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Purpose: Aldehyde dehydrogenase 1 (ALDH1) has been identified as a putative cancer stem cell (CSC) marker in lung cancer. However, the clinicopathological and prognostic value of this protein in lung cancer patients remains controversial. Thus, we performed a systematic review and meta-analysis of studies assessing the clinical and prognostic significance of ALDH1 expression in lung cancer.
Methods: An identification and review of publications assessing clinical or prognostic significance of ALDH1 expression in lung cancer until September 1, 2014 was undertaken. A meta-analysis was performed to clarify the association between ALDH1 expression and clinical outcomes.
Results: A total of 14 publications met the criteria and comprised 1926 cases. Analysis of these data showed that ALDH1 expression was not significantly associated with the patient age (OR = 0.82, 95% confidence interval [CI]: 0.45-1.50, P=0.52), tumour size (OR=0.68, 95% CI: 0.22-2.06, P=0.49), smoking status (OR=1.37, 95% CI: 0.85-2.22, P=0.19), or tumour grade (OR=1.65, 95% CI: 0.83-3.26, P=0.15). However, in the identified studies, ALDH1 expression was highly correlated with lymph node metastasis (OR=1.97, 95% CI: 1.16-3.34, P=0.01), tumour TNM staging (OR=1.68, 95% CI 1.28-2.22, P=0.0002), decreased overall survival (relative risk [RR]: 1.97,95% CI: 1.16-3.34, P =0.01) and decreased disease free survival (RR: 1.63, 95% CI: 1.01-2.64, P=0.05).
Conclusions: This meta-analysis shows ALDH1 expression in lung cancer is connected with decreased overall and disease free survival and thus marks a worse prognosis.
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http://dx.doi.org/10.1016/j.hlc.2015.03.021 | DOI Listing |
Genesis
October 2025
Eisai Co. Ltd. Kobe Research Laboratories, Kobe, Japan.
Astrocytes are a major glial cell type, playing multiple roles in the development, function, and pathogenesis of the brain. Accordingly, neuronal-astrocyte communication is an important research area. However, because these cell types share the same developmental origin, selective manipulation of each cell type is needed for precise mechanistic understanding.
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August 2025
Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
This study investigates the interplay between the Atypical chemokine receptors (ACKR1)/Decoy receptor for chemokines (DARC) and key molecular markers, including CCL8, c-MYC, ALDH1, and CHEK2, in breast cancer. DARC has been implicated in various aspects of cancer progression, including tumor growth, angiogenesis, and metastasis. By analyzing the expression patterns of these markers in breast cancer tissues, we aim to understand their collective impact on tumor behaviour and identify potential therapeutic targets.
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August 2025
Herbal and Traditional Medicines Research Center, Kerman University of Medical Sciences, Kerman, Iran.
Combination therapy with chemotherapy and phytochemical drugs is a promising cancer treatment method. In this study, noisome with Tween 20, span 40 and cholesterol in 80:20 ration was prepared for co-delivery of piperine (PIP) and doxorubicin (DOX) (Nio-DOX/PIP) using thin-layer hydration method. Niosomes indicated spherical structure, average size 653 ± 3.
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August 2025
Department of Mathematics, School of Medical Imaging, Hebei Medical University, Shijiazhuang, China.
Aldehyde dehydrogenase 1 family member A1 (ALDH1A1) gene is a member of aldehyde dehydrogenase (ALDH) family, and it is closely associated with cancer metastasis. However, the exact mechanism remains to be clarified. In the present study, we aimed to explore the specific mechanism and role of ALDH1A1 in colorectal cancer (CRC) metastasis.
View Article and Find Full Text PDFMar Drugs
July 2025
Department of Chemistry and Nanoscience, Ewha Womans University, Seoul 03760, Republic of Korea.
The discovery of bioactive natural compounds from microbes holds promise for regenerative medicine. In this study, we identified and characterized a steroid-like compound, 3,12-dioxochola-4,6-dien-24-oic acid (DOCDA), from a crude extract of sp. DOCDA significantly promoted wound healing by enhancing HaCaT cell invasion and migration.
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