scholarly journals Predictive value of ALDH1 and CD44 positivity for radiotherapy response and prognosis in early-stage glottic laryngeal squamous cell carcinoma

Author(s):  
Ozgur Surmelioglu ◽  
Kivilcim Eren Erdogan ◽  
Muhammed Dagkiran ◽  
Suleyman Ozdemir ◽  
Ozgur Tarkan ◽  
...  
Endoscopy ◽  
2008 ◽  
Vol 40 (S 02) ◽  
pp. E204-E205 ◽  
Author(s):  
T. Yoshida ◽  
Y. Shimizu ◽  
J. Hirota ◽  
M. Nakagawa ◽  
S. Ono ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (29) ◽  
pp. 48240-48247 ◽  
Author(s):  
Wan-Zhi Chen ◽  
Shi-Tong Yu ◽  
Rong Xie ◽  
Yun-Xia Lv ◽  
De-Bin Xu ◽  
...  

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Dong Xiao ◽  
Xiangyan Cui ◽  
Xin Wang

Abstract It is known that lncRNA PTCSC3 inhibits thyroid cancer and glioma and STAT3 promotes cancer development. We, in the present study, investigated the potential involvement of PTCSC3 in laryngeal squamous cell carcinoma (LSCC) and explored its interactions with STAT3. In the present study, we showed that plasma PTCSC3 was down-regulated in early stage LSCC patients, and the down-regulation of PTCSC3 separated in early stage LSCC patients from control group. LncRNA HOTAIR was up-regulated in early stage LSCC patients and was significantly and inversely correlated with PTCSC3 in LSCC patients. PTCSC3 overexpression led to the inhibition of HOTAIR, while PTCSC3 expression was not significantly affected by HOTAIR overexpression. PTCSC3 overexpression mediated the inhibited, while HOTAIR overexpression mediated the promoted proliferation of LSCC cells. However, cell invasion and migration were not significantly affected by PTCSC3 overexpression. In addition, HOTAIR overexpression reduced the inhibitory effects of PTCSC3 overexpression on cancer cell proliferation. Moreover, PTCSC3 overexpression mediated the down-regulation of STAT3 and STAT3 overexpression mediated the up-regulation of HOTAIR. Therefore, PTCSC3 may negatively interact with HOTAIR through STAT3 to inhibit LSCC cell proliferation.


BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Anke Schlüter ◽  
Patrick Weller ◽  
Oliver Kanaan ◽  
Ivonne Nel ◽  
Lukas Heusgen ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Tao Fan ◽  
Zhiliang Lu ◽  
Yu Liu ◽  
Liyu Wang ◽  
He Tian ◽  
...  

With the increasingly early stage lung squamous cell carcinoma (LUSC) being discovered, there is an urgent need for a comprehensive analysis of the prognostic characteristics of early stage LUSC. Here, we developed an immune-related gene signature for outcome prediction of early stage LUSC based on three independent cohorts. Differentially expressed genes (DEGs) were identified using CIBERSORT and ESTMATE algorithm. Then, a 17-immune-related gene (RPRM, APOH, SSX1, MSGN1, HPR, ISM2, FGA, LBP, HAS1, CSF2, RETN, CCL2, CCL21, MMP19, PTGIS, F13A1, C1QTNF1) signature was identified using univariate Cox regression, LASSO regression and stepwise multivariable Cox analysis based on the verified DEGs from 401 cases in The Cancer Genome Atlas (TCGA) database. Subsequently, a cohort of GSE74777 containing 107 cases downloaded from Gene Expression Omnibus (GEO) database and an independent data set consisting of 36 frozen tissues collected from National Cancer Center were used to validate the predictive value of the signature. Seventeen immune-related genes were identified from TCGA cohort, which were further used to establish a classification system to construct cases into high- and low-risk groups in terms of overall survival. This classifier was still an independent prognostic factor in multivariate analysis. In addition, another two independent cohorts and different clinical subgroups validated the significant predictive value of the signature. Further mechanism research found early stage LUSC patients with high risk had special immune cell infiltration characteristics and gene mutation profiles. In conclusion, we characterized the tumor microenvironment and established a highly predictive model for evaluating the prognosis of early stage LUSC, which may provide a lead for effective immunotherapeutic options tailored for each subtype.


Sign in / Sign up

Export Citation Format

Share Document