scholarly journals Increased resistin suggests poor prognosis and promotes development of lung adenocarcinoma

2018 ◽  
Author(s):  
Cui‑Cui Zhao ◽  
Jing Chen ◽  
Rui‑Fang Niu ◽  
Yan Liu ◽  
Chuan‑Gui Zhang
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis

scholarly journals Stromal FAP is an independent poor prognosis marker in non-small cell lung adenocarcinoma and associated with p53 mutation

Lung Cancer ◽  
2021 ◽  
Author(s):  
Pablo Moreno-Ruiz ◽  
Sara Corvigno ◽  
Nienke C. te Grootenhuis ◽  
Linnéa La Fleur ◽  
Max Backman ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
P53 Mutation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Prognosis Marker

scholarly journals Expression of nucleolar protein p120 predicts poor prognosis in patients with stage I lung adenocarcinoma

2001 ◽  
Vol 12 (8) ◽  
pp. 1121-1125 ◽  
Author(s):  
Y. Saijo ◽  
G. Sato ◽  
K. Usui ◽  
M. Sato ◽  
M. Sagawa ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Nucleolar Protein ◽  
Stage I

scholarly journals Decrease of FSTL1-BMP4-Smad signaling predicts poor prognosis in lung adenocarcinoma but not in squamous cell carcinoma

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jean Chiou ◽  
Chia-Yi Su ◽  
Yi-Hua Jan ◽  
Chih-Jen Yang ◽  
Ming-Shyan Huang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lung Adenocarcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Poor Prognosis ◽  
Smad Signaling

Paip1 predicts poor prognosis and promotes tumor progression through AKT/GSK-3β pathway in lung adenocarcinoma

2019 ◽  
Vol 86 ◽  
pp. 233-242 ◽  
Author(s):  
Yixuan Wang ◽  
Junjie Piao ◽  
Qianrong Wang ◽  
Xuelian Cui ◽  
Ziqi Meng ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Tumor Progression ◽  
Poor Prognosis ◽  
Gsk 3Β

Co-expression of β-arrestin1 and NF-кB is associated with cancer progression and poor prognosis in lung adenocarcinoma

Tumor Biology ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 6551-6558 ◽  
Author(s):  
Jianyu Yu ◽  
Liguang Wang ◽  
Tiehong Zhang ◽  
Hongchang Shen ◽  
Wei Dong ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Poor Prognosis

scholarly journals P2.09-32 Detached Epithelial Cell Cluster Size in Lung Adenocarcinoma is a Marker of Poor Prognosis

2018 ◽  
Vol 13 (10) ◽  
pp. S773
Author(s):  
A. Yoshizawa ◽  
K. Kondo ◽  
N. Nakajima ◽  
Y. Teramoto ◽  
M. Rokutan-Kurata ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Lung Adenocarcinoma ◽  
Cluster Size ◽  
Poor Prognosis ◽  
Cell Cluster

scholarly journals LncRNA FAM83H-AS1 Amplification is Associated With a Poor Prognosis in Lung Adenocarcinoma and Can Serve as A Therapeutic Target

2020 ◽  
Author(s):  
Siwei Wang ◽  
Chencheng Han ◽  
Tongyan Liu ◽  
Zhifei Ma ◽  
Mantang Qiu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Therapeutic Potential ◽  
Gene Annotation ◽  
Tumor Xenograft ◽  
Driver Gene ◽  
Clinical Prognosis ◽  
Crispr Interference ◽  
Oncogenic Driver

