In conclusion, hMLH1 and O6-MGMT promoter methylation are frequently present in AH, and thus considered to be early events in the carcinogenesis of EC, whereas P16 promoter methylation was mainly present in EC, and not in precursor lesions supporting a late event in the carcinogenesis.
In the FFPE samples, the immunohistochemistry of p16, which is considered appropriate to assess HPV-driven carcinogenesis in OPSCC according to the 8th American Joint Committee on Cancer TNM classification, may not be specific enough to become the diagnostic standard in the perspective of treatment deintensification. p16 may play a safer role in combination with another highly sensible assay.
Our study investigates the prevalence, prognostic, and clinicopathologic features of HPV-related oropharyngeal cancer in Northeast China and elucidates the involvement of p16 in the tumorigenesis and progression of OPSCC.
An impaired cell-cycle control and genetic material organization are crucial elements of carcinogenesis. p16 is a tumor suppressor protein which decelerates promotion of the cells from G<sub>1</sub> to S phase, whereas special AT-rich sequence-binding protein 1 (SATB1) is a nuclear matrix protein that binds to specific regions of the DNA and ensures its proper organization and function.
The activation of CDKN2A pathway in p53<sup>S/S</sup> MEF and tumors, and the accumulation of p19<sup>ARF</sup> protein in tumor tissues suggested p19<sup>ARF</sup> might contribute to the accumulation of mutant p53S protein in the tumor and promote tumorigenesis.
Although some LM-BN share several significant genetic alterations with leiomyosarcoma, including p16 and p53, the underlying tumorigenesis of LM-BN remains largely unknown.
This study showed that p16 and MDM2 polymorphisms do not play a decisive role in tumorigenesis, but some genotypes of these polymorphisms might be associated with follow-up characteristics of prolactinoma.
The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer.
Finally, the absence of differences in p53 and p16 expressions is at variance with other epithelia where the classical pathway is associated with human papillomavirus infection and can be explained by the fact that both AK pathways share identical mechanisms of actinic oncogenesis.
The current paradigm is that p16 and RB1 function in a linear pathway to suppress tumorigenesis; however p16 is preferentially lost in human cancers suggesting that p16 has critical tumor suppressive functions not mediated through RB1.
Ninety percent of examined murine B-ALL tumors showed loss of the wild-type <i>Ink4a/Arf</i> locus without acquisition of highly recurrent cooperating events, underscoring the role of <i>Ink4a/Arf</i> in restraining Kras-driven oncogenesis in the lymphoid compartment.
Therefore, in this study, we explored the possible association between the two important G1 cell cycle regulatory genes p16 and p53 and environmental risk factors and risk of esophageal carcinogenesis.
Our data confirm previous observations and suggest that losses of the MLH1 and CDKN2 genes and alterations of the TIMP3 gene play an important role in head and neck carcinogenesis.