scholarly journals In vivo dielectric measuring instrument using picosecond pulse for detection of oral cancer

2014 ◽  
Vol 2 (1) ◽  
pp. 1 ◽  
Author(s):  
A.A Ranade ◽  
M.M Joshi ◽  
R.S Deore ◽  
S.C Mehrotra
2014 ◽  
Vol 2 (1) ◽  
pp. 2 ◽  
Author(s):  
Olufoladare G Olorunsola ◽  
Steven H Kim ◽  
Ryan Chang ◽  
Yuo-Chen Kuo ◽  
Steven W Hetts ◽  
...  

2021 ◽  
Vol 133 ◽  
pp. 111057
Author(s):  
Chin-Shan Kuo ◽  
Cheng-Yu Yang ◽  
Chih-Kung Lin ◽  
Gu-Jiun Lin ◽  
Huey-Kang Sytwu ◽  
...  

2021 ◽  
Vol 22 (14) ◽  
pp. 7509
Author(s):  
Hai Huang ◽  
Jun-Koo Yi ◽  
Su-Geun Lim ◽  
Sijun Park ◽  
Haibo Zhang ◽  
...  

Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor.


Head & Neck ◽  
2018 ◽  
Vol 41 (5) ◽  
pp. 1260-1269 ◽  
Author(s):  
Cheng‐Yu Yang ◽  
Chih‐Kung Lin ◽  
Cheng‐Chih Hsieh ◽  
Chang‐Huei Tsao ◽  
Chun‐Shu Lin ◽  
...  

2011 ◽  
Vol 28 (10) ◽  
pp. 2599-2609 ◽  
Author(s):  
Kashappa-Goud H. Desai ◽  
Susan R. Mallery ◽  
Andrew S. Holpuch ◽  
Steven P. Schwendeman

2021 ◽  
Author(s):  
Patricia Maria Wiziack Zago ◽  
Luiza Rodrigues Hellmeister ◽  
Lucas Novaes Teixeira ◽  
Rui Barbosa de Brito Junior ◽  
Elizabeth Ferreira Martinez

Abstract ObjectivesThis study aimed to evaluate the in vitro antitumoral potential of different concentrations of EA against two OSCC cell lines with distinct tissue invasiveness profiles. Material and methodsNormal keratinocytes (NOK) and OSCC´s cells CAL-27 and SCC-9 were treated with concentrations of EA varying from 5 to 662 µM during 24, 48 or 72h. After each time of treatment, cells were submitted to viability analysis using MTT and the secretion of metalloproteinases (MMP-2 and MMP-9) and tissue metalloproteinases inhibitors (TIMP-1 and TIMP-2) were performed by Enzyme-Linked Immunoassay (ELISA). Data were submitted to ANOVA, followed by Bonferroni´s test, considering 5% as significance level. ResultsEA was cytotoxic to OSCC cells in all exposure times, rarely affecting normal cell viability, except for concentrations higher than 82 µM and after 72h treatment. For OSCC cells, EA decreased MMPs and increased TIMPs´s expression without effect on those enzymes for normal cell lines during all times of exposure. ConclusionEA is a promising therapeutic adjuvant to treat oral cancer, however, further in vivo studies are required to clinically validate its potential. Clinical RelevanceThe in vitro anticancer properties showed by Ellagic acid, a phenolic compound that could easily be accessed by oral cancer patients, provides data to base future clinical studies intended to develop a safe topical oral anticancer product.


2020 ◽  
Vol 99 (6) ◽  
pp. 604-612 ◽  
Author(s):  
Z.R. Fitzsimonds ◽  
C.J. Rodriguez-Hernandez ◽  
J. Bagaitkar ◽  
R.J. Lamont

Oral cancer, predominantly oral squamous cell carcinoma (OSCC), is the eighth-most common cancer worldwide, with a 5-y survival rate <50%. There are numerous risk factors for oral cancer, among which periodontal disease is gaining increasing recognition. The creation of a sustained dysbiotic proinflammatory environment by periodontal bacteria may serve to functionally link periodontal disease and oral cancer. Moreover, traditional periodontal pathogens, such as Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, are among the species most frequently identified as being enriched in OSCC, and they possess a number of oncogenic properties. These organisms share the ability to attach and invade oral epithelial cells, and from there each undergoes its own unique molecular dialogue with the host epithelium, which ultimately converges on acquired phenotypes associated with cancer, including inhibition of apoptosis, increased proliferation, and activation of epithelial-to-mesenchymal transition leading to increased migration of epithelial cells. Additionally, emerging properties of structured bacterial communities may increase oncogenic potential, and consortia of P. gingivalis and F. nucleatum are synergistically pathogenic within in vivo oral cancer models. Interestingly, however, some species of oral streptococci can antagonize the phenotypes induced by P. gingivalis, indicating functionally specialized roles for bacteria in oncogenic communities. Transcriptomic data support the concept that functional, rather than compositional, properties of oral bacterial communities have more relevance to cancer development. Collectively, the evidence is consistent with a modified polymicrobial synergy and dysbiosis model for bacterial involvement in OSCC, with driver mutations generating a conducive microenvironment on the epithelial boundary, which becomes further dysbiotic by the synergistic action of bacterial communities.


In Vivo ◽  
2020 ◽  
Vol 34 (5) ◽  
pp. 2461-2467
Author(s):  
HUNG-SHENG SHANG ◽  
KUO-WEI CHEN ◽  
JIANN-SHANG CHOU ◽  
SHU-FEN PENG ◽  
YUNG-LIANG CHEN ◽  
...  
Keyword(s):  

2013 ◽  
Vol 7 (3) ◽  
pp. 709-715 ◽  
Author(s):  
KAI ZHU ◽  
GUIJIE LI ◽  
PENG SUN ◽  
RUI WANG ◽  
YU QIAN ◽  
...  
Keyword(s):  

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