Abstract Background: Few oncogenic drivers of long noncoding RNAs (lncRNAs) have been identified and investigated. Identifying noncoding drivers provides potential strategies for novel interventions in lung adenocarcinoma (LUAD). Methods: We constructed a machine learning model for driver gene annotation using pan-cancer and clinical prognosis data from OncoKB and TCGA to predict potential oncogenic drivers of lncRNAs; then, we used zebrafish models to validate the biological function of candidate targets. The full length of FAM83H-AS1 was obtained by rapid amplification of the cDNA ends (RACE) assay. RNA pull-down, RNA immunoprecipitation (RIP), quantative mass spectrometry (QMS) and RNA sequencing (RNA-Seq) assays were utilized to explore the potential mechanisms. Additionally, we used CRISPR interference (CRISPRi) system and patient-derived tumor xenograft (PDTX) model to evaluate the therapeutic potential of targeting FAM83H-AS1 in vivo.Results: The results suggested that FAM83H-AS1 was a potential oncogenic driver from the chromosome 8q24 amplicon; increases in the expression of FAM83H-AS1 resulted in poor prognosis for LUAD patients both in JSCH and TCGA cohorts. Functional assays revealed that FAM83H-AS1 promotes malignant progression and inhibits apoptosis. Mechanistically, FAM83H-AS1 binds with HNRNPK to enhance the translation of oncogenes RAB8B and RAB14. Experiments using CRISPR interference (CRISPRi)-mediated xenografts and patient-derived tumor xenograft (PDTX) models indicated that targeting FAM83H-AS1 inhibited LUAD progression in vivo. Conclusions: Our work demonstrated that FAM83H-AS1 is a potential oncogenic driver that inhibits LUAD-mediated apoptosis via the FAM83H-AS1-HNRNPK-RAB8B/RAB14 axis. Importantly, we suggest targeting of FAM83H-AS1 as a potential therapeutic strategy for LUAD.

scholarly journals MUC5AC enhances tumor heterogeneity in lung adenocarcinoma with mucin production and is associated with poor prognosis

2020 ◽  
Vol 50 (6) ◽  
pp. 701-711
Author(s):  
Yujie Dong ◽  
Lijuan Zhou ◽  
Dan Zhao ◽  
Kun Li ◽  
Zichen Liu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Egfr Mutations ◽  
Driver Mutations ◽  
Kras Mutations ◽  
Mucin Production ◽  
Thyroid Transcription Factor 1 ◽  
Thyroid Transcription Factor ◽  
Transcription Factor 1

Abstract Objective The clinicopathological significance of Mucin5AC (MUC5AC) in lung adenocarcinoma with mucin production is still unclear. This study aimed to explore MUC5AC expression in lung adenocarcinoma with mucin production and its correlation with histological subtypes, common driver mutations and its impact on prognosis. Methods MUC5AC and thyroid transcription factor 1 immunohistochemistry was performed on surgical samples from 90 patients with lung adenocarcinoma with mucin production. Common driver mutations including EGFR and KRAS mutations and ALK rearrangement were detected by established methods. Results MUC5AC was significantly associated with lymphovascular invasion (P = 0.023) and tumors with intra-cytoplasmic mucin (P < 0.001). Moreover, MUC5AC was more significant in invasive mucinous adenocarcinoma (P < 0.001), as well as in tumors with KRAS mutations (P = 0.005) and a lack of thyroid transcription factor 1 expression (P < 0.001). Conversely, MUC5AC was less significantly detected in acinar predominant adenocarcinoma (P = 0.036) and tumors with EGFR mutations (P = 0.001). Notably, MUC5AC in non-pure mucinous subtype of lung adenocarcinoma with mucin production showed more aggressive behavior, distinct expression pattern and a lack of significant correlation with thyroid transcription factor 1 (P = 0.113) when compared with pure mucinous subtype. MUC5AC-positive tumors were significantly associated with a worse prognosis compared to MUC5AC-negative tumors (P < 0.001). A multivariate survival analysis showed that MUC5AC was an independent prognosis factor for poor prognosis (P = 0.006). Conclusions The clinicopathological features of non-pure mucinous subtype of lung adenocarcinoma with mucin production were distinct and should be distinguished from pure mucinous subtype. MUC5AC was associated with poor prognosis and could be a potential therapeutic target for this distinct type of lung adenocarcinoma that has few effective treatments.

Low expression of RGL4 is associated with a poor prognosis and immune infiltration in lung adenocarcinoma patients

2020 ◽  
Vol 83 ◽  
pp. 106454 ◽  
Author(s):  
Yidan Sun ◽  
Ying Zhang ◽  
Shiqi Ren ◽  
Xiaojiang Li ◽  
Peiying Yang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Immune Infiltration ◽  
Low Expression
Sign in / Sign up

Export Citation Format

Share Document