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Though some of the mice develop pituitary adenomas, spontaneous aggressive malignancies are rare.
MyrAKT p27 mice develop pituitary tumors early in life and died without the possibility of studying the role of p27 absence in the mammary gland (Data not shown).
Later in life, the hCGβ+ mice develop pituitary prolactinomas and mammary gland tumors (23, 26, 27).
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Interestingly, Rb1 D326V/+ mice developed pituitary tumors that originated from the intermediate lobe of the pituitary, despite selective inactivation of E2F1.
These results are consistent with the observations that Rb1 +/− mice developed pituitary tumors that originated from those cell types (Fig. 5c).
Importantly, the tumor spectrum found in the Rb1 D326V/+ mutants resembled those of E2F1 −/− :Rb1 +/− double-knockout mice reported previously, which only develop pituitary tumors but not thyroid tumors.
Among the 17 genes located within the common region (approximately 2.0 Mb), we focused on Rb1, because several Rb1-deficient mice have been reported to develop pituitary and thyroid tumors.
These mice also developed pituitary tumors in 81.1% of M1032 and 57.4% of M1033 heterozygotes (Fig. S1B).
We have recently shown that mice expressing a degradation-resistant mutant β-catenin in Rathke's pouch develop pituitary tumors that closely resemble human ACP [ Gaston-Massuet et al., 2011].
At first glance, this result is a little surprising taking into consideration that transgenic mice bearing human HMGA2 under the transcriptional control of cytomegalovirus (CMV) promoter have been reported to mainly develop pituitary adenomas.
Many people who have had a pituitary apoplexy develop pituitary hormone deficiencies and require long-term hormone supplementation.
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