scholarly journals Pineal gland protects against chemically induced oral carcinogenesis and inhibits tumor progression in rats

Oncotarget ◽  
2020 ◽  
Vol 11 (20) ◽  
pp. 1816-1831 ◽  
Author(s):  
Giseli Mitsuy Kayahara ◽  
Vitor Bonetti Valente ◽  
Rosani Belzunces Pereira ◽  
Felipe Yudi Kabeya Lopes ◽  
Marcelo Macedo Crivelini ◽  
...  
2007 ◽  
Vol 22 (2) ◽  
pp. 132-143 ◽  
Author(s):  
N.G. Shah ◽  
T.I. Trivedi ◽  
R.A. Tankshali ◽  
J.A. Goswami ◽  
J.S. Shah ◽  
...  

In this study an attempt was made to establish the significance of a battery of molecular alterations and thereby identify risk predictors in oral carcinogenesis. For this purpose, EGFR, Stat3, H-ras, c-myc, p53, cyclin D1, p16, Rb, Ki-67 and Bcl-2 were localized immunohistochemically in normal mucosa (n=12), hyperplasia (n=35), dysplasia (n=25), early stage carcinoma (n=65) and advanced stage carcinoma (n=70). Deregulation occurred at an early stage and the number of alterations increased with disease progression. Using multivariate logistic regression analysis, the significant risk predictor for hyperplasia from normal mucosa was Ki-67 (OR=5.75, p=0.021); the significant risk predictors for dysplasia from hyperplasia were EGFR (OR=12.96, p=0.002), Stat3 (OR=17.16, p=0.0001), p16 (OR=5.50, p=0.039) and c-myc (OR=5.99, p=0.052); the significant risk predictors for early stage carcinoma from dysplasia were p53 (OR=6.63, p=0.0001) and Rb (OR=3.81, p=0.056); and the significant risk predictors for further progression were EGFR (OR=5.50, p=0.0001), Stat3 (OR=4.49, p=0.0001), H-ras (OR=4.05, p=0.001) and c-myc (OR=2.99, p=0.015). Cyclin D1 holds a key position linking upstream signaling pathways to cell cycle regulation. Gene products of the mitogenic signaling pathway play an equally significant role as cell cycle regulatory proteins in the hyperplasia-dysplasia-early-advanced-carcinoma sequence and together may provide a reference panel of markers for use in defining premalignant lesions and predicting the risk of malignant transformation and tumor progression.


2007 ◽  
Vol 22 (2) ◽  
pp. 132-143 ◽  
Author(s):  
N.G. Shah ◽  
T.I. Trivedi ◽  
R.A. Tankshali ◽  
J.A. Goswami ◽  
J.S. Shah ◽  
...  

2011 ◽  
Vol 52 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Yian Wang ◽  
Ruisheng Yao ◽  
Song Gao ◽  
Weidong Wen ◽  
Yinqiu Du ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245190
Author(s):  
Flávia Alves Verza ◽  
Vitor Bonetti Valente ◽  
Lia Kobayashi Oliveira ◽  
Giseli Mitsuy Kayahara ◽  
Marcelo Macedo Crivelini ◽  
...  

Social isolation has affected a large number of people and may lead to impairment of physical and mental health. Although stress resulting from social isolation may increase cancer progression, its interference on tumorigenesis is poorly known. In this study, we used a preclinical model to evaluate the effects of social isolation stress on chemically induced oral carcinogenesis. Sixty-two 21-day-old male Wistar rats were divided into isolated and grouped groups. After 90 days of age, the rats from both groups underwent oral carcinogenesis with 4-nitroquinoline 1-oxide (4NQO) for 20 weeks. All rats were assessed for depressive-like behavior and euthanized for oral squamous cell carcinoma (OSCC) diagnosis and measurement of inflammatory mediators in the tumor microenvironment. Social isolation stress increased the OSCC occurrence by 20.4% when compared to control. Isolated rats also showed higher tumor volume and cachexia than the grouped rats. Social isolation did not induce changes in the depressive-like behavior after carcinogenic induction. Tumors from stressed rats had increased levels of the inflammatory mediators, TNF-alpha, IL1-beta and MCP-1. The concentrations of TNF-alpha and MCP-1 were significantly increased in the large tumors from isolated animals. Higher tumor levels of TNF-alpha, IL-6, IL1-beta and MCP-1 were positively correlated with OSCC growth. This study provides the first evidence that social isolation stress may facilitate OSCC occurrence and tumor progression, an event accompanied by increased local levels of inflammatory mediators.


1993 ◽  
Vol 14 (1) ◽  
pp. 163-166 ◽  
Author(s):  
Dong M. Shin ◽  
Paul J. Chiao ◽  
Peter G. Sacks ◽  
Hyung Ju Shin ◽  
Waun K. Hong ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document