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Additionally, a T2/OncZ transposon insertion in Snapc3 was observed in tumor 8T, a gene previously identified with a T2/Onc insertion in mouse tumor samples [11].

Furthermore, LKB1Ser431 (Ser428 in human) tends to be phosphorylated in mouse tumor samples harboring deregulated tyrosine kinase activities or increased mitogenic signaling, suggesting the direct participation of LKB1 in tumor biology.

We demonstrate that LKB1Ser428 residue is constitutively phosphorylated in cells harboring BRAFV600E activating mutations, and is found frequently phosphorylated in mouse tumor samples with an increased receptor tyrosine kinase activity suggesting a functional connection between BRAF oncogenic pathway and LKB1.

Paraffin-embedded mouse tumor samples were obtained as described before [ 8].

Mouse tumor samples were assayed with the Mouse ACTB-VIC/MGB probe (ABI) as an endogenous control and GPR110 probe Mm00505409_m1 (ABI).

To investigate whether gene expression was influenced by the strain of mouse, tumor samples isolated from C.B-17 SCID and Nu/Nu mice were also compared.

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Similar(52)

Sequencing for murine HD and PEST mutations in primary mouse tumors samples was performed as described [51].

To this end, we have built a database consisting of 1,172 mouse mammary tumor samples from 26 different major oncogenic mouse mammary tumor models.

Each mouse tumor DNA sample was isolated from fresh tumor tissues and hybridized against a reference DNA (spleen) obtained from the same animal to avoid picking up DNA copy number variations between mice.

MM cells were injected into the peritoneal cavity of NOD/SCID mice and tumor samples were collected for immunohistochemical analysis.

MPM cells were injected into pleura cavity of nude mice and tumor samples were collected for immunohistochemical analysis.

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