HPV E6 binds with EDD1 to ubiquitinate TIP60, leading to the degradation of TIP60, eventually resulting in
tumor tumorigenesis.
Not exact matches
The absence of
tumors in virgin Nrk mutant mice strongly suggests that the
tumorigenesis is closely related to the proliferation of mammary epithelial cells during pregnancy.
It has been known for a number of years that PREX2 is a GTP / GDP exchange factor that inhibits a
tumor suppressor protein called PTEN, and that this process can promote
tumorigenesis by activating the PI3K signaling pathway (Fine et al., 2009; Hodakoski et al., 2014; Figure 1A).
All this work supports the conclusion that the over-expression of PREX2 can increase PI3K - dependent
tumor growth (Fine et al., 2009), and that mutated PREX2 promotes
tumorigenesis by increasing RAC - dependent invasiveness (Mense et al., 2015).
The pancreas seems to require two oncogenic events to initiate and promote
tumorigenesis with
tumor suppressors acting later to increase progression to malignant disease.
We have found that the initiation of pancreatic cancer does not follow the classic paradigm seen in colon cancer where loss of a
tumor suppressor gene initiates
tumorigenesis and then acquisition of an oncogene promotes
tumor formation.
Activated Abl kinase inhibits oncogenic transforming growth factor - β signaling and
tumorigenesis in mammary
tumors.
These findings reinforce many things that we already know: that mutations acquire gradually with age, that most of the mutations in AML (and likely other
tumors) are random background events not contributing to
tumorigenesis, and that subsequent mutation and evolution can give rise to subclones that ultimately determine cancer progression and response to therapy.
TGFβ inhibits
tumor initiation and progression by inducing cell cycle arrest and apoptosis; however epithelial
tumorigenesis may escape this common antitumor mechanism by inducing aberrations in TGFβ signaling resulting in enhanced development and progression of human carcinomas.
The central focus of my future work is to elucidate the mechanisms by which
tumorigenesis results in the conversion of TGFβ from a suppressor of
tumor formation to a promoter of
tumor growth, invasion, and metastasis.
These observations support the notion that BECN1 is a haploid - insufficient
tumor suppressor gene and distinguish it from other classic
tumor suppressors that require both alleles be inactivated in promoting
tumorigenesis.
Interestingly, BRCA1 is not a haploid - insufficient
tumor suppressor gene; therefore monoallelic deletion may not affect its function or affect
tumorigenesis of those breast cancers bearing deletions.
Interestingly, neither dose of lycopene was able to significantly reduce
tumorigenesis (Tables 1 and 3), whereas 10 % whole tomato powder significantly reduced
tumor weights (P < 0.05).