemia (B-ALL) and are associated with accelerated progression and resistance to chemotherapy.
, however, so far, the specific role of this malignant tumor in NOTCH1 has not been fully defined.
study aims to assess the effects of Notch signal loss and overactivation of its pathology on CLL mouse models (IgH.TEm) that can faithfully reproduce human CLL pathological characteristics.
the use of RBP-J conditional infusion genes to abrogate classical Notch signaling in immature hematuration or B-cell ancestral cells can delay the induction of CLL and reduce the incidence of CLL mice.
, overactivation of the Notch signal increases the number of mice developing CLL and the onset of the disease earlier.
Comparing gene expression and metastattic characteristics of CLL cells carrying Notch functional acquisition mutations, it was found that Notch signal directly and indirectly regulates gene expression related to cell cycles, resulting in increased proliferation capacity of CLL cells carrying Notch functional acquisition mutations in the body.
in general, the results show that the Notch signal can promote the occurrence of CLL, and promote the proliferation of CLL cells and disease progression.
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