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Oropharynx
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Two diagnostic strategies are commonly used to detect HPV DNA within tumour cells—in situ hybridization (ISH) and polymerase chain reaction (PCR). Contamination or previous infection could render tests positive without confirming downstream biological activity of HPV; therefore, quantitative reverse transcription PCR (qRT-PCR) and RNA-based chromogenic ISH (RNA-ISH) can be used. More often, however, immunohistochemistry of p16 overexpression is used as a surrogate marker, although up to 30% of p16-positive tumours are HPV negative. Immunohistochemistry is inexpensive and widely available and is well established in treatment protocols. The overexpression of p16 correlates well with clinical outcome.
Postoperative Irradiation with or without Concomitant Chemotherapy for Locally Advanced Head and Neck Cancer
Published in Niall MH McLeod, Peter A Brennan, 50 Landmark Papers every Oral & Maxillofacial Surgeon Should Know, 2020
Stergios Doumas, Anastasios Kanatas
A major limitation in both studies (EORTC, RTOG) is that they were not stratified per tumour site and HPV status as they were conducted in the pre-HPV OPC era. It is now plausible that this particular group has different biological behaviours. Hence, the TNM 8th edition sub-classifies OPC into p16+ and p16− subgroups. p16 is the best surrogate marker of HPV infection in these tumours.3 Efforts are also being made to de-escalate treatment in HPV+ OPC.4
Oropharynx
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
Historically, oropharyngeal squamous cell carcinoma (OPSCC) was caused by exposure to cigarette smoke and/or alcohol. In a study by Hashibe et al. [18], the sum of the population attributed risk was 72%; tobacco causes 33% and alcohol 4%, however, synergistically the effect is 35%. More recently, a virally driven subset of cancers (human papillomavirus subtype 16 [HPV 16]) has emerged as the leading cause of squamous cell carcinoma (SCC) within the oropharynx. Though other subtypes (such as 18) have been identified in thee cancers, by far the most common in subtype 16. Today, up to 70% of oropharyngeal malignancies are thought to be driven by HPV 16 [19,20] This change in aetiology has been associated with a twofold increase in OPSCC in both the US and UK between 1990 and 2006 [21]. p16 is a tumour suppressor protein that can be detected using immunohistochemistry. It is used as a surrogate marker by pathologists to identify HPV positive (+) cases.
Protective effect of Pulsatilla saponin A on acute myocardial infarction via miR-24-3p/p16
Published in Toxicology Mechanisms and Methods, 2022
Feng Dong, Yanhua Pu, Yanfei Lv, Xiujuan Liu, Yimin Cao
In addition, p16 is a CDK inhibitor and acted as a tumor suppressor which suppresses the formation of the cyclin D1-CDK complex (Pezzuto et al. 2020). Cyclin D1 is a cell cycle regulatory protein, which can be associated with cyclin-dependent kinases (CDKs) and promote phosphorylation of retinoblastoma protein, to enhance cell proliferation (Li, Cui et al. 2016). Hence, the up-regulation of p16 and suppression of cyclin D1 after hypoxic treatment showed that hypoxia inhibited the proliferation of H9c2 cells. Zhang et al. showed that paracrine factors released from induced pluripotent stem cells (iPSCs), with or without oxidative stress, prevented stress-triggered senescence of H9C2 cells by inactivating both the p53-p21 and p16-pRb pathways (Zhang et al. 2014). Lycium barbarum polysaccharides strengthened cell viability, diminished p53, p21, and p16 protein expressions, promoted migration, and suppressed apoptosis in hypoxia-impaired H9c2 cells (Li et al. 2019). Our data suggested that knockdown of p16 could partly redeem the anti-apoptosis effect of PsA on hypoxia-exposed H9c2 cells applied with miR-24-3p inhibitor. We also verified that the silence of p16 boosted the viability and proliferation of H9c2 cells treated with hypoxia. Taken together, the influences of PsA on cell viability, proliferation and apoptosis in hypoxia-triggered toxicity to H9c2 cells were achieved by regulating the miR-24-3p/p16 axis.
Molecular markers for cervical cancer screening
Published in Expert Review of Proteomics, 2021
Coşkun Güzel, Jenny van Sten-van’t Hoff, Inge M.C.M. de Kok, Natalia I. Govorukhina, Alexander Boychenko, Theo M. Luider, Rainer Bischoff
As one of the major challenges in cervical cancer screening programs is to discriminate productive infections with hrHPV (those that produce viral particles but carry a low risk of transformation) from transforming infections (those that carry a high risk of transformation leading to cervical cancer), it is amenable that proteins that are implicated in regulating cell division and DNA replication may be candidates to make this discrimination. p16ink4a (referred to as p16 in this article) is a tumor suppressor and cell cycle regulatory protein that inhibits CDK 4 and 6, thereby suppressing cellular proliferation. Integration of viral genes coding for the oncoproteins E6 and E7 into the host genome leads to enhanced expression and cellular accumulation of p16 in epithelial cells of CIN2+ lesions undergoing transformation [102]. Ki-67 is a marker of proliferating cells routinely used in diagnostic settings. It is present during all phases of the cell cycle and is often increased in cervical lesions [103]. IHC staining for p16 and Ki-67 is used to discriminate lesions with a high short-term risk of transformation from those with a low risk [101].
Expression of α-Klotho Is Downregulated and Associated with Oxidative Stress in the Lens in Streptozotocin-induced Diabetic Rats
Published in Current Eye Research, 2021
Zhongxu Ma, Jing Li, Hao Jiang, Yanhua Chu
An early study reported that α-Klotho expression was regulated by proteins of P16 and P53, two key tumor suppressors.31 P16 blocks the progression of the cell cycle by binding to either cyclin-dependent kinase (CDK) 4 or CDK6.32 Expression of P16 dramatically increases with aging in most rodent and human tissues.33,34 Key functions of p53 are induction of cell cycle arrest, senescence, and apoptosis in response to DNA damage.31 Overexpression of P16 and P53 can reduce α-Klotho expression in HEK293 cells.31 P16 expression is increased in non-ocular tissue of STZ-induced diabetic rats.35 In addition, P16 is expressed in human lens epithelial cells.36 We speculate that reduced α-Klotho in the lens and circulation in STZ-induced diabetic rats may be due to increased expression of P16 in the lens and other tissues that generate soluble form of α-Klotho. γ-Klotho is a putative type I membrane protein that consists of N-terminal signal sequence, glycosidase domain, transmembrane region and short cytoplasmic tail. Despite its overall structural similarity to α-Klotho, the glutamic acid for the acid–base catalyst was not conserved in this protein.37 We could not exclude the possibility that the different molecular structure might increase resistance to DM-induced change in γ-Klotho expression.