Effect of gene on proliferation arrest in a non-small cell bronchopulmonary cancer line

a novel cancer stem cell marker, ALDH1 can be used for tumors whose corresponding normal tissues express ALDH1 in relatively restricted or limited levels such as breast, lung, ovarian or colon cancer

Data show that shRNA against NOTCH3 resulted in a significant decrease in ALDH(+) lung cancer cells, commensurate with a reduction in tumor cell proliferation and clonogenicity.

High ALDH1A1 expression is associated with aggressive lung cancer.

ALDH1 expression is associated with favorable outcome, in non-small cell lung cancer.

loss of ALDH1A1 expression is suggested to promote carcinogenesis especially in the smoking-related lung adenocarcinomas

levels of CD133, CD44, and ALDH1 had independent prognostic value to predict the recurrence of lung adenocarcinoma

The 5-year disease-free survival rate of non-small cell lung cancer patients with high aldehyde dehydrogenase 1 (ALDH1) expression levels in their cancer cells was significantly lower than those with a low ALDH1 level

This meta-analysis shows ALDH1 expression in lung cancer is connected with decreased overall and disease free survival and thus marks a worse prognosis.

High ALDH1 expression is associated with high-grade neuroendocrine carcinoma of the lung.

Results show that over-expression of both ALDH1 and CD133 were only found in non small cell carcinoma and adenocarcinoma (ADC) types of lung neoplasm but only, the low expression of ALDH1 was associated with more aggressive tumor in ADC patients.

Studies suggest that aldehyde dehydrogenase 1A1 (ALDH1A1) may be a stem cell marker in lung cancer (LC) and breast cancer (BC).

We ascertained the presence of strong association between ALDH1A1 expression and both histological subtype & tumor grade of non-small cell lung cancers. We report a fascinating finding; ALDH1A1 heterogeneity within adenocarcinoma can be mapped to its histological patterns.

disulfiram/copper complex targets ALDH1A1 to inhibit non-small cell lung cancer recurrence driven by ALDH-positive cancer stem cells

Results indicate that ALDH1A1 is associated with cisplatin resistance in human lung adenocarcinoma cell line A549/DDP cells, and that activation of the PI3K/AKT signal pathway may be the responsible mechanism.

High expression of ALDH1 is associated with non-small cell lung cancer.

this study identified TAZ as a novel inducer of lung cancer stem cells and the first transcriptional activator of the stem cell marker ALDH1A1

The expression of CD133, but not ALDHA1A, was significantly associated with poorer overall survival (p<0.0001) and shorter disease-free interval (DFI) (p<0.0001) in lung adenocarcinoma

NFATc2 enhances tumor-initiating phenotypes through the NFATc2/SOX2/ ALDH1A1 axis in lung adenocarcinoma.

ALDH1 could drive the stemness of circulating non-small-cell lung carcinoma cells and reduce the survival time of patients.

Aldehyde dehydrogenase 1A1 confers erlotinib resistance via facilitating the reactive oxygen species-reactive carbonyl species metabolic pathway in lung adenocarcinomas.

beta-escin inhibits tobacco carcinogen-induced lung tumor formation by modulating ALDH1A1-positive cells and RhoA/Rock signaling