Sentence examples for mouse lymphoma model from inspiring English sources

Interestingly, certain stromal components may have beneficial effects as a bright side such as tumor suppression, immune clearance, tissue repair (Ozdemir et al., 2014; Rhim et al., 2014), and particularly, chemosensitizing, for example, suppression of the secretion phenotype through NF-κB inhibition promoted resistance to chemotherapy in a mouse lymphoma model (Chien et al., 2011).

Interestingly, such a combination has recently shown efficacy in a mouse lymphoma model [ 66].

Thus, we tested the therapeutic efficacy in an EG7 mouse lymphoma model (EL4 cells expressing OVA as a surrogate tumour antigen).

For example, induction of Myc in a transgenic mouse lymphoma model stimulated surrounding macrophages to secrete TGFβ, which resulted in induction of cellular senescence [ 54].

It has demonstrated single-agent activity against certain human cancers transplanted into immunocompromised mice and induces remission in the Eμ-myc mouse lymphoma model when combined with doxorubicin.

Similar results have been reported in which disruption of the NF-κB-mediated SASP leads to chemo-resistance in a mouse lymphoma model (Chien et al, 2011; Jing et al, 2011).

It is presently unclear whether it has a major role during the evolution of disease, as shown in other tumoral models like mouse lymphoma models or in some mucosa-associated lymphoid tissue lymphomas, where continuous antigen stimulation has a key role and antigen withdrawal leads to regression of disease.

This was shown using a mouse thymic lymphoma model triggered by an oncogenic nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion kinase within the T-cell compartment (Chiarle et al, 2008).

Overexpression of the mir-17 mir-18a mir-19b-1 cluster was shown to accelerate mir-17 mir-18a mir-19b-1pment in a mouse B-clustermphoma model [ 61].

We have previously identified SatB1 as a factor that is required for the initiation of gene repression in a mouse T-cell lymphoma model (Agrelo et al., 2009).

In the Eμ-myc mouse B-cell lymphoma model, while the intact mir-17-92 mir-17-92 mir-17-92, its miR-92 component negactsely regulases the oncogenic cooperanioncogenec-Myc.